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Old 01-29-2007, 12:34 PM   #1
heblaj01
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Join Date: Apr 2006
Posts: 543
Karina,
Your remark about the change in cancer incidence in Japanese who emigrate to north America as related to diet, not genetics, is quite right . Even if these emigrants keep their traditional diet they may still be unwillingly prone to cancer due to differences in the quality of some foods.
For instance I already mentioned in an other post a comment by Dr M.J. Folkman in a lecture where he briefly discussed the variations of incidence related to soybean based food consumption.
He said that soybean grown in north America lacks the genetic make up for genestein while soybean grown in Japan includes genestein which is considered as a cancer preventative food.
So epidemiology studies show that those emigrants consumming imported soybeans are better off than those eating the local grown variety.
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Old 02-06-2007, 03:40 AM   #2
fullofbeans
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Join Date: Jan 2007
Location: UK
Posts: 617
Dear Hebla and R.B,

As you seem quite knowledgeable I was wondering if you could comment on the follwing statements:

"For two decades Dr. Perez Garcia has been using a treatment he calls Insulin Potentiation Therapy (IPT). It consists of giving a patient a dose of insulin followed by a tiny dose of chemotherapy.
Cancer cells have 15 times more insulin receptors than normal cells. The insulin dose helps to target chemotherapy into cancer cells because they have so many more insulin receptors. "

This could explain why keeping a low GI diet could be v.good in our case,

Still searching..

Best wishes
__________________

35 y/o
June 06: BC stage I
Grade 3; ER/PR neg
Her-2+++; lumpectomies

Aug 06: Stage IV
liver mets: 6 tumours
July 06 to Jan 07: 2*FEC+6*Taxotere; 3*TACE; LITT
March 07- Sept 07: Vaccination trial (phase 2, peptide based) at the UW (Seattle).
Herceptin since 2006
NED til Oct 09
Recurrence Oct 2009: to internal mammary gland since October 2009 missed on Oct and March 2010 scan.. palpable nodes in May 2010 when I realised..
Nov 2011:7 mets to lungs progressing fast failed hercp/tykerb/xeloda combo..

superior vena cava blocked: stent but face remains puffy

April 2012: Teresa Trial, randomised to TDM1
Nov 2012 progressing on TDM1
Dec 2012 blockage of my airways by tumours, obliteration of these blocking tumours breathing better but hoping for more- at mo too many tumours to count in the lungs and nodes.

Dec 2012 Starting new trial S-222611 phase 1b dual egfr her2+ inhibitor.



'Under no circumstances should you lose hope..' Dalai Lama
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Old 02-06-2007, 10:18 AM   #3
heblaj01
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Join Date: Apr 2006
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Karina,
Being much less knowledgeable than you think (no background in life sciences) I have to rely on what experts are saying & on common sense deductions from the evidence.
The main arguments against IPT from the standpoint of a layman are:
1. it has been around for a long time &
2. there is still no verifiable response data
3. there has been no research papers in PubMed
4. there has been no clinical trial

If the treatment was very effective at least one of the above negative points should have been answered positively.
Now, for a more scientific discussion of IPT here is the viewpoint of conventional medicine:
http://www.quackwatch.org/01Quackery...ancer/ipt.html
Why You Should Stay Away from Insulin Potentiation Therapy (IPT)
Robert Baratz, M.D., D.D.S., Ph.D.

P.S.
A quick search of PubMed gave me only one answer which seems to remotely relate to IPT:
http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
RNAi-mediated silencing of insulin receptor substrate 1 (IRS-1) enhances tamoxifen-induced cell death in MCF-7 breast cancer cells.
I don't fully understand this abstract, but if I read it correctly it, would seem to be somewhat the opposite of IPT.

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Old 02-06-2007, 03:40 PM   #4
fullofbeans
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Join Date: Jan 2007
Location: UK
Posts: 617
Hi Hebla,

Thanks for that, both articles came useful as confirming that cancer cells have insuline receptors stimulating growth. I was not suggesting to use IPT but I was interested in the fact that cancer cell have 20 times more insuline receptors than normal cells.

This to me would suggest that a good cancer diet would avoid having high peak of insuline i.e. a low G.I diet and therefore we should avoid sugars in the diet. At least it seems logical, I heard a lot that "sugar feeds cancer" well this seems to be another argument for it.
__________________

35 y/o
June 06: BC stage I
Grade 3; ER/PR neg
Her-2+++; lumpectomies

Aug 06: Stage IV
liver mets: 6 tumours
July 06 to Jan 07: 2*FEC+6*Taxotere; 3*TACE; LITT
March 07- Sept 07: Vaccination trial (phase 2, peptide based) at the UW (Seattle).
Herceptin since 2006
NED til Oct 09
Recurrence Oct 2009: to internal mammary gland since October 2009 missed on Oct and March 2010 scan.. palpable nodes in May 2010 when I realised..
Nov 2011:7 mets to lungs progressing fast failed hercp/tykerb/xeloda combo..

superior vena cava blocked: stent but face remains puffy

April 2012: Teresa Trial, randomised to TDM1
Nov 2012 progressing on TDM1
Dec 2012 blockage of my airways by tumours, obliteration of these blocking tumours breathing better but hoping for more- at mo too many tumours to count in the lungs and nodes.

Dec 2012 Starting new trial S-222611 phase 1b dual egfr her2+ inhibitor.



'Under no circumstances should you lose hope..' Dalai Lama
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Old 02-06-2007, 05:01 PM   #5
heblaj01
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Join Date: Apr 2006
Posts: 543
Karina,
I am personaly a believer that sugar is directly or indirectly helping cancer cell growth based on various research papers although most are not specifically devoted to prove the point.
But look at this extract from an article by a Mayo Clinic MD who may well know better:
http://www.mayoclinic.com/health/cancer/HO00033
Debunking cancer myths: An interview with a Mayo Clinic specialist
"People with cancer shouldn't eat sugar, since it can cause cancer to grow faster.

Sugar doesn't make cancer grow faster. All cells, including cancer cells, depend on blood sugar (glucose) for energy. But giving more sugar to cancer cells doesn't speed their growth. Likewise, depriving cancer cells of sugar doesn't slow their growth.

This misconception may be based in part on a misunderstanding of positron emission tomography (PET) scans. Doctors use PET scans to help determine the location of a tumor and see if it has spread.

During a PET scan, your doctor injects a small amount of radioactive tracer — typically a form of glucose — into your body. All tissues in your body absorb some of this tracer. But tissues that are using more energy — exhibiting increased metabolic activity — absorb greater amounts.

Tumors are often more metabolically active than healthy tissues. As a result, they may absorb greater amounts of the tracer. For this reason, some people have concluded that cancer cells grow faster on sugar. But this isn't true."

Here are a few of the articles that imply the opposite view:
http://www.news-medical.net/?id=1582
Glucose metabolism could be used to selectively destroy cancer cells

http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11039477
Physiological concentrations of insulin augment pancreatic cancer cell proliferation and glucose utilization by activating MAP kinase, PI3 kinase and enhancing GLUT-1 expression.

http://jnci.oxfordjournals.org/cgi/r...96/24/1805.pdf
Energy Boost: The Warburg Effect Returns in a New Theory of Cancer

http://www.ihop-net.org/UniPub/iHOP/...?pmid=12379472
Leptin and high glucose stimulate cell proliferation in MCF-7 human breast cancer cells: reciprocal involvement of PKC-alpha and PPAR expression.
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