Try a product called Gum and Tooth Tonic. It is not as harsh as peroxide or
alcohol based mouth washes. It is made with essential oils and independent
research showed that it is very effective in treating most oral infections and
sores.

Scott

PS It is not available retail but you can order it online.
----- Original Message -----
From: "Ruth Brucker" <ruthb1999@...>
To: CLLResearch@yahoogroups.com
Sent: Monday, November 23, 2009 10:01:49 AM GMT -07:00 US/Canada Mountain
Subject: [CLLResearch] mouth sores: what causes, which days are worst, how to
help prevent ...






My husband found that peroxide based mouth wash worked very well for mouth
sores.

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




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

My husband found that peroxide based mouth wash worked very well for mouth
sores.




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

From Lymphomation.org, twitter (likely Liz : )

Mayo Clinic on chemo mouth sores: what causes, which days are
worst, how to help prevent, how to cope. http://bit.ly/78jiYn

All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

Circulating CD52 and CD20 levels at end of treatment predict for progression and
survival in patients with chronic lymphocytic leukaemia treated with
fludarabine, cyclophosphamide and rituximab (FCR).
Gheath Alatrash, Maher Albitar, Susan O'Brien, Xuemei Wang, Taghi Manshouri,
Stefan Faderl, Alessandra Ferrajoli, Jan Burger, Guillermo Garcia-Manero, Hagop
M Kantarjian, Susan Lerner, Michael J Keating, and William G Wierda
Br J Haematol, November 6, 2009; .

From the Department of Stem Cell Transplantation & Cellular Therapy, U.T. MD
Anderson Cancer Center, Houston, TX.

Summary CD52 and CD20 antigens are important therapeutic targets for the
monoclonal antibodies (mAbs) alemtuzumab and rituximab respectively. Circulating
CD52 (cCD52) and CD20 (cCD20) have prognostic utility in lymphoid malignancies.
The efficacy of mAb therapy in patients with chronic lymphocytic leukaemia (CLL)
may be adversely affected by cCD52 or cCD20. In this report, blood and bone
marrow (BM) cCD52 and cCD20 were measured at response assessment in previously
treated (N = 235) patients with CLL who received fludarabine, cyclophosphamide,
and rituximab (FCR). Univariate and multivariate statistical models evaluated
correlations of pre- and response variables with progression-free (PFS) and
overall survival (OS). Response variables included 1996 National Cancer
Institute-Working Group (NCI-WG) response, polymerase chain reaction (PCR) for
immunoglobulin heavy chain (IGHV) in BM, and cCD52 and cCD20 levels (blood and
BM) at response assessment. Using multivariate analysis, response blood and BM
cCD52, blood cCD20, and NCI-WG response were significant independent predictors
of PFS. At the time of response assessment, BM cCD52 correlated with OS in
univariate analysis. cCD52 and cCD20, therefore appear useful in predicting
survival and may be important for monitoring patients following salvage FCR
(fludarabine, cyclophosphamide, rituximab) therapy. These data further indicate
that plasma may be a good target to evaluate for minimal residual disease using
cCD52/cCD20 levels.
PMID: 19895616


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A comprehensive evaluation of the prognostic significance of 13q deletions in
patients with B-chronic lymphocytic leukaemia.
Daniel L Van Dyke, Tait D Shanafelt, Timothy G Call, Clive S Zent, Stephanie A
Smoley, Kari G Rabe, Susan M Schwager, Jessica C Sonbert, Susan L Slager, and
Neil E Kay
Br J Haematol, November 6, 2009; .

Division of Laboratory Genetics at Mayo Clinic, Rochester, MN, USA.

Summary Deletion 13q14 on fluorescence in situ hybridization (FISH) analysis is
the most common cytogenetic abnormality in chronic lymphocytic leukaemia (CLL),
and is a favourable prognostic biomarker when detected as a sole abnormality. We
intensively interrogated clinical outcome in 323 consecutive, untreated CLL
patients with isolated 13q- identified within 2 years of diagnosis. We also
analyzed outcome in 217 additional patients with deletion 11q22.3 or 17p13.1, or
trisomy 12, based on whether these occurred in isolation or in conjunction with
13q-. Patients with a heterozygous 13q- and those with a homozygous deletion had
similar time to first treatment (TFT) and overall survival (OS). In contrast, a
higher percentage of 13q- nuclei was associated with significantly shorter TFT
(P < 0.001). The 5-year untreated rate was 79% for patients with isolated 13q-
in </=65.5% of nuclei compared to 38% among those with 13q- in >65.5% of nuclei
(P < 0.001). The percentage of nuclei exhibiting 13q- remained an independent
predictor of TFT after controlling for ZAP-70, IGHV, or CD38 (all P < 0.001).
Among patients with 13q- plus one other FISH abnormality, concomitant 13q-
appeared to attenuate the shorter survival associated with 17p- (P = 0.019). The
clinical implications of 13q- in CLL appear more complex than originally
appreciated.
PMID: 19895615

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Recruitment of PKC-betaII to lipid rafts mediates apoptosis-resistance in
chronic lymphocytic leukemia expressing ZAP-70.
C Meyer Zum Buschenfelde, M Wagner, G Lutzny, M Oelsner, Y Feuerstacke, T
Decker, C Bogner, C Peschel, and I Ringshausen
Leukemia, November 12, 2009; .

