http://www.medscape.com/viewarticle/508400


----------------------------------------------------------------------
----------



Mangafodipir Trisodium-Enhanced MRI, Whole-Body FDG-PET Comparable in
Detecting Patients With Liver Metastases


Laurie Barclay, MD;
Medscape Medical News 2005. © 2005 Medscape




July 18, 2005 — In patients with colon and pancreatic adenocarcinoma,
liver magnetic resonance imaging (MRI) with mangafodipir trisodium
enhancement provides more detail of liver metastases, whereas whole-
body fluorodeoxyglucose positron emission tomography (FDG-PET) may
offer additional information regarding extrahepatic disease,
according to the results of a study published in the July issue of
the American Journal of Roentgenology.

"MRI has been shown to be equal in sensitivity and specificity to
[computed tomography] CT arterioportography in the detection of focal
liver lesions," write Dushyant V. Sahani, MD, from Massachusetts
General Hospital in Boston, and colleagues. "PET with fluorine-18 FDG
is established as an important method for staging gastrointestinal
malignancies. A limited number of publications have directly compared
MRI and FDG-PET for the detection of liver metastases."

The investigators retrospectively reviewed imaging data of 34
patients who had undergone mangafodipir trisodium-enhanced liver MRI
and whole-body FDG-PET for the presence and number of liver
metastases. Age range was 44 to 78 years. There were 23 men and 11
women; and 27 patients had adenocarcinoma of the colon whereas seven
had adenocarcinoma of the pancreas. The standard of reference was
histopathology in 25 patients and follow-up imaging in nine patients.

Breathhold T1-weighted gradient-recalled echo, respiratory-triggered
T2-weighted fast spin-echo, and mangafodipir trisodium--enhanced
axial fat-saturated high-spatial-resolution (256 × 512) T1-weighted
gradient-recalled echo images were obtained on a 1.5-T scanner, and
FDG-PET was performed after the injection of 15-20 mCi (555-740 MBq)
FDG.

Based on the gold standard, 30 patients had a total of 79 hepatic
metastases, including 33 lesions that measured less than 1 cm, and
four patients had no hepatic metastases. Per-patient analysis yielded
sensitivities of 96.6% for MRI and 93.3% for FDG-PET, positive
predictive values of 100% and 90.3%, and accuracies of 97.1% and
85.3%, respectively.

Per-lesion analysis revealed sensitivities of 81.4% and 67.0%,
positive predictive values of 89.8% and 81.3%, and accuracies of
75.5% and 64.1%, respectively. MRI detected more hepatic metastases
than did FDG-PET (P = .016), and MRI detected all of the 33 confirmed
subcentimeter lesions, whereas only 12 were detected on FDG-PET (P
= .0001).

"In patients with colon and pancreatic adenocarcinoma, high-spatial-
resolution mangafodipir trisodium-enhanced liver MRI and whole-body
FDG-PET were comparable in the detection of patients with liver
metastases," the authors write. "FDG-PET provided additional
information about extrahepatic disease and was useful in initial
staging. However, significantly more and smaller liver metastases
were detected on MRI than on FDG-PET."

Study limitations include the retrospective nature of the data
collection and analysis, which may introduce inadvertent bias; lack
of histopathologic confirmation in nine patients; inclusion of only
patients who underwent liver MRI, whole-body FDG-PET, and surgery or
followup imaging within six weeks; and inability to determine the
impact on treatment strategy or survival benefit for patients in whom
additional lesions were detected or missed with either technique.

"In patients being considered for liver resection after initial
staging for metastatic disease, the treatment decision should be
based primarily on liver MRI because additional lesions detected on
MRI may alter or preclude such surgery," the authors conclude.

Am J Roentgenol. 2005;185:239-246

Reviewed by Gary D. Vogin, MD


----------------------------------------------------------------------
----------

Expert Interview
Treating Liver Metastases in Colorectal Cancer: An Expert Interview
With Michael Choti, MD



Medscape Hematology-Oncology.  2005; 8 (1):  ©2005 Medscape
Editor's Note
In 2005, it is estimated that more than 104,000 cases of colon cancer
will be diagnosed in the United States alone[1] and that more than
56,000 patients will die of this disease.[1] The liver is the most
common site of colon cancer metastasis, and patients who undergo
resection of liver metastases can have prolonged survival. One
quarter to one third of patients who are able to undergo resection of
liver metastases will live 5 years or longer, and median survival
after resection is between 24 and 40 months.[2] Unfortunately, even
for patients with metastatic disease confined to the liver, not all
liver lesions are resectable, and even after successful resection,
microscopic disease elsewhere can lead to disease recurrence and
death. As novel systemic therapies that are proven to improve
survival in metastatic colorectal cancer emerge,[3] there is
increasing interest in treating patients who are potential candidates
for resection of metastases with preoperative and/or postoperative
chemotherapy.

Dr. Michael Choti and colleagues discussed recent advances and
emerging strategies for the multidisciplinary management of liver
metastases from colorectal cancer in an education session at the 2005
annual meeting of the American Society of Clinical Oncology (ASCO).
[4] In an interview with Medscape, Dr. Choti explains the promise and
limitations of adding chemotherapy to liver surgery and how he
currently approaches patient management in this area.

Medscape: Dr. Choti, this morning you and your colleagues discussed
preoperative, or neoadjuvant, and postoperative, or adjuvant,
chemotherapy for patients with colorectal cancer and potentially
resectable hepatic metastases. If metastatic colorectal cancer is a
systemic disease, what is the rationale for treating metastases to
the liver with local therapy such as surgery?

Dr. Choti: That is an excellent question. We don't know why
necessarily by resecting metastases we improve outcomes and why some
patients can actually be cured, but it does happen. So, number one,
we need to base the rationale for resection on the empiric data
showing that some patients can be cured with surgery alone. Whether
in those selected patients these are the only sites of disease or you
are cytoreducing a tumor down to a volume of disease in which, for
some reason, microscopic residual disease does not progress, we don't
know. This, in particular, is why combining effective systemic
chemotherapy with resection is a theoretically good strategy.

Medscape: In terms of the scope of this problem, what percentage of
patients with metastatic colorectal cancer have liver-only disease
and are potential candidates for resection?

Dr. Choti: It depends on which series is looked at. Approximately two
thirds of patients have liver as their first site of metastatic
disease, but many of these patients also have extrahepatic disease.
Roughly one third of patients who develop metastatic disease appear
to have disease confined to their liver on imaging studies.

Medscape: What percentage of patients with liver-only disease can
undergo resection with current strategies?

Dr. Choti: That varies with the aggressiveness of the surgeon.
Somewhere in the range of one third to one half of patients with
liver-only metastatic disease may be candidates for resection.

Medscape: This morning, you and your colleagues were discussing the
use of preoperative, or neoadjuvant, chemotherapy as one means to
improve outcomes for patients with liver metastases. Can you explain
the rationale behind neoadjuvant chemotherapy?

Dr. Choti: There are a few issues. One is that even in patients with
resectable disease, although we are making dramatic improvements in
long-term outcomes with surgery, many of these patients without any
additional therapy still experience recurrence. The strategy is to
combine effective systemic chemotherapy with surgery to improve
outcomes. Then it becomes primarily a sequencing question. In a
patient with resectable disease, is it preferable to give
chemotherapy upfront and then perform the surgery after assessing
response? Or is it better to resect the disease and then give
chemotherapy postoperatively when there is no residual measurable
disease? We don't know the answer to this question.

As we have discussed at this conference, there are pros and cons to
giving chemotherapy first. In a patient who initially has resectable
disease, the goal is not to give long and extensive treatments with
chemotherapy but to give therapy of a relatively limited duration,
then get the tumor out, and perhaps give more chemotherapy after
surgery. In some patients who have marginally resectable or
unresectable disease, we would need to give chemotherapy first and
consider the option of operating on them if and when their disease
becomes resectable.

In our multidisciplinary conferences, we assess the individual
patient and discuss the best paradigm for any individual patient's
management. First, we think in terms of whether a patient may fit
into a curative intent paradigm or is the goal primarily palliative?
If the patient's disease is unresectable initially but may become
resectable, then we think about them in a curative intent mode and
tailor the strategy with that goal in mind. We attempt to maximize
the response through choice of initial chemotherapy regimen to
improve the chance of resection, at the same time trying to limit
hepatotoxicity, which may make liver surgery more difficult.

If resection is unlikely and we need to consider the overall
treatment as palliative, then we sometimes use the chemotherapy
differently and save regimens to maximize median survival and quality
of life. Occasionally, in patients in whom we have initially thought
treatment was palliative, we have been dramatically surprised by
response to therapy and are able shift the strategy to a curative
intent and consider liver resection or ablation. Similarly, when a
patient who we initially believe has resectable disease progresses
during preoperative chemotherapy and develops unresectable disease,
palliation is the primary goal.

Medscape: Are there factors that you can use to predict who is likely
to benefit from a curative approach? Do we have markers of
sensitivity that can help determine who is likely to respond to
neoadjuvant chemotherapy?

Dr. Choti: There are a variety of factors, some of which are related
to chemotherapy and chemosensitivity. Many are related to factors
such as the number and location of the metastatic disease within the
liver and elsewhere. Other factors, such as disease-free interval,
the histology of the primary tumor, and nodal status of the primary
tumor, also have prognostic implications. We consider a response to
chemotherapy as another favorable prognostic factor. Perhaps, in the
future, we will have methods such as tumor expression profiling,
proteomics, and molecular genetics to more accurately predict which
patients will derive the greatest benefit from aggressive liver
surgery and chemotherapy.

Medscape: You mentioned that chemotherapy can be administered before
surgery, after surgery, or both before and after surgery. Do we know
or are there studies planned to clarify whether the timing of therapy
affects survival or other end points in treating colorectal cancer
patients with liver metastases?

Dr. Choti: We do not currently have studies to answer this question.
In rectal cancer, we know that preoperative therapy can control local
disease and allow us to limit the extent of resection. In metastatic
colorectal cancer, we don't have information on how timing of
chemotherapy affects outcomes, but we are interested in these
questions. There is an EORTC [European Organization for Research
Treatment of Cancer] trial that I believe has completed accrual in
which they are looking at preoperative and postoperative chemotherapy
vs no chemotherapy, but this may only answer the question of whether
chemotherapy helps. It does not compare preoperative vs postoperative
chemotherapy.

In patients with resectable disease, we do not know whether
neoadjuvant chemotherapy is beneficial. There are trials under
development that will attempt to answer this question. We hope to
have a trial like this under way in the near future. Right now there
are theoretical reasons to consider chemotherapy before or after
resection. I believe that the strategy at present should be to
increase awareness of the potential role of systemic therapy and the
understanding that the optimal way to manage patients with liver
metastases may be the combination of surgery and chemotherapy,
however it is given.

Medscape: This suggests that good communication between medical
oncologists and surgical oncologists is an important factor in the
care of these patients. To what extent do you think adequate
communication is occurring today?

Dr. Choti: I think this is a very important point. Multidisciplinary
management is important when considering options. Medical oncologists
need to have an understanding of when disease is resectable and when
surgery should be offered. Similarly, the surgical oncologist or
liver surgeon needs to have a comprehensive understanding of the
various chemotherapeutic options available, including the benefit and
potential toxicities. I believe that sessions such as the discussion
of this topic this morning at ASCO are aimed at improving
communication and understanding. Providers need to appreciate that,
although we cannot cure many patients, there should no longer be an
automatic nihilistic approach to all patients with metastatic
disease. We need to integrate chemotherapy and surgery in
aggressively selected patients with advanced colorectal cancer.

I believe surgeons are developing a real understanding of the role of
chemotherapy, and this needs to be brought into the mainstream of
surgical education.

Medscape: Is neoadjuvant chemotherapy for patients with liver
metastases from colorectal cancer ready for the clinic?

Dr. Choti: There are several theoretical advantages to preoperative,
or neoadjuvant, chemotherapy.

One advantage of giving chemotherapy upfront is that we can determine
whether the tumor is responsive or not before resection, as opposed
to simply giving chemotherapy empirically after resection.

Additionally, in selected cases there may be progression if there is
a biologically aggressive tumor. Identification of this subset
preoperatively can spare a patient surgical resection, which is
unlikely to be beneficial.

Another reason is that giving systemic therapy earlier theoretically
may improve outcomes as the chemotherapy is started earlier. Finally,
a response from preoperative chemotherapy may reduce the size of
liver metastases, allowing for less extensive surgery.

The theoretical disadvantages include the possibility that a patient
who has initially resectable disease could progress to an
unresectable situation. Although this is uncommon, losing the window
of opportunity to attempt curative therapy is unfortunate. However,
as I mentioned in my discussion this morning, patients whose tumors
progress during chemotherapy are probably not those who are going to
do well even if they undergo resection.

In addition, chemotherapy can result in hepatotoxicity, particularly
when administered for prolonged duration. This liver steatosis, if
severe, can in fact decrease rather than increase resectability and
may actually make the liver resection riskier. What type of
chemotherapy -- and for what duration -- is associated with increased
hepatotoxicity is not clear. We have even less information on newer
biologic agents such as bevacizumab, which may also affect wound
healing or liver regeneration. I think we don't have enough
information regarding these issues at this time, but many of us are
trying to shed light on this subject. Let's wait and see.

There are currently no clinical trials open asking these questions,
so we manage our patients selectively. In some we offer preoperative
chemotherapy, and in some we go right to surgery first, depending on
various factors. In patients who are chemo-naive with multiple
metastases and stage 4 disease at presentation, we may be more
inclined to offer chemotherapy upfront. If a patient is marginally
resectable, in which case a response would improve the outcome of
resection, we may be aggressive about giving chemotherapy upfront as
well. If a patient has comorbidities or there is concern about
chemotherapy causing hepatotoxicity in a patient who will require a
large resection, I may be more inclined to go to surgery first.