3rd Department of Medicine, Hematology and Oncology, Technical University,
Munich, Germany.

ZAP-70 is a key signaling molecule in T cells. It couples the antigen-activated
T-cell receptor to downstream signaling pathways. Its expression in leukemic
B-cells derived from a subgroup of patients with chronic lymphocytic leukemia
(CLL) is associated with an aggressive course of the disease. However, its
implication for the pathogenesis of aggressive CLL is still unclear. In this
study, we show that the expression of ZAP-70 enhances the signals associated
with the B-cell receptor, recruiting protein kinase C-betaII (PKC-betaII) into
lipid raft domains. Subsequently, PKC-betaII is activated and shuttles from the
plasma membrane to the mitochondria. We unravel that the antiapoptotic protein
Bcl-2 and its antagonistic BH3-protein Bim(EL) are putative substrates for
PKC-betaII. PKC-betaII-mediated phosphorylation of Bcl-2 augments its
antiapoptotic function by increasing its ability to sequester more pro-apoptotic
Bim(EL.) In addition, the phosphorylation of Bim(EL) by PKC-betaII leads to its
proteasomal degradation. These changes confer leukemic cells to a more
antiapoptotic state with aggressiveness of the disease. Most importantly, these
molecular changes can be therapeutically targeted with the small molecule
inhibitor Enzastaurin. We provide evidence that this compound is highly active
in leukemic cells and augments the cytotoxic effects of standard
chemotherapeutic drugs.Leukemia advance online publication, 12 November 2009;
doi:10.1038/leu.2009.216.
PMID: 19907441

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Current and emerging treatments for chronic lymphocytic leukaemia.
T Robak, K Jamroziak, and P Robak
Drugs, January 1, 2009; 69(17): 2415-49.

Department of Hematology, Medical University of Lode, Copernicus Memorial
Hospital, Lodz, Poland. robaktad@...

Chronic lymphocytic leukaemia (CLL) is the most common adult leukaemia in Europe
and North America. The disease is characterized by proliferation and
accumulation of small CD5+ B cells in blood, lymph nodes, spleen, liver and bone
marrow. The natural clinical course of CLL is highly variable, and chemotherapy
is usually not indicated in early and stable disease. However, patients with
progressive and more advanced CLL require treatment. For many years,
chlorambucil with or without corticosteroids was used in previously untreated
patients with CLL. More recently, purine nucleoside analogues (PNAs)
[fludarabine, cladribine and pentostatin] have been included in treatment
approaches for this disease, and chlorambucil is no longer the leading standard
everywhere. Currently, this drug is rather recommended for the treatment of
older, unfit patients with co-morbidities, especially in European countries.
Significantly higher overall response (OR) and complete response (CR) rates in
patients treated initially with PNAs than in those treated with chlorambucil or
cyclophosphamide-based combination regimens have been confirmed in randomized,
prospective, multicentre trials. Moreover, PNAs administered in combination with
cyclophosphamide produce higher response rates, including CR and molecular CR,
compared with PNA as monotherapy. Recent reports suggest that the administration
of monoclonal antibodies (mAbs) can significantly improve the course of CLL. At
present, two mAbs have the most important clinical value in patients with CLL.
The first is rituximab, a human mouse antibody that targets CD20 antigens, and
the second is alemtuzumab, a humanized form of a rat antibody active against
CD52. Several recent reports suggest that in patients with CLL, rituximab
combined with a PNA can increase the OR and CR rates compared with PNA or
rituximab alone, with acceptable toxicity. In randomized trials, the combination
of rituximab with fludarabine and cyclophosphamide (FC-R regimen) demonstrated
higher rates of OR, CR and progression-free survival in patients with previously
untreated and relapsed or refractory CLL than fludarabine plus cyclophosphamide
(FC regimen). Several reports have confirmed significant activity with
alemtuzumab in relapsed or refractory CLL, as well as in previously untreated
patients. Recently, several new agents have been investigated and have shown
promise in treating patients with CLL. These treatments include new mAbs, agents
targeting the antiapoptotic bcl-2 family of proteins and receptors involved in
mediating survival signals from the microenvironment, antisense oligonucleotides
and other agents. The most promising are new mAbs directed against the CD20
molecule, lumiliximab and anti-CD40 mAbs. Oblimersen, alvocidib (flavopiridol)
and lenalidomide are also being evaluated both in preclinical studies and in
early clinical trials. In recent years, a significant improvement in
haematopoietic stem cell transplantation (HSCT) procedures in patients with
high-risk CLL has been observed. However, the exact role of HSCT, autologous or
allogeneic, in the standard management of CLL patients is still undefined.
PMID: 19911856

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SEER: Lymphoma incidence rates by subtype (2001-06)
http://bit.ly/8MGIXM

Can't say this would have happened without PAL's persistence ...
letters to SEER regarding the need, but it didn't hurt.

Subtypes stats are still not available under Quick Facts
however.
__________________
All the best,

Karl

Patients Against Lymphoma
www.Lymphomation.org


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

Blood First Edition Paper, prepublished online November 17, 2009; DOI
10.1182/blood-2009-08-236471.
Submitted August 10, 2009; accepted October 26, 2009.


Inhibition of Syk with fostamatinib disodium has significant clinical activity
in non Hodgkin's lymphoma and chronic lymphocytic leukemia
Jonathan W. Friedberg1,*, Jeff Sharman2, John Sweetenham3, Patrick B. Johnston4,
Julie M. Vose5, Ann LaCasce6, Julia Schaefer-Cutillo1, Sven De Vos7, Rajni
Sinha8, John P. Leonard9, Larry D. Cripe10, Stephanie A. Gregory11, Michael P.
Sterba12, Ann M. Lowe12, Ronald Levy2 and Margaret A. Shipp6
1 James P. Wilmot Cancer Center, University of Rochester, Rochester, NY; 2
Stanford University, Stanford, CA; 3 Cleveland Clinic, Cleveland, OH; 4 Mayo
Clinic, Rochester, MN; 5 University of Nebraska, Omaha, NE; 6 Dana-Farber Cancer
Institute, Boston, MA; 7 UCLA, Los Angeles, CA; 8 Emory University, Atlanta, GA;
9 Cornell University, New York, NY; 10 Indiana University, Indianapolis, IN; 11
Rush University, Chicago, IL; 12 Rigel Pharmaceuticals, South San Francisco, CA

* Corresponding author; email: jonathan_friedberg@...

Abstract

Certain malignant B-cells rely upon B-cell receptor (BCR)-mediated survival
signals. Spleen tyrosine kinase (Syk) initiates and amplifies the BCR signal. In
in vivo analyses of B-cell lymphoma cell lines and primary tumors, Syk
inhibition induces apoptosis. These data prompted a phase I/II clinical trial of
fostamatinib disodium, the first clinically available oral Syk inhibitor, in
patients with recurrent B-cell NHL. Dose-limiting toxicity in the phase I
portion was neutropenia, diarrhea and thrombocytopenia and 200 mg bid was chosen
for Phase II testing. 68 patients with recurrent B-NHL were then enrolled in 3
cohorts: DLBCL; FL, and other NHL, including MCL; marginal zone/MALT;
lymphoplasmacytic; and SLL/CLL. Common toxicities included diarrhea, fatigue,
cytopenias, hypertension and nausea. Response rates were 22% for (5/23) DLBCL,
10% (2/21) for follicular lymphoma, 55% (6/11) for SLL/CLL and 11% (1/9) for
mantle cell lymphoma. Stable disease was observed in an additional 22 patients,
including 11 with FL, 4 with DLBCL, 4 with MCL, 2 with SLL/CLL and 1 with
marginal zone lymphoma. Median progression-free survival was 4.2 months, and
median response duration exceeded 4 months. Disrupting BCR-induced signaling by
inhibiting Syk represents a novel therapeutic approach to NHL and SLL/CLL. This
study is registered at http://clinicaltrials.gov as NCT00446095.

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Published online first on November 17, 2009
[Cancer Research, 10.1158/0008-5472.CAN-09-2604]
A Novel Paradigm to Trigger Apoptosis in Chronic Lymphocytic Leukemia
Sandra Loeder1, Thorsten Zenz2, Andrea Schnaiter2, Daniel Mertens2, Dirk
Winkler2, Hartmut Döhner2, Klaus-Michael Debatin1, Stephan Stilgenbauer2 and
Simone Fulda1
1 University Children's Hospital; 2 Department of Internal Medicine III, Ulm
University, Ulm, Germany

Requests for reprints: Simone Fulda, University Children's Hospital, Eythstr.
24, D-89075 Ulm, Germany. Phone: 49-731-5005-7034; Fax: 49-731-5005-7058;
E-mail: simone.fulda@... .


Evasion of apoptosis is a hallmark of chronic lymphocytic leukemia (CLL),
calling for new strategies to bypass resistance. Here, we provide first evidence
that small-molecule X-linked inhibitor of apoptosis (XIAP) inhibitors in
combination with the death receptor ligand tumor necrosis factor-related
apoptosis-inducing ligand (TRAIL) present a novel approach to trigger apoptosis
in CLL, including subgroups with resistant disease or unfavorable prognosis.
XIAP, cellular IAP (cIAP) 1, and cIAP2 are expressed at high levels in primary
CLL samples. Proof-of-concept studies in CLL cell lines show that subtoxic
concentrations of XIAP inhibitors significantly enhance TRAIL-induced apoptosis
and also sensitize for CD95-mediated apoptosis. Importantly also in primary CLL
samples, XIAP inhibitor acts in concert with TRAIL to trigger apoptosis in 18 of
27 (67%) cases. This XIAP inhibitor-induced and TRAIL-induced apoptosis involves
caspase-3 activation and is blocked by the caspase inhibitor zVAD.fmk. The
cooperative interaction of XIAP inhibitor and TRAIL is even evident in distinct
subgroups of patients with poor prognostic features (i.e., with 17p deletion,
TP53 mutation, chemotherapy-refractory disease, or unmutated VH genes).
Interestingly, cases with unmutated VH genes were significantly more sensitive
to XIAP inhibitor-induced and TRAIL-induced apoptosis compared with VH
gene-mutated samples, pointing to a role of B-cell receptor signaling in
apoptosis regulation. By showing that XIAP inhibitors in combination with TRAIL
present a new strategy to trigger apoptosis even in resistant forms and poor
prognostic subgroups of CLL, our findings have important implications for the
development of apoptosis-based therapies in CLL. [Cancer Res
2009;69(23):8977-86]