The other factor we consider is whether a patient has been exposed to
chemotherapy or not, either in the metastatic setting or in the
adjuvant setting. If a patient has received adjuvant chemotherapy for
his or her primary disease and disease recurred early, then we may be
less inclined to use neoadjuvant or adjuvant chemotherapy with
resection of liver metastases.

Medscape: What are the next steps we need to take in this field in
terms of research?

Dr. Choti: There are several important issues. With rapidly changing
options for chemotherapy, including the combination of cytotoxic
agents and biologic therapies, we need to define the optimal regimens
in various clinical scenarios. We need to consider how we integrate
the biologics with chemotherapy, what cytotoxic regimens we use, and,
as we've discussed, the sequencing of therapy needs to be worked out.

In terms of the biologics, there are additional questions. For
example, bevacizumab presents potential issues regarding
administration around the time of extensive surgery. We don't know if
this will have an impact on wound healing, bleeding, or liver
regeneration. These questions will be emerging in the context of the
multimodality approach to patients with liver metastases.

An additional important issue regarding neoadjuvant chemotherapy is
how do we manage the type of resection, particularly in patients who
had unresectable disease and then responded. Do you need to resect
the volume of tissue in which the initial disease resided or can you
only take the nidus of residual disease? Does a tumor respond
circumferentially? We don't really understand how much one needs to
resect. Currently, we try to resect all sites within the liver that
contained disease, but this needs to be more clearly defined.

Response to initial therapy raises additional questions. If the
patient responds, we typically use the same regimen after surgery. If
the patient's cancer progressed or even if it is stable disease,
should we offer a different chemotherapy regimen in the postoperative
adjuvant setting, or should we not offer any chemotherapy? This is
completely unknown and requires further investigation.

What is the final word? Well, this is an exciting and evolving time
for patients with advanced colorectal cancer and physicians treating
them, but we have many unanswered questions. Stay tuned.

References
Jemal A, Murray T, Ward E, et al. Cancer statistics, 2005. CA Cancer
J Clin. 2005;55:10-30.
Choti MA, Sitzmann JV, Tiburi MF, et al. Trends in long-term survival
following liver resection for hepatic colorectal metastases. Ann
Surg. 2002;235:759-766.
Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus
irinotecan, fluorouracil, and leucovorin for metastatic colorectal
cancer. N Engl J Med. 2004;350:2335-2342.
Choti MA. Treatment of liver metastases: what are the limits? what
are the goals? Management of hepatic colorectal metastases. Proc Soc
Am Clin Oncol. 2005:302-306. Education Session.


Funding Information

Supported by an independent educational grant from Sanofi-Aventis.



Michael Choti, MD , Associate Professor of Surgery and Oncology, The
Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins,
Baltimore, Maryland


Disclosure: Jeffrey Peppercorn, MD, MPH, has no disclosed no relevant
financial relationships.

Disclosure: Michael Choti, MD, has disclosed no relevant financial
relationships.

Last Updated: June 09, 2005



NEW YORK (Reuters Health) - The combination of bevacizumab (Avastin),
fluorouracil, and leucovorin is effective in previously untreated
patients with metastatic colorectal cancer, according to a recent
report. "This is first direct test of the value of adding a
traditional cytotoxic versus adding a novel targeted agent on top of
a simplified platform of chemotherapy," Dr. Herbert I. Hurwitz told
Reuters Health.


Dr. Hurwitz from Duke University Medical Center in Durham, North
Carolina, and colleagues compared outcomes of 210 patients with
metastatic colorectal cancer treated either with the anti-VEGF
monoclonal antibody bevacizumab plus fluorouracil and leucovorin
(FU/LV/BV) or the combination of irinotecan, fluorouracil and
leucovorin (IFL).

The efficacy of the two regimens was similar, the investigators
report in the May 20th Journal of Clinical Oncology.

Median survival in patients treated with FU/LV/BV was 18.3 months,
the authors report, and in patients treated with IFL it was 15.1
months (p=0.25).

Median progression-free survival was also nonsignificantly higher in
patients treated with FU/LV/BV (8.8 months) than in patients treated
with IFL (6.8 months), the report indicates.

The percentage of patients with any grade 3 or 4 adverse event was
lower for FU/LV/BV (77.1%) than for IFL (81.6%), the results indicate.

A higher percentage of patients in the FU/LV/BV group had adverse
events causing withdrawal from the study and more FU/LV/BV patients
died from any cause within 60 days after randomization, the report
indicates, but adverse events leading to hospitalization occurred
with equal frequency in the two treatment arms.

"These data suggest modulating the targeted agents may be not only
less toxic, but may provide as much if not more anti-tumor activity
than adding cytotoxic agents," Dr. Hurwitz said. "This suggests one
approach to the development of new treatments will be to maximize
novel targeted agents upon a simplified chemotherapy platform."

This approach "needs clinical validation," Dr. Hurwitz
added. "Studies moving in this direction are now ongoing."





----------------------------------------------------------------------
----------

www.asco.org

Study published showing statins reduce risk of colorectal cancer
  Last Updated: May 25, 2005



NEW YORK (Reuters Health) - In a case-control study, the use of
statins for at least five years apparently halved the risk of
developing colorectal cancer. The findings are published in The New
England Journal of Medicine for May 26, but were reported last June
at a medical convention. This is the report filed at the time:


NEW ORLEANS, June 7, 2004 (Reuters Health) - In a population-based,
case-control study conducted in Israel, statin use was associated
with a 46% reduction in the risk of colorectal cancer (CRC) in
adjusted analyses.

These findings, reported at the 40th annual meeting of the American
Society of Clinical Oncology, support prior studies showing that HMG-
CoA reductase inhibitors have antitumor effects.

At a briefing with reporters, Dr. Stephen B. Gruber of the University
of Michigan said, "these observational data suggest that statins
deserve further investigation in chemoprevention and therapeutic
clinical trials."

The study involved 1849 Israeli colorectal cancer patients and 1959
healthy controls matched for age, gender, and ethnicity. Statin use,
most often pravastatin or simvastatin, was more common in controls
(11.3%) than in CRC cases (5.8%).

"In our study, use of statins for at least 5 years was associated
with a 51% reduction in the risk of colorectal cancer, with an odds
ratio of 0.49," Dr. Gruber reported. This association remained
largely unchanged in analyses adjusting for age,
hypercholesterolemia, ethnicity, aspirin or NSAID use, and APC
mutations, with an odds ratio of 0.54.

The use of non-statin cholesterol-lowering agents, such as fibrates,
was not associated with reduced risk of colorectal cancer, suggesting
that the protective effect is specific to statins.

Mechanistic studies provide support for the antitumor effects of
statins, Dr. Gruber said. "We know that statins inhibit RAS and RhoA,
two proteins that are potentially carcinogenic," he said.

In the current New England Journal, two editorialists hope the study
findings might move medicine beyond the "one drug, one disease"
model. "It's tempting to think," they say, "that systemically
targeting multiple diseases common to aging is not only theoretically
feasible but within our reach."

Does anyone knows that Herbal Medicines - Curcuma Zedoaria can prevent cancer ?

Thanks everyone.


---------------------------------
Yahoo! Mail Mobile
  Take Yahoo! Mail with you! Check email on your mobile phone.

[Non-text portions of this message have been removed]

Sperm may hold key to cancer, chimp study suggests
  Last Updated: May 19, 2005



WASHINGTON (Reuters) - The evolutionary path that separated humans
from chimps 5 million years ago may have made human sperm survive
better but paradoxically may have made humans prone to cancer.


A comparison of chimpanzee genes to human genes shows a concentration
of genes unique to people in areas associated with sperm production
and cancer, and suggests the changes that make humans unique also
make us uniquely prone to cancer.

"If we are right about this, it may help explain the high prevalence
of cancer," said Rasmus Nielsen of the University of Copenhagen in
Denmark, who led the study while at Cornell University in New York.

Nielsen and colleagues were studying the chimpanzee genome, the
collection of all DNA, for clues about what make chimps and humans
different. They used genetic sequences published by Maryland-based
Celera Corp.

For the report, published in the journal Public Library of Science
Biology, Nielsen's team at Cornell studied the 13,731 genetic
sequences that are the most different between humans and chimps.

They knew that genes having to do with smell, making sperm and
fighting bacteria and viruses were likely to be different.

"While we expected to find genes involved in olfaction,
spermatogenesis, and immune defense among the 50 annotated genes ...
we were surprised to find a very large proportion of cancer-related
genes, especially genes involved in tumor suppression, apoptosis, and
cell cycle control sequences," they wrote.

"It is surprising to find such a large proportion of genes that may
be related to tumor development and control."

In cancer, cells lose their ability to self-destruct when they become
faulty, a process called apoptosis. Cell cycling -- the process by
which cells activate, divide, and grow into two separate cells -- is
also disrupted in cancer.

"Eliminating cancer cells by apoptosis is one of the main processes
used by the organism to fight cancer," Nielsen said.

"The connection that we saw that these genes involved in
proliferation may be involved in spermatogenesis," Cornell's Andrew
Clark, who worked on the study, said in a telephone interview.

Apoptosis also kills many developing sperm cells before they mature.
But evolution could have interfered with this process, allowing more
sperm to reach maturity, thus carrying the mutation into the next
generation.

Clark said chimpanzees get cancer, too, but no one has been able to
study enough of them in captivity to see if they do so at the same
rate and in the same ways as humans do.

Cancer in people usually occurs in late adulthood, after they have
reproduced, and thus has not been removed by natural selection -- the
process that leads to evolution.

Radiofrequency Ablation: A New Revolution in the Treatment of Cancer
Jason R. Williams M.D.



Radiofrequency ablation (RFA) is a therapy that is gaining
significant ground in the treatment of cancer. The technique
involves inserting a needle under the guidance of computed
tomography (CT). The needle is placed directly into the tumor. A
radiofrequency is then sent through the needle. This RF energy
generates heat, which destroys the tumor. There is no radiation
involved, except for that from the CT scanner. Some patients can go
home the same day of treatment. Most patients will be observed
overnight.

There are many tumors which can be treated successfully with RFA.
Liver tumors are the most common. However, RFA is now being
performed in other areas of the body, such as the lungs, bones, and
adrenal glands. This offers a new treatment modality for a large
number of cancer patients.

The Treatment of Lung Tumors
There are many types of cancers that are found in the lungs. The
most common group of tumors that originate here are the non-small
cell type. The surgical resection of tumors generally gives the
patient the best hope for successful treatment. However, surgery is
associated with significant morbidity and mortality. For this reason
the majority of the patients diagnosed with lung cancer are not
considered surgical candidates.

RFA can be used to treat many tumors which cannot be removed
surgically. Patients may also consider RFA instead of an invasive
surgery. The recovery time is less, allowing patients to
aggressively continue chemotherapy.

Metastatic Cancer to the Lungs
Many types of tumors frequently spread to the lungs. This commonly
occurs in breast and colon cancer. The development of tumor
metastasis to the lungs is also a common problem for patients with
sarcomas. When the cancer spreads to the lungs, the prognosis is not
good. Metastatic tumors to the lung can be treated with RFA in the
same manner as primary lung tumors.

Liver Tumors
Radiofrequency ablation has been successfully used for many years in
the treatment of liver tumors. This includes primary (tumors that
originated in the liver), and metastatic tumors (tumors that have
spread to the liver). Patients treated with RFA recover much faster
than patients treated with a surgical resection. This success
prompted the FDA to approve the use of RFA for these tumors.

Other Tumors
RFA can be used in the treatment of certain bone tumors. This is
particularly helpful in relieving painful tumors. RFA can also be
used to successfully treat some tumors of the kidneys and adrenal
glands. Tumors located in the retroperitoneal area (such as some
sarcomas) can be treated with RFA as well.

Overview of RFA of Cancer
Radiofrequency ablation is an effective treatment for many types of
tumors, particularly in the lung and liver. Because of this success,
RFA is no longer considered an experimental therapy.

The treatment is quick and minimally invasive. The complication rate
is significantly less than that of surgery. With a simple needle
stick, all or a large amount of tumor can be destroyed using RFA.
The procedure is similar to a biopsy.

The treatment can be done using IV sedation only. The recovery time
is quick, thus allowing patients to feel well enough to immediately
begin chemotherapy. Patients may even have RFA while actively
receiving chemotherapy. RFA does not interfere with most standard
cancer therapies. Most insurance companies provide coverage for the
procedure, and most patients will require only an overnight stay in
the hospital.

In cases where the tumors cannot be entirely ablated, there is still
improvement in the patient's prognosis because of reduced tumor
burden. The RFA treatment can add a significant length of time to
the patient's life. In some patients it is possible to ablate all
visible tumor. These patients can potentially obtain a cure, when
there would have otherwise been little hope.

Jason R. Williams M.D.
The American Institute for Cancer Ablation
Gulf Shores, Alabama
jasonwilliams@...
www.cancerablation.com

See also Radiofrequency Ablation: A Minimally Invasive Technique For
Treating Cancer
Radiofrequency Ablation: A Minimally Invasive Treatment that is
Effective for Both Large and Small Tumors

Hello friends,
Some are saying that they didn't get the cancer STUDIES.

Here they are again. If you get them twice I am sorry.

Almost one out of every two people is expected to get cancer during
their lifetime.

Just about all of us have a LOVE ONE that has suffered from it.

I am sharing SEVEN, that's right SEVEN SCIENTIFIC STUDIES from
various Countries. About LIMU MOUI,S FUCOIDAN and Cancer.