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Encouaging results, but n is too small

Preliminary Results of a Phase II Study of Lenalidomide and Rituximab in
Relapsed / Refractory Indolent Non-Hodgkin's Lymphoma (NHL)
http://ash.confex.com/ash/2009/webprogram/Paper25195.html

Of 15 patients currently enrolled on study, 14 received >2 cycles of R2, and 12
are evaluable for response. Median age for evaluable patients is 60 yrs (range:
50-91), 5 pts are female, and histologies include FL (n=9), SLL (n=1), and
marginal zone lymphoma (n=2). Median time from diagnosis to treatment on study
was 7.5 years (3.3-19), median number of prior therapies was 4 (range:1-11), and
9 patients were considered heavily pretreated (defined as ? 3 prior courses of
therapy).  All patients received prior rituximab, 6 patients had
rituximab-resistant disease (defined as no response or relapse ? 6 months after
initiating rituximab), and 5 patients had received prior radioimmunotherapy.

Of 12 evaluable patients, 10 (83.3%) responded to R2, including 5 patients (41%)
with a CR and 4 patients (33%) with a PR. Responses occurred in 4 of 6 patients
(66%) with rituximab refractory disease, and in 7 of 9 (77%) heavily pretreated
patients.

Of 9 patients with R/R FL, 5 (55%) achieved a CR and 3 (33%) had a PR in
response to R2, for an 88% ORR. At a median follow-up of 12 months, the median
progression free survival has not been reached.

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

Karl
This is a last minute request re details of Indolent Lymphoma program tonight at
8:PM tonight.
Aviva




________________________________
From: "KarlS@..." <KarlS@...>
To: PAL-parent-support@yahoogroups.com; CLLResearch@yahoogroups.com;
cns-PAL@yahoogroups.com; MantleCell@yahoogroups.com; nhl-dlc@yahoogroups.com;
nhl-follic@yahoogroups.com; nhl-info@yahoogroups.com; nhl-malt@yahoogroups.com;
PAL-datafork@yahoogroups.com
Sent: Wed, November 18, 2009 2:06:23 PM
Subject: [CLLResearch] NCI bulletin: New Drug Blocks "Undruggable" Target in
Cancer Cells

 
Early but interesting.
==
New Drug Blocks "Undruggable" Target in Cancer Cells
http://www.cancer. gov/ncicancerbul letin/111709/ page3

Researchers have created a new type of cancer drug that blocks a
"master" protein considered to be untouchable by conventional
agents. A team from Harvard University used the drug to suppress
signals from a growth-promoting pathway, the Notch signaling
pathway, that switches on inappropriately in some cancers.
Cancer cells that depend on Notch signaling die when the pathway
is blocked, Drs. Gregory L. Verdine, James Bradner, and their
colleagues reported in the November 12 Nature.

The drug's primary target is Notch1, a transcription factor that
regulates genes involved in the growth and survival of cells.
Transcription factors are mutated in various cancers, but these
proteins have proved difficult to target directly because of
their structures.

To solve this problem, the Harvard team, led in the lab by
graduate student Raymond Moellering, designed a drug molecule
(called SAHM1) that enters cells and interferes with a
protein-protein interaction that is essential for the
transmission of cell growth signals via the Notch pathway.

The researchers tested the drug using cells from patients with
T-cell acute lymphoblastic leukemia (T-ALL) and a mouse model of
the disease. The Notch1 gene is mutated in half of patients with
T-ALL and produces an inappropriately active Notch1 protein.
Activated Notch signaling has been seen in several other
cancers, including lung, ovarian, and pancreatic cancer, and
melanoma.

"We've drugged a so-called undruggable target," said Dr.
Verdine. "This study validates the notion that you can target a
transcription factor by choosing a new class of molecules,
namely stapled peptides." The strategy may work for other
transcription factors because the molecular logic of these
proteins is similar to that of Notch1, he added.

In an accompanying editorial, Drs. Paramjit Arora and Aseem
Ansari said that the group's "remarkable results highlight the
potential of molecules that mimic the secondary structures of
proteins to target normally intractable protein-protein
interactions. "
All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation. org | Current News: http://bit.ly/f2A0T

How to Help: www.lymphomation. org/how-to- help.htm







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

Early but interesting.
==
New Drug Blocks "Undruggable" Target in Cancer Cells
http://www.cancer.gov/ncicancerbulletin/111709/page3

Researchers have created a new type of cancer drug that blocks a
"master" protein considered to be untouchable by conventional
agents. A team from Harvard University used the drug to suppress
signals from a growth-promoting pathway, the Notch signaling
pathway, that switches on inappropriately in some cancers.
Cancer cells that depend on Notch signaling die when the pathway
is blocked, Drs. Gregory L. Verdine, James Bradner, and their
colleagues reported in the November 12 Nature.

The drug's primary target is Notch1, a transcription factor that
regulates genes involved in the growth and survival of cells.
Transcription factors are mutated in various cancers, but these
proteins have proved difficult to target directly because of
their structures.