Tou will want to save this letter. Print it out. Show it to your
Doctor. You will find that Many Doctors haven't heard about them.
They are FASCINATING!

You will begin to understand ,maybe, why it is that we get GLOWING
testimonies from cancer patients.

LOOK THESE OVER. Then Get Some Limu Moui NOW!

I HATE HYPE. You know how I always let the Scientists speak for
themselves. The scientific  minded will have little problem
understanding the studies.



REMEMBER, you can always SKIP to the scientists CONCLUSION. It,s
always fairly clear. You also can print this out , or email it to
your DOCTOR.



Once you see and understand the studies, you may want to get LIMU
MOUI AS SOON AS POSSIBLE. I will show you 2 ways right now.



     TO GET LIMU do  EITHER one below:



1. CALL (407)804-1931 and use ID 7649701

                  OR
2.http://ginasgift.originallimu.com/

                  OR

3. To hear more about Limu with FUCOIDAN go here and hear what it has
done for others:  http://www.angelfire.com/ar/maybe4u2/limu.html

          NOW THE AMAZING STUDIES


Antitumor activity and immunological properties of marine algal
polysaccharides, especially fucoidan, prepared from Sargassum
thunbergii of Phaeophyceae.



Itoh H, Noda H, Amano H, Zhuaug C, Mizuno T, Ito H.



Laboratory of Marine Biochemistry, Faculty of Bioresources, Mie
University, Japan.



Marine algal polysaccharide, GIV-A from Sargassum thunbergii markedly
inhibited the growth of Ehrlich ascites carcinoma at the dose of 20
mg/kg per day X10 with no sign of toxicity in mice. GIV-A is
suggested to be a hexouronic acid containing L-fucan sulfate,
fucoidan by the analyses of physicochemical properties and IR- and
NMR-spectra. The results of carbon clearance activity with fucoidan
demonstrated that it is acting as a so-called activator of the
reticuloendothelial system. Fucoidan enhanced the phagocytosis and
chemiluminescence of macrophages. By the immunofluorescent method,
binding of the third component of complement (C3) cleavage product to
macrophages and the proportion of C3 positive cells were increased.
In crossed immunoelectrophoresis, human serum C3 was converted by
fucoidan and appeared as the 3rd peak (converted C3). The height of
the 3rd peak was directly proportional to the doses of fucoidan. The
residual CH50 units of human serum decreased dose-dependently. These
results suggest that the antitumor activity of fucoidan is related to
the enhancement of immune responses. The present results indicate
that fucoidan may open new perspectives in cancer chemotherapy.



PMID: 8297113 [PubMed - indexed for MEDLINE]












Polysulfated heparinoids selectively inactivate heparin-binding
angiogenesis factors.



Zugmaier G, Favoni R, Jaeger R, Rosen N, Knabbe C.



Department of Hematology/Oncology, Philipps-University, Marburg,
Germany.



Angiogenesis is a prerequisite for tumor expansion and metastasis.
The angiogenic potential of the heparin-binding growth factors acidic
fibroblast growth factor (FGF) and basic FGF has been demonstrated in
various publications. We studied the inhibitory effects of suramin
and the polysulfated heparinoids pentosan polysulfate, dextran
sulfate, and fucoidan on the action of FGF. As an experimental model,
we used the adrenal cancer cell line SW 13, whose anchorage-
independent growth depends on the presence of FGF. The polysulfated
heparinoids inhibited FGF-induced growth and binding to the receptor
at an IC50 of 0.5-3 micrograms/ml. Suramin inhibited FGF at an IC50
of 100 micrograms/ml. The polysulfated heparinoids exerted no effect
on IGF-1 or TGF alpha-related growth. Suramin inhibited the anchorage-
independent growth induced by IGF-1 or TGF alpha only at an IC50 of
100 micrograms/ml. Our results indicate that suramin inhibits growth
factors in a nonselective way. By contrast, polysulfated heparinoids
exert a selective inhibitory effect on heparin binding angiogenesis
factors at an IC50, which is 100 times below the IC50 of suramin.
Therefore, the administration of polysulfated heparinoids might
become a novel approach to tumor therapy based on blocking
angiogenesis.



PMID: 10667230 [PubMed - indexed for MEDLINE]








Antitumor and antiproliferative effects of a fucan extracted from
ascophyllum nodosum against a non-small-cell bronchopulmonary
carcinoma line.



Riou D, Colliec-Jouault S, Pinczon du Sel D, Bosch S, Siavoshian S,
Le Bert V, Tomasoni C, Sinquin C, Durand P, Roussakis C.



ISOMer (Institut des Substances et Organismes de la Mer), SMAB,
Laboratoire de Pharmacologie Marine, Faculte de Pharmacie, Nantes,
France.



Fucans, sulfated polysaccharides extracted from brown seaweeds, have
been shown to be endowed with inhibitory effects cell growth in
various experimental models. We studied both the antiproliferative
and antitumor properties of a fucoidan extract (HF) obtained from the
brown seaweed Ascophyllum nodosum on a cell line derived from a non-
small-cell human bronchopulmonary carcinoma (NSCLC-N6), this type of
carcinoma is particularly chemo-resistant. HF exerts in vitro a
reversible antiproliferative activity with a block observed in the G1
phase the cell cycle. Studies performed with the NSCLC-bearing nude
mice show antitumor activity at subtoxic doses. These preliminary
results indicate that HF exhibits inhibitory effect both in vitro and
in vivo and is very potent antitumor agent in cancer therapy.



PMID: 8702239 [PubMed - indexed for MEDLINE]







Immunological analysis of inhibition of lung metastases by fucoidan
(GIV-A) prepared from brown seaweed Sargassum thunbergii.



Itoh H, Noda H, Amano H, Ito H.



Laboratory of Marine Biochemistry, Faculty of Bioresources, Mie
University, Tsu, Japan.



The antimetastatic effect of GIV-A (fucoidan) and/or 5-FU was
examined in an experimental model of lung metastases induced by Lewis
lung carcinoma in mice. Injection of GIV-A i.p. after removal of the
implanted primary tumor inhibited the development of lung metastases.
Combination treatment with GIV-A and 5-FU inhibited significantly the
lung metastases. The number of peritoneal macrophages, total cells
and macrophages in the lung increased in mice treated with GIV-A.
Binding of the third component of complement (C3) cleavage products
(C3b) to the C3 receptor on peritoneal macrophages after i.v.
injection of GIV-A was enhanced, as shown by the fluorescent antibody
technique. Lung metastases were inhibited by i.v. injection of
peritoneal macrophages activated with GIV-A. GIV-A depressed aniline
hydroxylase and aminopyrine demethylase activities of the hepatic
microsomal drug-metabolizing system in tumor-bearing mice. Moreover,
the concentration of 5-FU in the tissues (lung, liver, kidney, spleen
and blood) was increased significantly by coadministration of GIV-A.
The picryl chloride-induced delayed type hypersensitivity (PC-DTH)
response in mice was depressed after the implantation of tumor and
treatment with 5-FU. GIV-A restored the suppression of PC-DTH by 5-
FU, but did not increase the PC-DTH of normal mice. GIV-A not only
enhanced the degree of spleen cell-mediated sheep red blood cell
(SRBC) hemolysis (quantitative hemolysis of SRBC), the indexes of the
spleen and thymus and the number of spleen cells, but also restored
the suppressive effect of 5-FU. In the group receiving GIV-A, the
percentages of splenic Thy1.2-, L3T4- and asialo GM1-positive cells
were significantly increased as compared with the tumor-bearing mice
treated with saline. Furthermore, the L3T4+/Lyt2+ ratio showed a
tendency to increase, and the Lyt2+/Thy1.2+ ratio was decreased.
These results suggest that the antitumor effect of GIV-A may be
correlated with the changing pattern of the Thy1.2-, L3T4- and asialo
GM1-positive cells, C3 activation, macrophage activation and
depression of the hepatic microsomal drug-metabolizing system. These
findings raise the possibility that GIV-A may have clinical value in
the prevention of cancer metastasis.



PMID: 8572581 [PubMed - indexed for MEDLINE]








Antitumor active fucoidan from the brown seaweed, umitoranoo
(Sargassum thunbergii).



Zhuang C, Itoh H, Mizuno T, Ito H.



United Graduate School of Agricultural Sciences, Gifu University
(Shizuoka University), Japan.



Neutral and acidic polysaccharides and their protein complexes were
fractionated and purified from the brown seaweed umitoranoo
(Sargassum thunbergii) by fractional extraction, iron-exchange
chromatography, and gel filtration. Thirty-one polysaccharide
fractions were obtained and tested for antitumor activity in mice
with Ehrlich carcinoma transplanted i.p. Two of the fractions, GIV-A
([alpha]25D -127 degrees and mol. wt., 19,000) and GIV-B ([alpha]25D -
110 degrees and mol. wt., 13,500) had such activity. On the basis of
chemical and spectral analyses, these compounds were found to be a
fucoidan or L-fucan containing approx. 30% sulfate ester groups per
fucose residue, about 10% uronic acid, and less than 2% protein.



PMID: 7772818 [PubMed - indexed for MEDLINE]








Inhibitory effect of oversulfated fucoidan on invasion through
reconstituted basement membrane by murine Lewis lung carcinoma.



Soeda S, Ishida S, Shimeno H, Nagamatsu A.



Department of Biochemistry, Faculty of Pharmaceutical Sciences,
Fukuoka University.



We investigated the effects of native, oversulfated, and desulfated
fucoidans and heparin on the invasion of 3 LL cells through Matrigel.
Of the four polysaccharides tested, oversulfated fucoidan was the
most potent inhibitor of tumor cell invasion and inhibited most
potently and specifically the tumor cell adhesion to laminin. Sodium
dodecyl sulfate-polyacrylamide gel electrophoretic analysis of the
binding of elastase-cleaved laminin to fucoidan- and heparin-
Sepharoses showed that both polysaccharides bound to the 62 and 56
kDa fragments. Pretreatment of 3LL cells with native or oversulfated
fucoidan reduced their adhesive potency to laminin. The two fucoidans
inhibited further the laminin binding of 3 LL cells which had been
pretreated with a laminin-based pentapeptide, YIGSR. These results
suggest that fucoidan specifically binds to not only the heparin
binding domain(s) of laminin but also site(s) other than the cell
surface laminin receptor. 3 LL cells secreted a 50 kDa form of
urokinase-type plasminogen activator (u-PA). The extracellular level
of u-PA activity was increased 1.7 times by addition of laminin but
not type IV collagen. Oversulfated fucoidan most potently reduced the
increased u-PA levels. Therefore, the reduction in in vitro
invasiveness of 3 LL cells in response to either fucoidan or its
oversulfated derivative may result from an inhibition of physical
interaction between the tumor cells and the Matrigel (laminin),
followed by a suppression of the laminin-induced increase in
extracellular u-PA.



PMID: 7829400 [PubMed - indexed for MEDLINE]







Blocking of lectin-like adhesion molecules on pulmonary cells
inhibits lung sarcoma L-1 colonization in BALB/c-mice.



Roszkowski W, Beuth J, Ko HL, Uhlenbruck G, Pulverer G.



National Institute of Lung Diseases and Tuberculosis, Warsaw, Poland.



Adhesion and inhibition experiments with pulmonary cells of BALB/c-
mouse origin and syngeneic sarcoma L-1 cells indicated that L-fucose
specific lectin-like adhesion molecules, presumably situated on
pulmonary cell surfaces are (at least partly) responsible for the
specificity of this cell-cell interaction. Addition of specific
sugars and glycoconjugates (L-fucose and fucoidan, respectively) to
the incubation medium evidently inhibited the adhesion process as
quantified using radiolabelled tumor cells. Unspecific carbohydrates
(e.g. D-galactose) did not affect the cellular interaction. In vivo,
repeated administration of fucoidan (but not of unspecific
glycoconjugates) significantly inhibited the settling of metastatic
sarcoma L-1 cells in the lungs of BALB/c-mice. Therefore, when lectin-
like adhesion molecules on pulmonary cells were blocked with
competitive glycoconjugates, tumor cell colonization of the lung
could be significantly inhibited.



PMID: 2737266 [PubMed - indexed for MEDLINE]



+++++++++++++++++++++++++++++++++++++++++++++++++++++++
To read some MORE scientific study summaries ABOUT OTHER  ILLNESSES
go here: http://www.angelfire.com/ar/maybe4u2/limu.html or email me
at gina1906@...
_______________________________________________________



  Have a wonderful weekend
http://www.angelfire.com/ar/maybe4u2/limu.html

The latest British health service guidelines on triple therapy with
irinotecan, oxaliplatin and raltitrexed for palliative treatment of
advanced colon cancer:
http://www.nice.org.uk/page.aspx?o=98342

Interesting document links are at the bottom of the page, so do scroll
down. There is quite a good overview at:
http://www.nice.org.uk/page.aspx?o=250578


- Darren



The content of this email is confidential and for the
addressee only. If you are not the addressee of this
email (or responsible for the delivery of this message
to such person) you may not copy, forward, disclose
or otherwise use it or any part of it in any form
whatsoever. If you have received this email in error
please email the sender by replying to this message
and delete this message thereafter.

Opinions, conclusions and other information in this
message that do not relate to the official business
of our Company shall be understood as neither
given nor endorsed by it.

Since colon cancer often metastasises to the liver, readers (especially
British) may find this interesting:
http://www.nice.org.uk/ipcat.aspx?o=239507

The most common indication for laparoscopic liver resection is a
solitary liver metastasis from a colorectal cancer, but it may also be
used for hepatocellular carcinoma (HCC) and for benign liver tumours or
cysts.

Open surgical resection, to remove the affected part of the liver, is
the standard treatment for patients with localised colorectal liver
metastases and HCC. This procedure is performed through a large incision
across the abdomen. A number of alternative therapies have also been
developed, including hepatic artery infusion chemotherapy, percutaneous
ethanol injection, cryoablation, microwave coagulation therapy,
laser-induced thermotherapy, and radiofrequency ablation.

Benign liver tumours are usually treated only if they are causing
symptoms. The standard treatment is open surgical resection.

Laparoscopic liver resection is performed under a general anaesthetic.
The abdomen is insufflated with carbon dioxide and a number of small
incisions are made to provide access for the laparoscope and surgical
instruments. The resected liver is enclosed in a bag and removed,
through a small incision in the umbilical area.

Hand-assisted laparoscopic liver resection allows the surgeon to place
one hand in the abdomen while maintaining the pneumoperitoneum required
for laparoscopy. An additional small incision is made which is just
large enough for the surgeon's hand and an airtight 'sleeve' device is
used to form a seal around the incision.


- Darren



The content of this email is confidential and for the
addressee only. If you are not the addressee of this
email (or responsible for the delivery of this message
to such person) you may not copy, forward, disclose
or otherwise use it or any part of it in any form
whatsoever. If you have received this email in error
please email the sender by replying to this message
and delete this message thereafter.

Opinions, conclusions and other information in this
message that do not relate to the official business
of our Company shall be understood as neither
given nor endorsed by it.

Hello,

I am new to this group and thought I'll share the Health Listing of
hi-fiweb.
To get the complete health listing you may go to
http://www.hi-fiweb.com/health

Good day!
Kathy

Cancer Information From CancerConsultants.com

This article can be viewed at
http://patient.cancerconsultants.com/print_tnpv.aspx?id=691

Stage IV Colon Cancer
Overview
Colon cancer is classified as stage IV (D) if the final evaluation
following surgical removal of the cancer shows that the cancer has
spread to distant locations in the body, which may include the
liver, lungs, bones, or other sites. The common perception is that
patients diagnosed with stage IV colon cancer have few treatment
options.  However, certain patients can still be cured of their
cancer, and others derive significant benefit from additional
treatment.

Patients with stage IV colon cancer can be broadly divided into two
groups:

Those with cancer that has metastasized to a single site , and
Those with unresectable cancer , or cancer that cannot be treated
with surgery.
When the site of metastasis is a single organ, such as the liver,
and the cancer is confined to a single defined area within the
organ, patients may benefit from local treatment directed at that
single metastasis.

The majority of patients have unresectable or widespread disease.
Historically, these patients have been considered incurable and were
offered treatment with chemotherapy for the purpose of prolonging
their survival and alleviating symptoms from progressive cancer. New
chemotherapy combinations have lead to increased survival.
Combinations approved in early 2004 include:

Eloxatin®/5-FU/LV
AvastinT/5FU/LV
Treatments that are currently being evaluated include the oral
chemotherapy drug Xeloda® (capecitabine), vaccines, and the
monoclonal antibody ErbituxT (cetuximab), which was approved in
early 2004 for recurrent colon cancer and may be available to
patients with stage IV disease through a clinical trial.

The following is a general overview of treatment for stage IV colon
cancer. Treatment may consist of surgery, radiation, chemotherapy,
biological therapy, or a combination of these treatment techniques.
Multi-modality treatment, which is treatment using two or more
techniques, is increasingly recognized as an important approach for
increasing a patient's chance of cure or prolonging survival. In
some cases, participation in a clinical trial utilizing new,
innovative therapies may provide the most promising treatment.
Circumstances unique to each patient's situation may influence how
these general treatment principles are applied. The potential
benefits of multi-modality care, participation in a clinical trial,
or standard treatment must be carefully balanced with the potential
risks. The information on this website is intended to help educate
patients about their treatment options and to facilitate a mutual or
shared decision-making process with their treating cancer physician.

Treatment of Unresectable Stage IV Colon Cancer
For over 30 years, single-agent fluorouracil (5-FU) chemotherapy
with or without leucovorin (LV) was the standard treatment for non-
localized stage IV colon cancer. In 2001, Camptosar®/5-FU/LV was
found to significantly improve patient outcomes and became the new
standard treatment.[1]Significant advances have been made in the
treatment for non-localized stage IV colon cancer over the last few
years, including the following (see data in table 1):

In 2002, patients treated with Eloxatin®/5-FU/LV (FOLFOX) were shown
to be cancer-free longer and live longer than those treated with
Camptosar®/5FU/LV. Importantly, patients reported fewer severe side
effects when treated with Eloxatin®/5-FU/LV than with Camptosar®/5-
FU/LV.[2]Eloxatin® was approved for first-line treatment of advanced
colon cancer in January 2004.
The most recent advance is the combination AvastinT/5FU/LV , which
was approved for initial treatment of advanced colon cancer in
February 2004.[3]Patients who received Avastin® were cancer-free for
longer and lived longer than patients treated with only 5FU/LV.
Additionally, patients treated with AvastinT/Camptosar®/5-FU/LV have
been shown to live longer and be cancer-free longer than those
treated with Camptosar®/5FU/LV.[4]
Table 1 Advances in chemotherapy regimens for advanced colorectal
cancer


  Response rate
  Progression free survival (months)
  Overall survival (months)

Camptosar®/5FU/LV
  33%
  6.9 (time to progression)
  14.6

Eloxatin®/5FU/LV
  45%
  8.8 (time to progression)
  19.4






5FU/LV
  24%
  5.2
  13.6

Avastin®/5FU/LV
  40%
  9.0
  17.6






Camptosar®/5FU/LV
  35%
  7.1
  15.6

Avastin®/
Camptosar®/5-FU/LV
  45%
  10.4
  20.3


While results from different studies cannot be definitively
compared, these findings suggest that the recent developments in
treatment for advanced colon cancer have resulted in better
treatment options and that AvastinT plus chemotherapy may hold the
most promise.

Bevacizumab (AvastinT): AvastinT is a new class of drug known as an
angiogenesis inhibitor. Angiogenesis is the process of developing
new blood vessels. Cancer cells require food, oxygen, and proteins
in order to grow and spread. New blood vessels are necessary to
deliver these essential components of cellular growth.

Inhibition of angiogenesis is a growing area of cancer research. Two
key proteins that are necessary for the process of angiogenesis are
called vascular endothelial growth factor (VEGF) and matrix
metalloproteinases (MMPs). VEGF causes endothelial cells (cells
comprising the innermost layer of blood vessels) to replicate and
migrate from existing blood vessels to the cancer. Endothelial cells
secrete MMPs, which create an opening in existing tissues
surrounding the cancer, allowing the endothelial cells to move near
the cancer and form new blood vessels to "feed" the cancer.
Researchers have been evaluating targeted treatment approaches which
hinder or reduce the effects of VEGF and thus, slow cancer
progression.

AvastinT produces its anti-angiogenic effects by binding to VEGF and
inhibiting or reducing the growth of new blood vessels that are
necessary for cancer cell growth. Two studies have demonstrated that
the addition of AvastinT to standard chemotherapy treatment improves
survival in patients with metastatic colorectal cancer.

Researchers from the United States recently conducted a multi-
institutional clinical trial to evaluate the addition of AvastinT to
a standard chemotherapy combination in patients with metastatic
colorectal cancer. This trial involved over 100 patients who were
treated with one of the following regimens: fluorouracil (FU) and
leucovorin (LV), FU/LV and low-dose AvastinT or FU/LV and high-dose
AvastinT. The patients that received AvastinT showed a greater anti-
cancer response, longer time before their cancer progressed, and
higher overall survival rate. Low-dose AvastinT appears to be more
effective than high-dose (see Table 2). Side effects for patients
treated with AvastinT included blood clots, high blood pressure,
protein in the urine, and bloody nose.[5]

Table 2 Effect of AvastinT in patients with metastatic colorectal
cancer



FU/LV
  FU/LV plus
low-dose AvastinT
  FU/LV plus
high-dose AvastinT

Anti-cancer response
  17%
  40%
  24%

Time to cancer progression (months)

5.2

9.0

7.2

Overall survival (months)
  13.8
  21.5
  23


According to results of a large trial published in mid-2004, the
addition of AvastinT to chemotherapy showed that patients treated
with AvastinT lived longer and were more likely to experience
shrinkage of their cancer, a delay in cancer progression than
patients not treated with AvastinT (see table 3). Side effects were
similar between the two groups of patients; however, high blood
pressure was more prevalent in the group treated with AvastinT.[6]

Table 3 Results of a large trial demonstrating the effect of
AvastinT in patients with metastatic colorectal cancer


  Camptosar®/5FU/LV plus AvastinT
  Camptosar®/5FU/LV plus placebo

Response rate
  44.8%
  34.8%

Complete response rate
  3.7%
  2.2%

Time to cancer progression (months)
  10.4
  7.1

One-year survival
  74.3%
  63.4%

Median survival (months)
  20.3
  15.6


Oral chemotherapy: Several new chemotherapy agents are being
developed that can be taken orally. The most common are the
fluoropyramidines, which may provide the same or greater benefit as
intravenous (IV) fluorouracil (5-FU) without requiring intravenous
administration. Results from recent clinical trials have
demonstrated that the oral chemotherapy agent Xeloda® (capecitabine)
provides similar treatment outcomes to 5-FU/LV and allows patients
to be treated at home with fewer side effects.

Three trials have been completed in the last several years comparing
oral Xeloda® to IV 5-FU/LV in the treatment of patients with
advanced colon cancer. Two trials published in 2001 demonstrated no
difference in response to treatment, the length of time before the
cancer progressed, and duration of survival between the oral and IV
treatments.[7][8]A trial presented at the 2004 meeting of the
American Society of Clinical Oncology showed that more patients
treated with oral Xeloda® were free of cancer for 3 years or more
compared to patients treated with IV 5FU/LV (65.5% vs. 61.1%,
p=0.0407). All of these trials reported significantly fewer side
effects with Xeloda®, including low white blood cell count,
diarrhea, and nausea/vomiting. The only side effect that was more
prevalent with Xeloda® was hand/foot syndrome, which is a thickening
of the skin on the hands and feet.[9]

Treatment of Colon Cancer that has Metastasized to a Single Site
Stage IV colon cancer commonly spreads to the liver or the lungs.
Treatment for patients with colon cancer that has spread to one of
these locations may include surgery or specialized delivery of
chemotherapy that targets the cancer. Surgical removal of the cancer
metastasis has been shown to provide benefit, or even cure for some
patients. For patients with liver metastases, chemotherapy treatment
delivered into the blood vessel that supplies the liver (hepatic
artery infusion) has been shown to provide some benefit. Patients
with colon cancer that has spread to the liver or lungs should be
evaluated by doctors in a medical center that has significant
experience treating patients with these circumstances.

Surgery for liver and lung metastases: Physicians from the Mayo
Clinic have determined that select patients with colon cancer that
has metastasized to the liver and lungs may have an increased chance
for long-term survival with surgical removal of these metastases.
This trial involved 58 patients with colon cancer who had metastases
to both the liver and lungs, but no relapse of their cancer at the
original site. All patients underwent the surgical removal of their
metastases at the Mayo Institution between 1980 and 1988. There were
no deaths during surgery. Five years following surgery, 55% of
patients remained cancer-free. The patients that responded best to
treatment did not have thoracic lymph node involvement and did not
have an elevated carcinoembryonic antigen, which is a type of
protein found on the surface of cancer cells.[10]

Hepatic artery infusion: The infusion of chemotherapy directly into
the vessel that delivers blood to the liver is called hepatic artery
infusion. This technique is used to treat patients with colon cancer
that has metastasized to the liver. The pooled results of several
small studies indicate that hepatic artery infusion produced more
anti-cancer responses and caused patients to live longer than those
treated with traditional systemic chemotherapy[11](see table 4).

Table 4 Outcomes with hepatic artery infusion or systemic
chemotherapy


  Hepatic artery infusion
  Systemic chemotherapy

Response rate
  41%
  14%

Average duration of survival
  16 months
  12 months


Also, treatment with hepatic artery infusion plus traditional
chemotherapy has been shown to increase duration of survival and
reduce recurrences compared to treatment with systemic chemotherapy
only (see table 5).[12]


  Hepatic artery infusion plus systemic chemotherapy
  Systemic chemotherapy

Average duration of survival
  72 months
  59 months

Cancer recurrence rate
  10%
  60%


Liver-directed treatment approaches, such as hepatic artery
infusion, are highly specialized procedures and are best performed
by experienced individuals. Furthermore, this approach is only
appropriate for select patients. The benefit of the procedure must
outweigh the risk, and these must be carefully compared to the
benefit and risk of undergoing standard surgical removal and
systemic chemotherapy.

Treatment of the Elderly
A large percentage of patients with advanced colorectal cancer are
65 years or older. Because elderly patients commonly have concurrent
illnesses or other medical difficulties that are perceived to
exacerbate the side effects of chemotherapy, elderly patients are
often treated with reduced doses of chemotherapy.  Clinical studies
have shown however, that elderly patients get the same benefit from
chemotherapy treatment as younger patients. While a dose reduction
or delay may sometimes be necessary, it may also compromise the
optimal treatment of some patients.  All patients over 65 should be
closely monitored for toxic side effects of chemotherapy, especially
during their initial chemotherapy administration cycle.  Moreover,
The NCCTG trial demonstrated that Eloxatin® when combined with 5-
FU/LV had fewer side effects than Camptosar® and may represent a
better treatment option for elderly patients.