To solve this problem, the Harvard team, led in the lab by
graduate student Raymond Moellering, designed a drug molecule
(called SAHM1) that enters cells and interferes with a
protein-protein interaction that is essential for the
transmission of cell growth signals via the Notch pathway.

The researchers tested the drug using cells from patients with
T-cell acute lymphoblastic leukemia (T-ALL) and a mouse model of
the disease. The Notch1 gene is mutated in half of patients with
T-ALL and produces an inappropriately active Notch1 protein.
Activated Notch signaling has been seen in several other
cancers, including lung, ovarian, and pancreatic cancer, and
melanoma.

"We've drugged a so-called undruggable target," said Dr.
Verdine. "This study validates the notion that you can target a
transcription factor by choosing a new class of molecules,
namely stapled peptides." The strategy may work for other
transcription factors because the molecular logic of these
proteins is similar to that of Notch1, he added.

In an accompanying editorial, Drs. Paramjit Arora and Aseem
Ansari said that the group's "remarkable results highlight the
potential of molecules that mimic the secondary structures of
proteins to target normally intractable protein-protein
interactions."
All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

A finding that surprised investigators I suspect.  Did me.   ~
Karl

==
Folic acid plus vitamin B12 may increase risk of cancer, death
in heart-disease patients.

Canada's Globe and Mail (11/18, Weeks) reports that, according
to research published Nov. 18 in the Journal of the American
Medical Association, "heart-disease patients treated with a
combination of folic acid and vitamin B12 had an increased risk
of cancer and death, compared to patients who didn't receive the
vitamins as treatment." The finding "fuels fears that mandatory
fortification of the food supply with folic acid could yield
unintended consequences."

         The Los Angeles Times (11/17, Dennis) "Booster Shots"
blog reported that the researchers "analyzed data from 6,837
people with ischemic heart disease treated with folic acid, B6
and B12; folic acid and B12; just B6 or a placebo," finding that
"those treated with folic acid and B12 had higher rates of
cancer, cancer deaths, and deaths in general over the course of
several years."

         In fact, 10 percent "of patients getting folic acid and
vitamin B12 developed cancer, compared with 8.4 percent who
didn't receive this treatment," Bloomberg News (11/18, Cortez)
reports. Meanwhile, "four percent died from cancer and 16
percent died from any cause among those getting folic acid and
vitamin B12" compared to "2.9 percent of people who died from
cancer and 13.8 percent who died from any cause among those who
didn't get the combination."

         Notably, "the most common cancers associated with folic
acid were colorectal, lung, prostate, and blood cancer,"
HealthDay (11/17, Reinberg) reported. But, "other researchers
cautioned that the results should not turn women away from
normal folic acid supplements that can help prevent birth
defects," MedPage Today (11/17, Walsh) reported. WebMD (11/17,
Boyles) also covered the story.

All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

This I expect would apply to CNS-lymphoma, primary or secondary
http://bit.ly/3s8M9k


All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

This study is not recruiting, but worth calling attention to.
Prospective Study of Possible Infectious Disease - Associated
Antigen Drive in Previously Untreated Indolent Lymphoma
http://clinicaltrials.gov/ct2/show/NCT00582270
The purpose of this study is to determine if an infectious
disease may be associated with the new lymphoma diagnosis.

Infections to be tested include:

   1.. Helicobacter pylori (H. pylori): This is a bacteria
sometimes found in the stomach that has been associated with a
particular kind of lymphoma, gastric MALT. We are interested to
learn if the H. pylori infection may be associated with other
indolent lymphomas.
   2.. Hepatitis C: This virus infection of the liver has been
found in association with non-follicular lymphomas in Italy. We
want to determine if the infection is associated with lymphomas
in the United States.
   3.. Bacterial overgrowth of the small bowel: Since indolent
lymphomas often affect the lymph nodes surrounding the small
bowel, it may be possible that an infection within the bowel is
stimulating lymphoma growth. This has never been demonstrated to
date, and will be studied in this clinical study.
   4.. Epstein-Barr virus: This is the virus that causes
infectious mononucleosis or "mono." It has been associated with
other rapidly growing lymphomas, but not indolent lymphoma.

All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

Greetings,

Occupational studies have been done on dental health
professionals ...those presumably exposed to mercury vapors at
the highest levels ... and no association with mortality from
cancer - beyond that for the general population.

See for example: http://bit.ly/2gxQWf

And related PubMed abstracts: http://bit.ly/1omNac

The only proven benefit would be financial - to the dentist who
replaces them. If a filling must be removed for other reasons,
other materials are available I believe.

Further, even if such exposures were associated with higher risk
of CLL, removing them would likely do no good after the fact.

All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

Here's the source report:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699384/?tool=pmcentrez

Seems an important finding in that it was a prospectively
designed study.

Worth a mention, that switching to a vegetarian life style after
the diagnosis (even if good for other reasons) is not likely to
influence the clinical course of an existing cancer ... (just as
quitting smoking is not likely to reverse a lung cancer)

copying from the Discussion:

"We observed a striking difference between the dietary groups in
the risk for the group of cancers of the lymphatic and
haematopoietic tissues, on the basis of 257 cancers overall.

The risk for these cancers was not significantly reduced among
fish eaters, but among vegetarians the risk was substantially
lower than that among meat eaters.

Among the three major cancer types contributing to this
grouping, the risks for non-Hodgkin's lymphoma and multiple
myeloma, but not leukaemia, were significantly lower in
vegetarians than in meat eaters.

Previous research has suggested inconsistently that consumption
of meat and/or exposure to live animals and raw meat among
farmers and butchers might be associated with an increased risk
for some of these cancers (Zhang et al, 1999; Alexander et al,
2007). Potential mechanisms could include mutagenic compounds
and viruses (Cross and Lim, 2006; Alexander et al, 2007)."

==
I suppose for this to become definitive would require an
independent group to repeat the experiment and have a similar
finding.
All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

Thanks.  Just a note that results with regional deep
hyperthermia is not likely to be applicable for a systemic
(i.e., blood) cancer.  Karl

A Victory for Hyperthermia in Bladder Cancer
Sunday, 15 November 2009

There was another victory for the use of regional deep
hyperthermia in the
treatment of cancer. The latest victory occurred in the
treatment of
high-risk bladder cancer. Heat treatment, delivered via the BSD
2000
machine, improved such patients' five-year survival rate from 67
to 80
percent. The local tumor control rate went from 63 to 81
percent. In
addition, the disease-specific survival was 88 percent,
metastasis-free
survival was 89 percent, and the bladder-preserving rate was 96
percent at
three years.

By Ralph W. Moss

Full story
http://www.cancerdecisions.com/content/view/285/2/lang,english/

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Prudent guidelines for adults as well when in treatment or if
immune suppressed. ~ Karl

==
The Effectiveness of the Neutropenic Diet in Pediatric Cancer
Patients
http://clinicaltrials.gov/ct2/show/NCT00726934

Participants will be randomized to one of two dietary
guidelines: the neutropenic diet or the food safety guidelines
endorsed by the FDA. Both diets include the same guidelines
regarding Food Shopping, Food Storage, Food Preparation, Safe
Cooking, and Safe Serving of Food. The Neutropenic

Diet Guideline includes the following additional
recommendations:

Avoid raw vegetables and fruit (Oranges and bananas are okay.)
Avoid take-out foods and fast foods and fountain drinks.
Avoid aged cheese (blue, Roquefort, Brie).
Cook all produce to well done. Eggs must be hard-boiled.
Avoid deli meats.
No raw nuts, nuts roasted in shell, or freshly ground nutbutters
from a healthfood store.
No well water
No yogurt

All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

A Victory for Hyperthermia in Bladder Cancer
Sunday, 15 November 2009

There was another victory for the use of regional deep hyperthermia in the
treatment of cancer. The latest victory occurred in the treatment of
high-risk bladder cancer. Heat treatment, delivered via the BSD 2000
machine, improved such patients' five-year survival rate from 67 to 80
percent. The local tumor control rate went from 63 to 81 percent. In
addition, the disease-specific survival was 88 percent, metastasis-free
survival was 89 percent, and the bladder-preserving rate was 96 percent at
three years.

By Ralph  W. Moss

Full story
http://www.cancerdecisions.com/content/view/285/2/lang,english/

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Vegetarians have less cancers
In the last issue of icon we told you that meat caused inflammation in the body,
and inflammation was a known precursor to cancer. Now comes a repeat of a study
from several years ago. Last time an Oxford study concluded that overall
vegetarians had 40 per cent less cancers; this time it was just 12 per cent but
the figure varied enormously by cancer type (British Journal of Cancer). This
study followed more than 61,000 people for over 12 years, during which 3,350 of
the participants were diagnosed with cancer. The study looked at 20 different
types of cancers

The risk of being diagnosed with cancers of the stomach, bladder and blood was
lower in vegetarians than in meat eaters, but the most striking difference was
in cancers of the blood including leukaemia, multiple myeloma and non-Hodgkin
lymphoma. The risk of these diseases was 45 per cent lower in vegetarians than
in meat eaters. Professor Tim Key of Cancer Research UK Epidemiology Unit at
Oxford University, was lead author.

Importantly this study ruled out other influencing factors. The differences in
risks between vegetarians and meat eaters were independent of other lifestyle
behaviours including smoking, alcohol intake and obesity which also affect the
chance of developing cancer.

http://www.canceractive.com/cancer-active-page-link.aspx?n=2466#10

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Study of Repeat Intranodal Injection of Memgen's Cancer Vaccine,
Ad-ISF35, in Subjects With Non-Hodgkin's Lymphoma (Follicular,
Diffuse Large Cell, Mantle Cell, and Small Lymphocytic
Lymphoma/Chronic Lymphocytic Leukemia

http://clinicaltrials.gov/ct2/show/NCT00942409

University of California, San Diego Moores Cancer Center

Contact: Vineeta Prasad     858-822-0337     vprasad@...
Contact: Mary Carpenter     (858) 822-5635
mcarpenter@...