Strategies to Improve Treatment of Stage IV Colon Cancer
The development of more effective cancer treatments requires that
new and innovative therapies be evaluated with cancer patients.
Clinical trials are studies that evaluate the effectiveness of new
drugs or treatment strategies. Future progress in the treatment of
stage IV colon cancer will result from the continued evaluation of
new treatments in clinical trials. Participation in a clinical trial
may offer patients access to better treatments and advance the
existing knowledge about treatment of this cancer. Patients who are
interested in participating in a clinical trial should discuss the
risks and benefits of clinical trials with their physician. Areas of
active exploration to improve the treatment of stage IV colon cancer
include the following:

Epidermal Growth Factor Receptor (EGFR) Inhibitors
ErbituxT(IMC-225)
COX-2 inhibitors
Celocoxib (Celebrex®)
Other treatments
Managing side effects
Liver-directed therapies
Biological therapy
Vaccines
Phase I clinical trials
Epidermal Growth Factor Receptor (EGFR) Inhibitors
Epidermal growth factor receptors (EGFR) are small proteins that are
found on the surface of all cells. EGFR binds exclusively to small
proteins circulating in the blood called growth factors. The binding
action between EGFR and growth factors stimulates biological
processes within the cell to promote growth of a cell in a strictly
controlled manner. However, in many cancer cells, EGFR is either
abundantly overexpressed or the EGFR biological processes that
normally stimulate cell growth are constantly active, leading to the
uncontrolled and excessive growth of the cancer cell. It is
estimated that approximately 70% of patients with colon cancer are
positive for EGFR.

ErbituxT(IMC-225): ErbituxT is a monoclonal antibody that blocks the
binding action between EGFR and growth factors. Monoclonal
antibodies are proteins that have been manufactured in a laboratory
to bind to specific sites on designated cells. ErbituxT binds to
EGFR so that growth factors are unable to bind to EGFR. This
ultimately slows or stops the growth process of EGFR-positive cancer
cells. In addition, ErbituxT appears to augment anti-cancer activity
of chemotherapy agents through biological processes not yet
elucidated.

In February 2004, the Food and Drug Administration (FDA) approved
ErbituxT for the treatment of recurrent colorectal cancer that
expresses the epidermal growth factor receptor (EGFR). The FDA
indication specifies that ErbituxT be used in combination with the
chemotherapy agent Camptosar® in patients who stopped responding to
previous therapy with Camptosar®, or as a single agent in patients
who are not able to tolerate Camptosar®-based chemotherapy. ErbituxT
may be available to patients with stage IV disease through a
clinical trial.

Cox-2 Inhibitors
Clinical trials evaluating Cox-2 inhibitors in combination with
Camptosar® are ongoing in an attempt to improve the treatment of
colon cancer. Clinical studies have suggested that the regular use
of non-steroidal anti-inflammatory drugs reduces the risk for
developing colorectal cancer.

Celocoxib (Celebrex®): Non-cancerous tumors, called adenomatous
polyps, may grow in the colon or rectum. In some individuals, these
polyps eventually become cancerous and develop into colorectal
cancer. Familial adenomatous polyposis (FAP) is a genetic disease
that most often affects adolescents and young adults, causing
hundreds of adenomatous polyps to form in the colon and rectum.
Because of the presence of these polyps, many of these people
develop colorectal cancer at an early age. In 2000, the Food and
Drug Administration approved Celebrex®, previously approved for the
treatment of individuals with arthritis, to be used in conjunction
with the usual therapy for individuals with FAP. Celebrex® has been
reported to reduce the number of colon polyps that develop in
individuals with FAP, thus significantly reducing their risk for
developing colorectal cancer.

Other Treatments
Managing side effects (supportive care): Treatment designed to
prevent or control the side effects of cancer and cancer therapies
are called supportive care. Side effects not only cause patients
discomfort, but also may prevent the delivery of therapy at its
planned dose and schedule. In order to achieve optimal outcomes from
treatment and improve quality of life, it is imperative that
treatment is delivered as planned and that side effects resulting
from cancer and its treatment are appropriately managed. For more
information, visit Managing Side Effects .

Liver-directed therapies: Continued development and refinement of
hepatic artery infusion, chemoembolization, and other liver-directed
therapies is ongoing. For patients with liver dominant disease,
these strategies are being utilized to shrink the cancer and
increase the number of patients eligible for surgical removal of
their cancer.

Biological therapy: Biologic therapy consists of naturally occurring
or synthesized substances that direct, facilitate, or enhance the
body's normal immune defenses. Examples of compounds used for
biological therapy include interferons, interleukins, vaccines and
monoclonal antibodies. In an attempt to improve survival rates,
these and other agents are being tested alone or in combination with
chemotherapy in clinical trials.

Vaccines: The purpose of a vaccine is to help the patient's immune
system destroy the cancer by activating the patient's immune cells
against the cancer. Vaccines have already been shown to improve the
survival of certain patients with colorectal cancer and continue to
be evaluated in clinical trials. The majority of colorectal cancer
cells display a protein on their surface called the carcinoembryonic
antigen (CEA). Through mechanisms not clearly elucidated, CEAs are
not recognized by the patient's immune system when they are
presented on cancer cells in the body. Researchers have recently
been investigating novel strategies to stimulate the immune system
to recognize CEA as foreign which would cause an attack on cancer
cells presenting this antigen.

Human chorionic gonadotropic (hCG) hormone is a hormone that is
normally only produced during pregnancy. However, researchers have
discovered that many cancer cells express hCG and have been
developing a vaccine that specifically targets hCG. Avicine® is a
vaccine that is comprised of parts of the hCG hormone and is linked
to the diphtheria toxin. Once injected, a patient's immune system
recognizes the whole vaccine complex as "foreign" and researchers
speculate that the immune system recognizes the whole vaccine
complex as "foreign" and researchers speculate that the immune
system neutralizes hCG in the body and its possible growth
stimulatory effects on cancer, as well as stops the growth of the
cancer cells expressing hCG.

Results from a recent clinical trial including 12 medical centers in
the United States involved 77 patients with stage IV colorectal
cancer who were treated with Avicine®. Of these patients, 56
patients demonstrated an immune response against hCG. The overall
survival of all patients in the trial was 34 weeks. Patients who
developed an immune response to the vaccine had an average survival
of 45 weeks. Patients who developed an immune response to two
segments of hCG had an average survival of 66 weeks. Avicine® was
very well tolerated.[13]

Vaccines are also being developed which are made from the actual
cancer cells removed from the patient. This is referred to as an
autologous vaccine. The difficulty in preparing vaccines is that the
patient's cancer cells must be processed immediately following
surgery. Therefore, patients and their surgeon must be prepared in
advance to ensure that the removed cancer cells can be handled
properly for vaccine preparation.

Phase I clinical trials: New chemotherapy drugs continue to be
developed and evaluated in patients with recurrent cancers in phase
I clinical trials. The purpose of phase I trials is to evaluate new
drugs in order to determine the best way of administering the drug
and whether the drug has any anti-cancer activity in patients.

References


---------------------------------------------------------------------
-----------

[1] Saltz LB, Cox JV, Blanke C, Rosen LS, et al. Irinotecan plus
Fluorouracil and Leucovorin for Metastatic Colorectal Cancer. New
England Journal of Medicine 2000;343(13):905-914.

[2] Sanofi-Synthelabo. EloxatinT (oxaliplatin for injection)
Approved in the United States for the 1st Line Treatment of
Metastatic Colorectal Cancer. Available at: http://www.sanofi-
synthelabous.com/news/2004/20040112.html. Accessed January 2003.

[3] Hurwitz H, et al. Late-Breaking Oral Presentation. Proceedings
of the 39th Meeting of the American Society of Clinical Oncology
2004; Abstract #3646.

[4] Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus
Irinotecan, Fluorouracil, and Leucovorin for Metastatic Colorectal
Cancer. New England Journal of Medicine. 2004;350:2335-2342.

[5] Hurwitz H, et al. Late-Breaking Oral Presentation. Proceedings
of the 39th Meeting of the American Society of Clinical Oncology
2004; Abstract #3646.

[6] Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus
Irinotecan, Fluorouracil, and Leucovorin for Metastatic Colorectal
Cancer. New England Journal of Medicine. 2004;350:2335-2342.

[7] Hoff PM, Ansari R, Batist G, et al. Comparison of oral
capecitabine versus intravenous fluorouracil plus leucovorin as
first-line treatment in 605 patients with metastatic colorectal
cancer: results of a randomized phase III study. J Clin Oncol.
2001;19:2282-2292.

[8] Van Cutsem E, Twelves C, Cassidy J, et al. Oral capecitabine
compared with intravenous 5-fluorouracil plus leucovorin in patients
with metastatic colorectal cancer: results of a large phase III
study. J Clin Oncol. 2001;19:4097-4106.

[9] Cassidy J, Scheithauer W, McKendrick J, Kroning H, et al.
Capecitabine (X) vs bolus 5-FU/leucovorin (LV) as adjuvant therapy
for colon cancer (the X-ACT study): Efficacy results of a phase III
trial. Proceedings from the 40th annual meeting of the American
Society of Clinical Oncology, held in New Orleans LA, June 5-8,
2004; Abstract #3509.

[10] Headrick JR, Miller DL, Nagorney DM, Allen MS, et al. Surgical
treatment of hepatic and pulmonary metastases from colon cancer.
Annals of Thoracic Surgery 2001;71:975-980.

[11] Harmantas A, Rotstein LE, Langer B. Regional versus systemic
chemotherapy in the treatment of colorectal carcinoma metastatic to
the liver: Is there a survival difference?--Meta-analysis of the
published literature. Cancer 1996;78:1639-1645.

[12] Kemeny N, Huang Y, Cohen AM, Shi W, et al. Hepatic Arterial
Infusion of Chemotherapy after Resection of Hepatic Metastases from
Colorectal Cancer. New England Journal of Medicine 1999;342:2039-
2048.

[13] AVI Biopharma. Available at:
http://www.avibio.com/html/NFFrameSet.htm. Accessed August 7, 2002.


---------------------------------------------------------------------
-----------




CancerConsultants.com© 1998 - 2004, last updated 09/04, Authored by
Charles H. Weaver, M.D., Managing Editor and C. D. Buckner, M.D.,
Scientific Editor. CancerConsultants.com, All Rights Reserved.

These materials may discuss uses and dosages for therapeutic
products that have not been approved by the United States Food and
Drug Administration. All readers should verify all information and
data before administering any drug, therapy or treatment discussed
herein. Neither the editors nor the publisher accepts any
responsibility for the accuracy of the information or consequences
from the use or misuse of the information contained herein.

Posted: April 07, 2005


NEW YORK (Reuters Health) - Hepatic arterial infusion of oncolytic
vesicular stomatitis virus (VSV) in a rat model of colorectal cancer
with multifocal hepatic metastases significantly improves survival,
researchers report in the April 20th issue of the International
Journal of Cancer.


"Viruses that specifically replicate in and kill cancerous, but not
normal, cells are being developed as a novel class of therapeutic
agents to treat cancer,"

senior investigator Dr. Savio L. C. Woo told Reuters Health

Dr. Woo and colleagues at Mount Sinai School of Medicine, New York
report that VSV "can reach and replicate efficiently in multifocal
lesions of colorectal cancer in the liver of rats after vascular
delivery, which led to substantial tumor necrosis and prolongation of
survival."

Control animals began to die of tumor progression in as little as 9
days and all of these animals had died within 19 days. However, VSV-
treated animals survived for up to 24 days. No vector-associated
toxicities were observed and there was no apparent damage to the
hepatic parenchyma.

"With additional improvements on the tumor-killing potential of the
virus through molecular engineering," Dr. Woo concluded, "the virus
can be developed as an effective and safe agent to treat colorectal
as well as other cancers that have spread to the liver, where
prognosis is usually poor."

Hi all ~

A few months back I had introduced myself to the group and then I was
unable to reply again since. I did get some replies and I am
grateful! Unfortunately, I have been thru the nightmare we all fear
most: my husband of 20 years and the father of our three daughters,
passed away on March 10th as a result of suspended chemo due to
infections from long term hospitalization and TPN. Some friends ours
online have created a memorial site to him…if anyone is interested at
viewing it. www.freewebs.com/ray-borden

I thank you all for being there even if I couldn't get online to talk…
just knowing there were folks there that understood what my family
was going thru helped a bunch. Hugs all around…

I am not in a place yet to be very supportive of others, but I'm sure
I will get to that place eventually. I will remain a member of this
group, but I am going to no mail for a while. If you wish to email me
personally, since I will not get what is posted through the group,
please send it to pewterthistles@... . Thanks!

With Love and Best Wishes to You All ~
Mrs. Denise Borden

Polysulfated heparinoids selectively inactivate heparin-binding
angiogenesis factors.



Zugmaier G, Favoni R, Jaeger R, Rosen N, Knabbe C.



Department of Hematology/Oncology, Philipps-University, Marburg,
Germany.



Angiogenesis is a prerequisite for tumor expansion and metastasis.
The angiogenic potential of the heparin-binding growth factors
acidic fibroblast growth factor (FGF) and basic FGF has been
demonstrated in various publications. We studied the inhibitory
effects of suramin and the polysulfated heparinoids pentosan
polysulfate, dextran sulfate, and fucoidan on the action of FGF. As
an experimental model, we used the adrenal cancer cell line SW 13,
whose anchorage-independent growth depends on the presence of FGF.
The polysulfated heparinoids inhibited FGF-induced growth and
binding to the receptor at an IC50 of 0.5-3 micrograms/ml. Suramin
inhibited FGF at an IC50 of 100 micrograms/ml. The polysulfated
heparinoids exerted no effect on IGF-1 or TGF alpha-related growth.
Suramin inhibited the anchorage-independent growth induced by IGF-1
or TGF alpha only at an IC50 of 100 micrograms/ml. Our results
indicate that suramin inhibits growth factors in a nonselective way.
By contrast, polysulfated heparinoids exert a selective inhibitory
effect on heparin binding angiogenesis factors at an IC50, which is
100 times below the IC50 of suramin. Therefore, the administration
of polysulfated heparinoids might become a novel approach to tumor
therapy based on blocking angiogenesis.



PMID: 10667230 [PubMed - indexed for MEDLINE]

My son-in law, 27 and a U.S. Marine; was diagnosed with colon cancer.
He, my daughter, and grandson, visited us , over the Christmas
holidays. He had been in constant pain from September; and was
diagnosed with colon cancer in November. He also had a tumor, in his
left side; diagnosed malignant. He was scheduled for chemo; after
returning from leave. He could eat very little; and was vomiting
blood; and defecating blood. I had been making my own oxygenated-
colloidal silver, at home; using a low-tech method, with four 9-volt
batteries in series; with 2 pure silver bars; spaced 2" apart, in
distilled water. For oxygen, I used a capful of off-the-shelf 3%
peroxide, to the distilled water. This  is a general antibiotic and
antivirus. Also; I had been using the herb Graviola; as a cancer
prevental. Using Google, for Graviola: I read that it was supposed
to be 10,000 times more effective against colon cancer, than the
best Chemotherapy. With his doctors permission; as she said that;"He
had nothing to lose",; by trying it. I gave him both.
  The effects were so immediately successful; that I did not believe
it. He seemed to be in perfect health; active; and able to eat
anything, for the 10 days, that he was here. I told him; not to get
his hopes up; until he went back; and was tested. His tests were
completely negative; including a benign fibrous tumor. His doctor
did not believe the tests; and insisted on a retest, two weeks
later. These tests were also negative.
He marched 200 miles; while playing his French Horn, during Mardi
Gras week, with the Marine band, in New Orleans.
  All I want; is for needing people;to give it a try. The information
can be had; by looking it up, on Yahoo, or Google. Look up Colloidal
Silver, and Graviola. I have no financial interest. It is all public
information. Through synergy and serendipity; I may have hit on a
"miracle" combination.
As an aside; I may have cured a 20-yr. old male; who was told that
he had a massive dose of HIV virus in his blood. He was tested
negative afterwards; but believes that he was deliberately misled;
by the doctor who told him; that he had the virus.

See: http://www.quackwatch.org/00AboutQuackwatch/altseek.html

      Be Aware !

                  Best,

                      Ed

The link to Yahoo Health Day where this article appears today is:
http://news.yahoo.com/news?tmpl=index&cid=97

Drug Stops Cancer in Its Tracks

Mon Mar 14, 7:02 PM ET


MONDAY, March 14 (HealthDay News) -- An experimental drug that stops
cancer cell division and triggers tumor death has been developed by
researchers at Temple University.

Yahoo! Health
Have questions about your health?
Find answers here.






The drug, called ON01910, interferes with the activity of a gene
called Plk1, which plays an important role in cancer spread. Previous
research found that Plk1 is present at higher levels in tumors and in
cancer patients with poor survival rates. That work also discovered
that when Plk1 is blocked cancer cells can't divide and tumors die.


The Temple team tested ON01910 on 94 different human cancers.


"We found that ON01910 was a potent inhibitor of human tumor growth
and also worked well with several existing cancer drugs, often
inducing complete regression of tumors. Someday it might work either
as a single drug or in combination with other drugs," research leader
Prem Reddy, a professor of biochemistry and director of the Fels
Institute for Cancer Research at Temple, said in a prepared statement.


"Our drug stops tumor cells from reaching normal cells three ways.
First, it blocks invasion, next it blocks angiogenesis [the growth of
surrounding blood vessels] and finally, it induces tumor cell death,"
Reddy said.


The study appears in the March issue of Cancer Cell.


Currently, ON01910 is being assessed in a Phase I clinical trial
involving up to 56 people with advanced and metastatic cancers.


More information


The American Cancer Society (news - web sites) offers a guide to
cancer drugs.

Men get prostate screen, balk at colon cancer test
  Last Updated: March 07, 2005



NEW YORK (Reuters Health) - Men apparently find it quite acceptable
to get a PSA test to screen for prostate cancer, but don't go along
so readily with being screened for colorectal cancer, findings from a
new study indicate.


Dr. Ruth Carlos wants doctors to approach PSA testing as a "teachable
moment" for informing men about tests aimed at cutting colon cancer
risk.

"Men are already paying attention to their cancer risk in one area,"
she noted in a statement. "If we can take advantage of that
consciousness to educate them about another cancer risk, it might
lead to more early detection of colorectal cancer."

Carlos, at the University of Michigan in Ann Arbor, and her
colleagues analyzed data from 22,304 men who participated in the 2002
Behavioral Risk Factors Surveillance Survey.

The analysis showed that 62 percent of men underwent prostate cancer
screening, while just 48 percent went along with colon cancer
screening, according to a report in the Journal of the American
College of Surgeons.

The team found that men who had a PSA test were three times more
likely to get a colon cancer test.

"If we can turn the PSA test into an opportunity to encourage men to
get their colons checked too, it would take advantage of the public
demand for PSA testing," said Carlos.

She also pointed out that colorectal screening might pay bigger
dividends than prostate screening. "Colon cancer screening is proven
to be effective at reducing deaths from colon cancer, while the
effectiveness of the PSA test in reducing mortality continues to be
debated," Carlos explained.





----------------------------------------------------------------------
----------

www.asco.org c Copyright 2002 American Society of Clinical Oncology
All rights reserved worldwide.

Heated chemotherapy prolongs survival in abdominal cancer
  Last Updated: March 07, 2005



NEW YORK (Reuters Health) - Intraperitoneal injection of hyperthermic
chemotherapy (IPHC) following cytoreductive surgery lengthens overall
survival in patients with peritoneal dissemination of GI neoplasms,
according to studies reported at the Society of Oncology Surgeons
national meeting in Atlanta.


In one of the presentations, co-investigator Dr. Perry Shen and his
colleagues at Wake Forest University in Winston-Salem, North
Carolina, reported the results of six patients with peritoneal
carcinomatosis secondary to small bowel adenocarcinoma who underwent
IPHC after cytoreductive surgery.

"We first do surgery to reduce the bulk of the tumor, ideally to less
than 5 mm deposits or just microscopic deposits," Dr. Shen said in an
interview with Reuters Health.

Patients are cooled to a core temperature of 34 to 35 degrees C. Then
mitomycin C heated to 39 degrees Centigrade is perfused through
inflow and outflow catheters placed percutaneously into the abdominal
cavity, at a flow rate of approximately 800 mL/min for approximately
2 hours.

Heating the drug serves two purposes, Dr. Shen explained: "It
potentiates the effect of chemotherapy and decreases tumor resistance
to chemotherapy." Intraperitoneal perfusion also increases the
concentration of the drug delivered to the tumor compared with
conventional systemic chemotherapy, he added.

Median survival after IPHC was 45.1 months, the investigators report.
In comparison, median survival is 3.1 months when patients are
treated conventionally.

In a second presentation, Dr. Shen, working with another team at the
same institution, described 110 cases of peritoneal dissemination of
appendiceal neoplasms treated with cytoreductive surgery and IPHC
between 1993 and 2004.

The 1-year survival rate was 83.8%, and the 5-year survival rate was
56.8%.

A third presentation illustrated the benefit of cytoreductive surgery
and IPHC in treating peritoneal carcinomatosis arising from multiple
sites, including the appendix, colon/rectum, mesothelium, ovary and
stomach.

Assessments performed for 86 patients every 3 months for up to 1 year
showed significant improvements in overall quality of life, with
physical functioning improved at 6 months.

With these data, Dr. Shen hopes that clinicians will be more likely
to refer patients for cytoreductive surgery and IPHC when they first
present with peritoneal spread of primary cancers.

"For those people who have a good performance status and have disease
localized to abdomen, if you can surgically debulk that tumor down to
minimal size, this procedure would be the treatment of choice," he
said.

Colorectal cancer survival lower in Europe than in US
  Last Updated: February 16, 2005



NEW YORK (Reuters Health) - Overall colorectal cancer survival is
lower in Europe than in the United States, largely due to differences
in diagnosis and treatment, according to a report in the February
edition of Gut.


These findings suggest that the "differences in survival observed
between the USA and Europe are real, and reflect earlier diagnosis in
the USA," Dr. Laura Ciccolallo from Istituto Nazionale per lo Studio
e la Cura dei Tumori, Milan, told Reuters Health. "This is important,
because it suggests in turn that the lower survival in Europe is a
problem that is potentially remediable if adequate attention can be
given to earlier diagnosis and more rapid investigation and
treatment."

Dr. Ciccolallo and colleagues used data from 10 population-based
cancer registries to examine the extent to which disease stage,
staging procedures, and treatment explain the differences in
colorectal cancer survival between European and US populations in
1990.

The relative excess risk of death 3 years after diagnosis of
colorectal cancer was 1.26- to 2.21-fold higher in Europe than in the
US, the authors report. The relative excess risks were even higher
after adjustment for age, sex, and primary site.

Excess mortality in Europe was highest during the first year after
diagnosis, the investigators note, and was higher for women and for
patients of advanced age.

More cancers in the US (54%) than in Europe (48%) were diagnosed at
Dukes' stage A or B, the report indicates, and more patients in the
US (92%) than in Europe (85%) were surgically resected.

More than twice as many patients in the US (28%) than in Europe (13%)
had 12 or more lymph nodes examined by the pathologist, the results
indicate.

Within the same category of Dukes' stage and number of nodes
examined, 3-year survival was similar in Europe and the USA, the
researchers note.

"The differences in survival between the USA and Europe are likely to
reflect differences in the speed of diagnosis and the stage of
disease at least as much as any differences in the efficacy of
treatment," Dr. Ciccolallo added.

Next month is Colon Cancer Awareness Month.
There are a few things going on.

--------------------------------------------------------------------------------

The Colossal Colon is on tour again - but a much smaller tour than before.
http://www.rollingtorecovery.com/colossalcolon.htm


--------------------------------------------------------------------------------

CCNetwork has a show on colon cancer on PBS Healthy Bodies Healthy Minds.
(Date to be determined)


--------------------------------------------------------------------------------

Digestive Disease National Coalition is arranging visits with your legislators
to talk about the need to screen all adults.
March 6 & 7
www.ddnc.org
Please, if you can come, go to their website and sign up and join in.  It rocks
the boat to have constituents show up in mass at their Washington DC offices.


--------------------------------------------------------------------------------

Most cancer centers will have some kind of flyers up or information on colon
cancer especially made available.


--------------------------------------------------------------------------------

Colorectal Cancer Screening Legislation
17 states and the District of Columbia have colorectal cancer screening
legislation.

       California
       Connecticut
       Delaware
       Georgia
       Illinois
       Indiana
       Maryland
       Missouri
       Nevada North Carolina
       Oklahoma
       Rhode Island
       Tennessee
       Texas
       Virginia
       Washington, D.C.
       West Virginia
       Wyoming



If your state isn't on the list it's time to demand that they join the list.  If
they are already on the list remember, they are only covering from 50 on up.  So
you need to educate them about just who is getting colon cancer.


--------------------------------------------------------------------------------

Wear Awareness items.

There are two colors for colon cancer.  For about 15 years the ribbon has been
brown.  A few years ago the American Cancer Society decided they didn't like the
ribbon that patients were wearing at that time and so they changed it to blue. 
CCNetwork stayed with brown.  We have a few objections to the blue.  The main
objection to the brown is that it is of course poop colored.  But it is unique
and had the ability to have one recognizable meaning.  The blue ribbon is best
known for Internet Freedom of Speech and for Stopping Child Abuse.  So there is
no way to have the solidarity that the pink ribbon has for breast cancer, the
light blue ribbon has for prostate cancer, and the red ribbon has for AIDS. 
CCNetwork feels strongly that we need to have something that is unmistakeable. 
So we had the colon with the 'no' red circle with the line crossing through it
(as in No Smoking, etc).  It is recognizable.   We have put it on some of the
tshirts at CafePress and can put it on anything else you want.

http://www.colorectal-cancer.net/individual.htm
Go to this page and click on the icon near the bottom that says CafePress in its
lower right hand corner.

So wear the brown ribbon.  Wear the blue ribbon.  But wear something and tell
someone.


--------------------------------------------------------------------------------

Colon Cancer Challenge Race March 13, 2005 NYC Central Park
http://www.coloncancerchallenge.org/
But be aware that money that goes to this will strengthen keeping the screening
age at 50.

--------------------------------------------------------------------------------

Scope It Out 5k Run/Walk for CRC AwarenessWashington, DC

Call 703-408-0614 for more information.  March 19th

Again though, be an educated consumer.  You are supporting the 50 screening age
with any events but CCNetworks.   It may sound like sour grapes.  But  if we
want the right thing to be done we have to not support the wrong goal.


--------------------------------------------------------------------------------


Advances in the Treatment of Colorectal Cancer  March 22

Teleconference

Call 800-813-HOPE for more information or register online now!

This is a CancerCare teleconference jointly sponsored by CCNetwork and other
groups.


--------------------------------------------------------------------------------


Now, what would be really cool, would be each of you hosting a small Mardi Gras
to Stop Colon Cancer party in March.    Use viral email marketing (that's when
you send an email notice and ask that the reader send it on to 10 people - or
more)  to advertise it and send a PSA to the radio stations.Charge $25 to come.
Encourage party wear and costumes.  Hire a DJ or do the music yourself or check
with a local college to see if there is an up and coming DJ who would do it for
free.   If you do, we'll send you "Stop Colon Cancer - Moon A Doc"
bumperstickers for each of them.  And then we'd have a lot more awareness events
for colon cancer next month.