* ASCO report - Phase I data: http://bit.ly/3EtN5x


All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

A Genomic Approach to Improve Prognosis and Predict Therapeutic Response in
Chronic Lymphocytic Leukemia
   1.. Daphne R. Friedman1,2,
   2.. J. Brice Weinberg1,4,
   3.. William T. Barry2,
   4.. Barbara K. Goodman3,
   5.. Alicia D. Volkheimer4,
   6.. Karen M. Bond4,
   7.. Youwei Chen4,
   8.. Ning Jiang4,
   9.. Joseph O. Moore1,
   10.. Jon P. Gockerman1,
   11.. Louis F. Diehl1,
   12.. Carlos M. Decastro1,
   13.. Anil Potti1,2 and
   14.. Joseph R. Nevins2
+ Author Affiliations

   1.. Authors' Affiliations:1Divisions of Hematology, Oncology, and Cellular
Therapy, 2Duke Institute for Genome Sciences and Policy, and 3Department of
Pathology, Duke University Medical Center; and 4Department of Medicine, Durham
VA Medical Center, Durham, North Carolina
   1.. Requests for reprints:
   Joseph R. Nevins, Institute for Genome Sciences and Policy, 101 Science Drive,
2121 Ciemas Building, Durham, NC 27708. Phone: 919-684-2746; Fax: 919-681-8973;
E-mail: j.nevins@... .
Abstract
Purpose: Chronic lymphocytic leukemia (CLL) is a B-cell malignancy characterized
by a variable clinical course. Several parameters have prognostic capabilities
but are associated with altered response to therapy in only a small subset of
patients.

Experimental Design: We used gene expression profiling methods to generate
predictors of therapy response and prognosis. Genomic signatures that reflect
progressive disease and responses to chemotherapy or chemoimmunotherapy were
created using cancer cell lines and patient leukemia cell samples. We validated
and applied these three signatures to independent clinical data from four
cohorts, representing a total of 301 CLL patients.

Results: A genomic signature of prognosis created from patient leukemic cell
gene expression data coupled with clinical parameters significantly
differentiated patients with stable disease from those with progressive disease
in the training data set. The progression signature was validated in two
independent data sets, showing a capacity to accurately identify patients at
risk for progressive disease. In addition, genomic signatures that predict
response to chlorambucil or pentostatin, cyclophosphamide, and rituximab were
generated and could accurately distinguish responding and nonresponding CLL
patients.

Conclusions: Thus, microarray analysis of CLL lymphocytes can be used to refine
prognosis and predict response to different therapies. These results have
implications for standard and investigational therapeutics in CLL patients.
(Clin Cancer Res 2009;15(22):6947-55)

Note: Supplementary data for this article are available at Clinical Cancer
Research Online (http://clincancerres.aacrjournals.org/).

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From Anjou

FYI Subject: [nhl-info] talking science with patient advocates
Laurie: There is a schism between ardent supporters of
evidence-based medicine and patients who feel strongly about the
value of CAM. Why do you think it is so appealing to patients
with chronic illness, despite the lack of research to support
it?

Dr. Val: It's really hard to accept the limits of modern
medicine. We can't cure every disease, we can't effectively
treat every symptom, and we can't prevent death indefinitely. It's
human nature to want to control our destinies, to reject the
cards we've been dealt. In that sense I have the utmost sympathy
for people who choose to turn over every treatment stone in the
face of a daunting diagnosis, or when they are suffering from
disease.

However, we have to recognize how vulnerable we are to snake oil
when we are sick. There are entire industries that prey on the
ill, ...

full text: http://www.sciencebasedmedicine.org/?p=2625

Karl

Just listening now. Inspirational, for anyone ...

==
Of the webcast with Wendy Harpham on the Art of Survivorship,
Anjou writes: "Fabulous show, worth a listen." Indeed, Wendy
shared some wonderful, uplifting nuggets we can all use and put
into practice.

Direct link: http://bit.ly/13wbJG

Wendy loves feedback - if you listen and want to comment, please
do, either here and by emailing me at lymphomationlive@...

Thanks,
Betsy

==

All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

Re: Wendy Harpham on The Art of Survivorship

Anjou wrote: Fabulous show-- worth a listen @
http://bit.ly/4vYgWf

Indeed!  Direct link to recorded interview  http://bit.ly/13wbJG

Karl



===
--- In nhl-info@yahoogroups.com, "Betsy de Parry" <betsy@...>
wrote:
>
> Webcast: The Art of Survivorship with Dr. Wendy Harpham
>
> Wed., 11/11/09, 8:00 pm EST
>
> Listen live or later http://bit.ly/4vYgWf
>
>
>
>
> Diagnosed with follicular non-Hodgkin lymphoma in 1990, Dr.
> Wendy Harpham has since become one of the most respected
> voices on survivorship. Wendy is a doctor of internal
> medicine, mother of three and best-selling author whose
> beautifully written books are manuals on how to live with
> lymphoma (or any other chronic illness).
>
>
>
> I'll be talking with Wendy on the Art of Survivorship - what
> it is and how we can learn to find happiness despite cancer
> and how to tap into those special moments of happiness than
> can sometimes even occur because of it.
>
>
>
> So mark your calendars for Wednesday night - this is one
> episode you won't want to miss!
>
>
>
> Betsy
>
>
> [Non-text portions of this message have been removed]
>

Below are reusable queries to locate studies that include
genetic analysis.