Priscilla A. Savary
Executive Director
Colorectal Cancer Network
PO Box 182, Kensington MD 20895
301-879-1500
psavary@...
www.colorectal-cancer.net
_________
Like to help CCNetwork? Go shopping!
That's right, go head and buy something for yourself -- a new CD, the latest
bestseller, essentials like toothpaste or vitamins, even a computer. But first
join www.iGive.com/CCNetwork . Every time you shop at one of the over 500
name-brand stores in the Mall at iGive.com, we'll receive a donation of up to
26% of each purchase you make, at no cost to you.
Remember, donating to CCNetwork won't cost you a thing.  But we'll miss out on a
lot of extra dough, if you don't join. So visit www.iGive.com/CCNetwork now.
Membership is free and your privacy is guaranteed.

Click here to join:  http://www.iGive.com/CCNetwork




[Non-text portions of this message have been removed]

New Cancer Treatment Causes Fewer Side Effects
By JOHN McKENZIE ABC NEWS


Feb. 3, 2005 — A study published in today's New England Journal of
Medicine offers encouraging news about a novel way to fight cancer.
It finds that injecting a type of liquid radiation, called Bexxar,
into patients with lymphoma — a cancer of the immune system — can
fight the disease more quickly and with fewer side effects that
existing treatments. The approach might eventually be used on a
variety of cancers.
"This is the first time we're using injectable radiation to treat
cancer," said Dr. Andrew Zelenetz, a hematologic oncologist at
Memorial Sloan-Kettering Cancer Center in New York.
The radioactive drug is delivered intravenously and works like a
guided missile. It travels throughout the body, homing in on a
specific protein found on the cancer cells.
"And when it latches on to it, it now has radiation attached to it
and the radiation is essentially there at the site where you want it,
radiating the tumor and not radiating other tissues," said Dr. Mark
Kaminski, director of the Multidisciplinary Lymphoma Clinic at the
University of Michigan Cancer Center.
When Bexxar was used to combat non-Hodgkin's lymphoma, 59 percent of
patients remained cancer-free during the five years of study.
"These results are very similar to the results we're getting with
state-of-the-art chemotherapy," said Zelenetz. "However, the distinct
advantage here is that it is much more user-friendly for the
patient."
Few Side Effects
The liquid radiation treatment is completed in just one week,
compared to the 4½ months often required for chemotherapy. There are
remarkably few side effects — no hair loss, less nausea and a lower
risk of infection. Fatigue is the most common side effect.

Thursday, Jan 27, 2005


Preliminary Positive Results From Phase III Trial Of Avastin Plus
FOLFOX4 Chemotherapy Presented At ASCO GI Meeting


Hollywood, Fla.  --  January 27, 2005 --  Genentech, Inc. (NYSE: DNA)
today announced that a randomized Phase III study (E3200) of Avastin™
(bevacizumab) plus the FOLFOX4 chemotherapy regimen (oxaliplatin/5-
FU/leucovorin), compared to FOLFOX4 alone in second-line metastatic
colorectal cancer patients achieved its primary endpoint of improving
overall survival. These data, first announced by the National Cancer
Institute (NCI) and Genentech in November 2004, were presented by
Bruce J. Giantonio, M.D., of the Abramson Cancer Center at the
University of Pennsylvania in Philadelphia at the Second Annual
Gastrointestinal Cancers Symposium. Avastin is currently approved as
a first-line treatment for metastatic colorectal cancer in
combination with intravenous 5-FU-based chemotherapy.
Results from a preliminary analysis of the E3200 study demonstrated
that patients receiving Avastin plus FOLFOX4 had a 26 percent
reduction in the risk of death (a hazard ratio of 0.74), the primary
endpoint, compared to patients who received FOLFOX4 alone. Median
survival for patients receiving Avastin plus FOLFOX4 was 12.5 months,
compared to 10.7 months for those receiving FOLFOX4 alone, a 17
percent improvement.

"Avastin is the only targeted therapy to demonstrate an improvement
in survival in first-line metastatic colorectal cancer patients, who
on average face a two-year life expectancy upon diagnosis. The data
presented today show that Avastin in combination with the FOLFOX4
regimen may be an effective treatment for second-line metastatic
colorectal cancer," said Gwen Fyfe, M.D., Genentech's vice president,
Clinical Hematology/Oncology. "The results from this study add to the
growing body of data showing that the addition of Avastin to 5-FU-
based chemotherapy regimens can result in meaningful clinical benefit
to patients with metastatic colorectal cancer, and we have initiated
discussions with the FDA to determine a filing strategy for the use
of Avastin plus FOLFOX in the second-line population."

Adverse events in this Phase III study were consistent with those
seen in previous Avastin and FOLFOX4 clinical trials in metastatic
colorectal cancer. The most frequent adverse events were hypertension
and sensory neuropathy, with six percent of patients (17/286) in the
Avastin plus FOLFOX4 arm experiencing Grade 3 or 4 hypertension
compared to two percent (5/282) in the FOLFOX4 arm. Grade 3 and 4
sensory neuropathy occurred at a rate of 15 percent (44/286) in the
Avastin plus FOLFOX4 arm, compared to a rate of nine percent (26/282)
in the FOLFOX4 arm. The most serious adverse events were bleeding,
which occurred at a rate of 2.8 percent (8/286) in the Avastin +
FOLFOX4 arm and less than one percent (1/282) in the FOLFOX4 arm,
gastrointestinal perforation, which occurred at a rate of one percent
(3/286) in the Avastin plus FOLFOX4 arm, and thrombosis, which
occurred in 4.5 percent of patients (13/286) treated with Avastin
plus FOLFOX4 and compared to 2.8 percent of patients (8/282) treated
with FOLFOX4.

About the E3200 Study
This Phase III study was a randomized, controlled, multicenter trial
that enrolled 829 patients with advanced colorectal cancer who had
previously received a 5-FU-based therapy and irinotecan, either alone
or concurrently, for advanced disease or if their disease had
relapsed within six months of concluding adjuvant treatment with
these chemotherapy agents. The patients enrolled in this trial were
randomized to receive treatment with the FOLFOX4 regimen with or
without Avastin. Randomization to a third arm of the study evaluating
single-agent Avastin was suspended in March 2003 on the
recommendation of the Data Monitoring Committee overseeing the study
when review of early results suggested that overall survival for
patients in that group might be lower compared to that of patients
treated in the other two arms. Results from this treatment arm have
not yet been disclosed.

The trial was sponsored by the National Cancer Institute (NCI), part
of the National Institutes of Health, and conducted by a network of
researchers led by the Eastern Cooperative Oncology Group (ECOG).
Genentech provided Avastin for the trial under the Cooperative
Research and Development Agreement (CRADA) with the NCI for the
clinical development of Avastin.

About Avastin
Avastin is a therapeutic antibody designed to inhibit Vascular
Endothelial Growth Factor (VEGF), a protein that plays an important
role in tumor angiogenesis and maintenance of existing tumor vessels.
By binding to VEGF, Avastin is designed to interfere with the blood
supply to tumors, a process that is critical to tumor growth and
metastasis. For full prescribing information, including Boxed
Warnings for Avastin and information about Avastin and angiogenesis,
visit www.gene.com or www.avastin.com.

The FDA approved Avastin on February 26, 2004 as a first-line
treatment for metastatic colorectal cancer in combination with
intravenous 5-FU-based chemotherapy. Approval was based on data from
two trials. The pivotal trial was a large, placebo-controlled,
randomized study of 925 patients that demonstrated a prolongation in
the median survival of patients treated with Avastin plus the IFL (5-
FU/leucovorin/CPT-11) chemotherapy regimen by approximately five
months, compared to patients treated with the IFL chemotherapy
regimen alone (20.3 months versus 15.6 months). In addition, this
study demonstrated an improvement in progression-free survival (PFS)
of more than four months (10.6 months in the Avastin/IFL arm compared
to 6.4 months in the IFL-alone arm). The survival and PFS results
observed when Avastin is added to first-line chemotherapy are the
longest ever reported in a randomized, Phase III study of patients
with metastatic colorectal cancer.

Last year the National Comprehensive Cancer Network (NCCN), an
alliance of 19 of the world's leading cancer centers, updated their
Colorectal Clinical Practice Guidelines and added Avastin in
combination with 5-Fluorouracil-based regimens -- including those
using oxaliplatin or irinotecan -- to its list of treatment options
for first-line advanced colon or rectal cancer.

Based on data showing that VEGF may play a broad role in a range of
cancers, Genentech is pursuing a late-stage clinical development
program with Avastin evaluating its potential use in adjuvant and
metastatic colorectal, renal cell (kidney), breast and non-small cell
lung cancers. Avastin is also being evaluated in earlier stage trials
as a potential therapy in prostate, ovarian, and several types of
solid tumor cancers and hematologic malignancies and melanoma.

Avastin Safety Profile
Avastin has a well-established safety profile. In Genentech-sponsored
studies, the most serious adverse events associated with Avastin were
infrequent, and included gastrointestinal perforation, wound healing
complications, hemorrhage, arterial thromboembolic events,
hypertensive crisis, nephrotic syndrome and congestive heart failure.
The most common Grade 3-4 adverse events (occurring in greater than
two percent of patients in the Avastin arm, compared to the control
group) were asthenia, pain, hypertension, diarrhea and leukopenia.
The most common adverse events (occurring in greater than two percent
of patients in the Avastin arm, compared to the control group) of any
severity were asthenia, pain, abdominal pain, headache, hypertension,
diarrhea, nausea, vomiting, anorexia, stomatitis, constipation, upper
respiratory infection, epistaxis, dyspnea, exfoliative dermatitis and
proteinuria.

About VEGF and Tumor Angiogenesis
The link between angiogenesis and cancer growth has been discussed by
many researchers for decades. It wasn't until 1989 that a key growth
factor influencing the process, VEGF, was discovered by Napoleone
Ferrara, M.D., a staff scientist at Genentech. Dr. Ferrara and his
team cloned VEGF, providing some of the first evidence that a
specific angiogenic growth factor existed. This research was
published in the journal Science in 1989. Dr. Ferrara then created a
mouse antibody to this protein. In 1993, Dr. Ferrara and his team at
Genentech, in a study published in Nature, demonstrated that the
antibody directed against VEGF could suppress angiogenesis and tumor
growth in preclinical models, providing compelling evidence that VEGF
can play a critical role in tumor growth. Clinical studies with a
humanized version of the antibody, Avastin, began in 1997.

About Genentech BioOncology
Genentech is committed to changing the way cancer is treated by
establishing a broad oncology portfolio of innovative, targeted
therapies with the goal of improving patients' lives. The company is
the leading provider of anti-tumor therapeutics in the United States.
Genentech is leading clinical development programs for Rituxan®
(Rituximab), Herceptin® (Trastuzumab), Avastin™ (bevacizumab) and
Tarceva™ (erlotinib), and markets all four products in the United
States alone (Avastin and Herceptin), with Biogen Idec Inc. (Rituxan)
or with OSI Pharmaceuticals (Tarceva). Genentech has licensed
Rituxan, Herceptin, and Avastin, and OSI Pharmaceuticals has licensed
Tarceva to Roche for sale by the Roche Group outside of the United
States.

The company has a robust pipeline of potential oncology therapies
with a focus on four key areas: angiogenesis, apoptosis (i.e.
programmed cell death), the HER pathway and B-cell biology. Potential
oncology therapies directed at the HER pathway include a therapeutic
antibody currently in Phase II trials. Also in early development are
a small molecule directed at the hedgehog pathway, a soluble human
protein targeting apoptosis and a humanized anti-CD20 antibody for
hematology/oncology indications.

Genentech is a leading biotechnology company that discovers,
develops, manufactures, and commercializes biotherapeutics for
significant unmet medical needs. A considerable number of the
currently approved biotechnology products originated from, or are
based on, Genentech science. Genentech manufactures and
commercializes multiple biotechnology products directly in the United
States, and receives royalties or other income from companies that
are licensed to market its products outside of the United States. The
company has headquarters in South San Francisco, Calif., and is
traded on the New York Stock Exchange under the symbol DNA. For
additional information about the company, please visit
http://www.gene.com.


# # #
For full prescribing information, including Boxed Warnings for
Avastin, please call 1-800-821-8590 or visit www.gene.com.

Please go over to the companion support site to this one at:
http://health.groups.yahoo.com/group/colon_cancer_support/
There, you'll get the info you're looking for and and a prompt
response. At this site mostly  postings regarding general colon
cancer treatments are to be found. Hope this helps.

                  Best Regards,
                            Ed

Genentech updates Avastin label with thromboembolic risk
  Last Updated: January 06, 2005



NEW YORK (Reuters) - Genentech Inc. said on Thursday it has updated
information on the package insert for its colon cancer drug Avastin
(bevacizumab) to reflect an increased risk of thromboembolism that
can lead to MIs and stroke.


The company, which first announced the potential risk last year, has
also sent a letter to physicians notifying them of the label change.
The final label reflects discussions with the U.S. Food and Drug
Administration, which analyzed information disclosed by Genentech.

Genentech, which is majority owned by Roche Holding AG, said last
August that the thromboembolic risk for patients taking Avastin plus
chemotherapy was as much as 5% compared with 1.9% in patients taking
chemotherapy alone. The risk in patients taking Avastin has now been
determined to be 4.4%, the company said.

The company said the risk of blood clots increased in patients over
the age of 65.

Avastin, which was approved in February last year, is the first U.S.-
approved anti-angiogenesis drug. It has been shown to extend the life
of colon cancer patients by an average of 5 months.

The warning last August has done little to affect sales of Avastin,
which costs $4,400 a month.





----------------------------------------------------------------------
----------

This online resource is supported by: Sanofi-Synthelabo
www.asco.org c Copyright 2002 American Society of Clinical Oncology
All rights reserved worldwide

Hi

My name is Denise and my husband, Ray, was diagnosed with
stage four colon cancer just this past November. He appeared
healthy as a horse until August. Then there was chronic
stomach pain, which he attributed to stress...since it was
a stressful year for our family all around.

By late October, he had lost about 15-20 lbs from lack of
appetite and nausea. We went to a local emergency room
and were told that he probably had the beginnings of an
ulcer...to take Prilosec...and follow up with a regular MD.
We were planning a move and decided that the follow up
could wait for two more weeks...he had meds to see him
through the move.

In early November, our family was packing all our belongings
and moving from Mississippi to Michigan...to start our
new business and a new life that looked to be a great
improvement over the prior situation.

We arrived in Michigan on November 10th and by the 14th,
Ray was in the emergency room again...in great pain...and
was admitted with a tentative diagnosis of Crohn's disease.

5 days of testing later was surgery...a small, simple
resection of the small bowel...but it was more once the
surgeon got in there. He had to remove ALL of Ray's
large bowel and create an ileostomy.

But that's not all...

5 days after that...pathology reports come in and show that
it isn't Crohn's at all...but cancer...eating away at his
bowels from the outsides in...and metastacized on his
abdominal wall.

They gave this ridiculous prognosis of 2 months to 4 years,
and said it was dependent on his reactions to chemo...but
chemo was our only hope. Both love and fear kept me at his
side in the hospital for two whole weeks.

All this after he was released from his employment of over
17 years for reasons of absenteeism...most which were for
stomach ailments etc...

So here we are...no jobs...no money to speak of...two
teenage daughters...one adult daughter who is a new mom...
all living in a new state...with no family, only some
really good friends...on "assistance" for the first time in
nearly 20 years...

Ray has started chemo now and is reacting well so far...but
so far to go...blockages keep coming and going in his small
bowel...caused by the cancer and/or the chemo...still don't
know which for certain.

It seems like life is on hold waiting for the next bit of
news on Ray...and the visits to the hospital (a 50 minute
drive from our friends' home, where we are staying
temporarily) are eating up what money we get on assistance.

I'm sorry if I sound whinny or anything...I am just frustrated
and feeling very alone...he was always the breadwinner and
the final word...and now I have so many new roles.

HELP!!! please... Any advice or sharing would be gold to me
right now.

Thanks for "listening"...

Denise aka Butterfly

See the article below regarding NPI-2358

Priscilla A. Savary
Executive Director
Colorectal Cancer Network
PO Box 182, Kensington MD 20895
301-879-1500
psavary@...
www.colorectal-cancer.net
_________
Like to help CCNetwork? Go shopping!
That's right, go head and buy something for yourself -- a new CD, the latest
bestseller, essentials like toothpaste or vitamins, even a computer. But first
join www.iGive.com/CCNetwork . Every time you shop at one of the over 500
name-brand stores in the Mall at iGive.com, we'll receive a donation of up to
26% of each purchase you make, at no cost to you.
Remember, donating to CCNetwork won't cost you a thing.  But we'll miss out on a
lot of extra dough, if you don't join. So visit www.iGive.com/CCNetwork now.
Membership is free and your privacy is guaranteed.

Click here to join:  http://www.iGive.com/CCNetwork


____________________________________
Nereus, Vitae Raise Funds For Clinical Trials In 2005

By Jennifer Boggs

Staff Writer

Two companies started the new year on a high note. Nereus Pharmaceuticals Inc.
and newly named Vitae Pharmaceuticals announced they had raised funds to push
their products into clinical trials in 2005.

Marking its fourth financing round, San Diego-based Nereus will be receiving a
$42.6 million private placement in two tranches. The first, already closed,
amounted to $24.3 million.

The second tranche will be $18.3 million upon completion of development
milestones, said Nereus President and CEO Kobi Sethna.

"We'll draw down the rest once we reach our milestones, which are
investigational new drug applications for our two lead compounds," he told
BioWorld Today. "Then we'll have funding in place for conducting clinical
trials."

In its first three rounds, Nereus raised $38 million, Sethna said.

New investors HBM BioVentures Ltd., of Baar, Switzerland, and HBM BioCapital LP,
of Research Triangle Park, N.C., led the fourth round, along with returning
investors Alta Partners, of San Francisco; Forward Ventures, of San Diego; GIMV,
of Antwerp, Belgium; Novartis Bioventure Fund, of Basel, Switzerland; Pacific
Venture Group, of San Francisco; and Lotus BioScience Ventures, of Hong Kong.

Sethna estimated that the $42.6 million will sustain the company for the next
two to three years.

"It depends on how the clinical trials go and whether we partner the compounds,"
Sethna said. "We've been talking to pharmaceutical companies about possible
joint development projects, so that could change the picture."

He said Nereus hopes the funds will get its first compound, NPI-2358, a vascular
disrupting agent, into Phase II trials and its second compound, NPI-0052, a
proteasome inhibitor, into Phase I studies.

"Then we'll see what the market looks like and decide whether to go public or
seek additional private funds or partner with pharmaceutical companies," Sethna
said. "In two or three years, I think, if all goes well with the clinical
trials, there's a good chance we'll probably seek some public funds."

NPI-2358, a cancer product that works as a targeted compound rather than a
cytotoxic drug, is a selective tumor vascular disrupting agent (VDA) designed to
treat solid tumors. The parent molecule of the compound was isolated from a
marine fungus that provided the chemistry.

"The compound works on its own and synergistically with chemotherapy and
radiotherapy," Sethna said, adding that the company plans to begin human trials
in a few months.

The compound initially will be tested by itself, but Sethna said later "it will
be tried in combination as we move along in the process."

He added that while VDA is a scientifically proven treatment, a VDA compound has
yet to be approved by the FDA.

"So we're on the cutting edge here," he said.

Nereus' second targeted compound, NPI-0052 (salinosporamide), is derived from a
marine-obligate actinomycete and is designed as a second-generation proteasome
inhibitor to treat multiple myeloma. The concept of looking for treatments by
inhibiting proteasomes has been a popular concept since the FDA approved
Cambridge, Mass.-based Millennium Pharmaceuticals' Velcade in 2003, Sethna said.

In vitro data presented at the American Society of Hematology meeting in
December by Nereus and Harvard Medical School's Dana-Farber Cancer Institute
showed that the compound was active in multiple myeloma cells resistant to
Velcade, as well as desamethasone and doxorubicin, though exact mechanisms still
were under investigation. (See BioWorld Today, Dec. 10, 2004.)

"This is a very exciting compound for us," Sethna said of NPI-0052. "Also, on a
preclinical basis, it shows more safety and does not have the same kind of toxic
effects of other chemotherapy treatments."

Nereus has filed an accelerated investigational new drug application for
NPI-0052, and Sethna said the company hopes to begin Phase I trials by the
latter part of the year.

Using its marine microbial drug discovery platform, Nereus has "a host of other
compounds in the wings that will be studied for potential use as anti-cancer,
anti-inflammatory and anti-infectious agents," he said. "We'll be making
selections of compounds to begin development in 2006 and 2007."

Created in 1998, Nereus began work in late 2001 isolating marine microbes.
Sethna said in the last two years, the company "has grown exponentially."

Nereus also recently named three new directors to its board: incoming Director
Gary Shearman, of HBM Advisors USA; Jason Fisherman, of Advent; and Nina
Kjellson, of Interwest Partners.

Vitae's $34M Part Of 'Rapid Evolution'

Fort Washington, Pa.-based Vitae Pharmaceuticals, formerly Concurrent
Pharmaceuticals, introduced its new name and secured $34 million in equity
financing to accelerate the company's product programs.

Tuesday's announcements encapsulate "the rapid evolution of our company," said
Vitae CEO Jeff Hatfield. "The name change emblemizes that revolution."

Vitae, a Latin word meaning "life," reflects the company's efforts to mark
itself as a product-focused drug development company, Hatfield said.

He described Vitae as being "at the forefront of the trend of rapid product
creation," with plans for four products to begin clinical trials in 2005.

"What's really important about all our efforts is the trend to rapidly create
valuable products," he said.

Vitae has raised $75 million to date, including the $34 million in funding from
two new investors - Atlas Venture, of Boston, and Wellcome Trust, of London -
and existing investors Prospect Venture Partners, of Palo Alto, Calif.; Venrock
Associates, of New York; and New Enterprise Associates, of Menlo Park, Calif.

The money will be used to accelerate product candidates as they begin human
trials and, later, to help expand research and commercialization, Hatfield said.

"I hope this will sustain the company for a two- to three-year horizon," he
said, adding that funds will be used to pay for upcoming clinical trials for
four of Vitae's products.

The company's lead cancer program is set to start human trials in the first half
of this year. Initial studies will focus on lymphoma, though the compound might
also be tested for additional cancer indications.

Also in the pipeline is a compound aimed at treating myeloid leukemia. The
company is developing a selective modulator of a nuclear receptor subtype
thought to play a role in neutrophil differentiation and, based on preclinical
studies, might be applied to treat and prevent chemo-radiotherapy-inducted
neutropenia and to enhance peripheral blood progenitor-cell mobilization in
transplantation.

A third product, a topical agent designed to treat psoriasis, eventually might
be extended to the treatment of acne and photo-aging, based on results from
clinical trials to begin this year.

The fourth product in preclinical development is an orally available renin
inhibitor to manage hypertension and end-organ protection. Renin, an aspartyl
protease, is the rate-limiting enzyme in the renin-angiotensin system that plays
a key role in regulating blood volume, arterial pressure and vascular function.

Clinical studies have shown that inhibition of renin can control blood pressure,
though most programs have not been successful in finding orally available
small-molecule compounds suitable for development. Hatfield said Vitae is using
its technology to generate non-peptidic renin inhibitors and has discovered
multiple series of small-molecule inhibitors of the enzyme.

"Vitae selected this as our target challenge," he said. "We believe in a unique
approach that combines the talent of drug discovery skills to achieve innovative
products."

In May, the company bought a portfolio of near-clinical compounds from Allergan
Inc.'s retinoid and rexinoid nuclear receptor drug program. Vitae, then known as
Concurrent, gave Allergan undisclosed equity plus potential future milestone
payments and royalties in exchange for exclusive license rights to compounds for
diabetes and cancer. (See BioWorld Today, May 27, 2004.)


[Non-text portions of this message have been removed]

I have recently created a memorial for colon cancer victims.  If you have lost
someone to colon cancer, please go to www.coloncancermemorial.com to submit your
memorial.
If you have any suggestions for the site, please send them my way, too!
Thank you.

--
Colon Cancer Victims Memorial http://www.coloncancermemorial.com

[Non-text portions of this message have been removed]

Fecal DNA test promising for colorectal cancer detection
  Last Updated: December 23, 2004



NEW YORK (Reuters Health) - A non-invasive test that analyzes mutated
DNA in feces may be a useful method of detecting colorectal cancer in
average risk, asymptomatic individuals, according to a study in the
December 23rd issue of The New England Journal of Medicine.


In the study, 4404 average-risk adults age 50 or older underwent
fecal occult-blood testing with the Hemoccult II, fecal DNA testing,
as well as colonoscopy -- the reference standard.

Dr. Thomas F. Imperiale from the Indiana University School of
Medicine and the Regenstrief Institute in Indianapolis and
multicenter colleagues compared test results in a random subgroup of
2507 subjects seen in private-practice or university-based settings.

The fecal DNA test detected just over half (16 of 31) of all invasive
colorectal cancers (TNM stage I, II, or III), for a sensitivity of
51.6%, they report.

"The fecal DNA test was better than the Hemoccult II, the current
standard noninvasive screening test," Dr. Imperiale told Reuters
Health, noting that the Hemoccult II detected only 4 of 31 invasive
colorectal cancers in the same population, for a sensitivity of 12.9%.

Moreover, the sensitivity of the fecal DNA test was "more than twice"
that of Hemoccult II for detecting adenomas containing high-grade
dysplasia (32.5% vs 15.0%). Among 418 individuals with advanced
neoplasia, the DNA fecal test had a sensitivity of 18.2% compared
with a sensitivity of 10.8% for Hemoccult II.

"Specificity in subjects with negative findings on colonoscopy was
94.4% for the fecal DNA panel and 95.2% for Hemoccult II," the
authors also report.

Dr. Imperiale and colleagues point out that while "the majority of
neoplastic lesions identified by colonoscopy were not detected by
either noninvasive test, the multitarget analysis of fecal DNA
detected a greater proportion of important colorectal neoplasia than
did the Hemoccult II without compromising specificity."

They emphasize, however, that the place of DNA fecal testing in
colorectal cancer screening remains to be determined.

Dr. Steven H. Woolf, from the Virginia Commonwealth University in
Richmond, agrees, noting in an editorial that while testing stool for
DNA is a "potentially smarter strategy" than testing it for occult
blood, numerous questions remain including issues of
generalizability, superiority, testing intervals, not to mention
affordability.

The price tag for fecal DNA testing is $400 to $800 compared with a
cost of $3.00 to $40 for fecal occult blood testing, he notes.

The current study was funded by grants from EXACT Sciences, Inc.,
manufacturer of the stool DNA panel.





----------------------------------------------------------------------
----------

This online resource is supported by: Sanofi-Synthelabo
www.asco.org c Copyright 2002 American Society of Clinical Oncology
All rights reserved worldwide