"Genetic analysis" generally means the evaluation of biospecimen
(tumor or other) for the purpose of correlating outcomes to
unique characteristics of the tumor or patient, such as:  *
Polymorphisms (normal inherited variations affecting the immune
system or how you metabolize drugs), * Gene expression of tumor
cells (which genes are over-active or silent), or * Cytogenetic
mutations (additions, deletions, transpositions of base pairs
(TCGA) within a gene in tumor cells).

Reusable, because as the clinicaltrials.gov registry is updated,
the same query will provide new results.

* Follicular lymphoma OR CLL  http://bit.ly/4iGb70

* Follicular only: http://bit.ly/3hVVKC  (37 studies)

* CLL only: http://bit.ly/1Spmoz (49)

* DLBCL only http://bit.ly/2ntw6a (41)

* Lymphoma unspecified http://bit.ly/41yTCh (89)

All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

Copying from Cancer Myths:

"Cancer surgery causes tumors to spread.

Surgery is an effective type of cancer treatment. And although
it's possible that the medical team may find the cancer more
widespread than previously thought, the operation does not cause
a tumor to spread. For more information on cancer treatment,
please read Types of Treatment."


Source http://bit.ly/23P9lg  (Cancer.net)

More specific to lymphoma, cell ingratiation appears to be
regulated internally (programmed by gene expression within each
cell) and also by signals from the host microenvironment.  That
is, it is not random or determined by physical boundaries.

However, lymphocytes have "license" to travel if needed, unlike
breast or prostate cells. This ability to move is required in
order to fight infection in the body.   So lymphoma is
considered a systemic condition ... unless caught very early
...it's expected be widespread in the lymph and blood, but
again, tending to home to specific regions, such as to skin,
mucosal tissue, bone marrow, and lymph nodes - depending in part
on the type of lymphoma ... the cell of origin.

... Which could be why massage is not considered a dangerous
practice for lymphoma survivors, nor is walking, which is
probably the best way to encourage lymphatic circulation.

All the best,

~ Karl

Patients Against Lymphoma
Patients Helping Patients
Non-profit | Independent | Evidence-based
www.lymphomation.org | Current News: http://bit.ly/f2A0T

How to Help:  www.lymphomation.org/how-to-help.htm

Preliminary data on the involvement of B, C and D hepatitis viruses in the
etiopathogenesis of chronic lymphoproliferative syndromes in Romania.
V Molagic, V Arama, AS Cercel, N Irimescu, AM Vladareanu, M Olariu, SS Arama, A
Rafila, C Dobrea, S Costoiu, M Marza, D Otelea, S Paraschiv, D Maxim, M Popa, H
Bumbea, C Ciufu, C Baicus, and R Mihailescu
Rom J Intern Med, January 1, 2009; 47(1): 25-34.

"Professor Dr. Matei Bal?" National Institute of Infectious Diseases, Bucharest.

THE AIMS OF THE STUDY: Evaluation of the prevalence of HBV, HCV, HDV infection
in patients with chronic lymphoproliferative diseases (CL), identification of
the most involved viral genotypes, correlation between viremia dynamics and CL
evolution, detection of molecular mechanisms implicated in CL pathogenesis,
identification of lymphocytic receptors for viral antigens and biologic markers
for early diagnosis of CL. METHODS: We present preliminary results of the first
year of our research grant. This is a prospective, analytic, observational study
in patients diagnosed with CL and HBV, HCV, HDV chronic infection. We included
the following forms of CL: non-Hodgkin malignant lymphoma (NHL), Hodgkin
lymphoma (HL) and chronic lymphocytic leukemia (CLL). We used the following
commercial test kits: HCV RNA Real time PCR on a COBAS TaqMan (Roche
Diagnostics) analyzer with 28 to 140.000.000 UI/ml detection range for HCV
viremia, HBV DNA Real time PCR on a COBAS TaqMan (Roche Diagnostics) analyzer
with 6 to 110.000.000 UI/ml detection range for HBV and the Roboscreen-RoboGene
AJ kit with 10-10.000.000 replica/ml detection range for HDV. RESULTS: We have
included 20 patients with CL and chronic hepatitis infection so far. Median age
of the patients was 61 years. The identified CL forms were: B cell NHL (15
cases), T cell NHL (1 case), CLL (3 cases), Hodgkin lymphoma (1 case), equally
distributed in aggressive and indolent forms of CL. HCV infection was diagnosed
in 10 patients with CL, HBV infection was found in 10 patients with CL, 3 of
them having co-infection HBV + HDV. In 4 patients with HBV infection viremia was
over 20.000 IU/ml and the pattern of the CL was the aggressive form of the
disease. The feature of the co-infection HBV + HDV was the predominance of
indolent forms of CL. Among patients with HCV infection, only 3 cases were
detected with viremia over 600.000 IU/ml and CL was represented by aggressive
forms of the disease. We also have immunohistochemical data available in 19
cases, which seem to confirm the role of hepatitis viruses in
lymphoproliferative disease etiopathogenesis. CONCLUSIONS: We ascertained an
almost equally represented prevalence of HCV and HBV infection in patients with
CL. The levels of HBV, HCV and HDV viremia were low in most of the cases. The
most frequent form of CL was B cell NHL. We found an equal distribution between
indolent and aggressive forms of NHL associated to hepatitis virus infection.
PMID: 19886066

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