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Dr Trevor Marshall
Foundation Staff
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Posted: Fri Dec 18th, 2009 15:02 |
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http://bit.ly/8Lfj5y"The renin-angiotensin pathway plays an important role in promoting cancer growth, explained Dr. Chae on December 11. The AT1 receptor is functionally expressed in several tumor types, including ovarian cancer. Prior retrospective studies have documented lower cancer incidence among users of ACE inhibitors/ARBs compared with nonusers, and 1 randomised trial showed a protective effect of these agents on the development of major skin cancers, he said. No studies, however, have looked at the relationship between ACE inhibitors/ARBs and cancer recurrence. For the study, Dr. Chae and colleagues reviewed the medical records of female patients diagnosed with stage II/III breast cancer at Albert Einstein between 1999 and 2005, and who later reached no evident disease (NED) after curative therapy. A user of ACE inhibitors/ARBs was defined as a patient who took the medication in the NED stage for at least 6 months. The mean follow-up period was 4.4 years and the maximum follow-up was 9.8 years. About one-fourth (23.3%) of the patients, overall, were prescribed an ACE inhibitor or ARB, including 49.0% of the 164 patients with hypertension. Fourteen percent (23/164) of the women who took either an ACE inhibitor or ARB developed a tumour recurrence, compared with 23.3% (125/541) of nonusers ([P = .01).
The 5-year disease-free survival was 0.85 in the ACE inhibitor/ARB users and 0.756 in the nonusers (P < .01)"
75 to 85% survival rate at 5 years. Interesting data in and of itself.
One of the problems with studies like this is that they clump all the drugs into one class - for example - 'ARBs' - without realizing that each of the ARB drugs is a little bit different. They also assume that ACEI have a similar mechanism of action - a sad commentary on the lack of precision in modern medicine.
Still - this is confirmation that Benicar should not increase the rate of relapse with cancers, even if it doesn't yet have the (study) strength to back up my suspicions as to why the MP has essentially wiped out metastasis in our cohort...
http://www.youtube.com/watch?v=y8AfUg3aJVk
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Freddie Ash
Member in Phase 3
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Posted: Fri Dec 18th, 2009 18:19 |
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HI ALL
This is Fred in WV . I just got my email from the Doctor's Guide today and that is the main story in it. Thanks for posting that for all to see. Another reason to take Benicar.
Remember, we are all in this together and I am pulling for us.
Your friend in Sarcoidosis
Freddie
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Freddie: dx-sarc 2/82 lymph; skin, eyes, joints, esophagus, intestines, spleen, heart,lungs-meds digitek, L-thyroxine, nexium, furosemide, nattokinase36mg,eat cinnamon w/meals,25D-7; 125-D43
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Bane
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Posted: Fri Dec 18th, 2009 21:59 |
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Impact of angiotensin I converting enzyme inhibitors and angiotensin II type 1 receptor blockers on survival in patients with advanced non-small-cell lung cancer undergoing first-line platinum-based chemotherapy.
http://www.ncbi.nlm.nih.gov/pubmed/19399518
Application of angiotensin II receptor blocker in prostate cancer
http://www.ncbi.nlm.nih.gov/pubmed/19348246
Ets-1 and hypoxia inducible factor-1alpha inhibition by angiotensin II type-1 receptor blockade in hormone-refractory prostate cancer.
http://www.ncbi.nlm.nih.gov/pubmed/19760626
Angiotensin II Type 1 Receptor Antagonist as an Angiogenic Inhibitor in Urogenital Cancer.
http://www.ncbi.nlm.nih.gov/pubmed/19463103
Synergistic inhibitory effect of gemcitabine and angiotensin type-1 receptor blocker, losartan, on murine pancreatic tumor growth via anti-angiogenic activities.
http://www.ncbi.nlm.nih.gov/pubmed/19578777
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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Ruth Goold
Health Professional
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Posted: Fri Dec 18th, 2009 23:06 |
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And here is some info on (one of the) ways in which olmesartan (Benicar) mediates it's anticancer effects:
The Host Defense Peptide Cathelicidin Is Required for NK Cell-Mediated Suppression of Tumor Growth
http://www.ncbi.nlm.nih.gov/pubmed/19949065
And from the same issue of the Journal of Immunology, yet another study outlining a clever way in which intracelluar pathogens compromise the immune response (albeit, in mice in this case):
Dissemination of Mycobacteria to the Thymus Renders Newly Generated T Cells Tolerant to the Invading Pathogen
http://www.ncbi.nlm.nih.gov/pubmed/19949112
Happy Holidays,
Ruth
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03/02/07 Ph 1 MP; 2001: Pulmonary sarc; 01/04/07: 125 D=110pmol/L(45.8 pg/ml)| 25D=20.8 ng/ml: 04/07 19.2: 07/07 11?: 09/07 16.5: 11/07 <10.0: 01/08 <10.0: 05/08 10 ng/ml. Ca. Elocom (ears). diphenhydramine 25 mg. Adidas EE glasses outside. NoIRs
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Dr Trevor Marshall
Foundation Staff
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Posted: Fri Dec 18th, 2009 23:31 |
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Ah yes, the Thymus - so they can pervert the function of AIRE
Great find Ruth - I just hadn't put two and two together...
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ChrisMavo
Member in Phase 2
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Posted: Sat Dec 19th, 2009 00:16 |
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Great STUFF!
So not only can we cure ourselves from chronic Th1 diseases... but we can protect ourselves from the Big C too....
Great stuff INDEED!!!
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PLS/ALS, speech difficulty, dizziness, leg weakness, overly emotional, Ph1Aug2609, 11/09: 25D-20, 9/09: 25D-27, 7/09: 25D-38, 1,25D-46, Mod Ph2Oct09, 100mg Mino + 150mg Clindy
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Phil Schoner
Member in Phase 3
| Joined: | Wed Jan 25th, 2006 |
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Posted: Sun Dec 20th, 2009 15:07 |
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Trevor,
You state "the MP has essentially wiped out metastasis in our cohort..."
Epidemiologically speaking, have we developed the percentages of expected cancer metastasis in the cohert versus the (nearly?) zero percent experienced?
Phil
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Phil Schoner, MP Support Spouse, no symptoms, 1,25D 74 5/08, 25D 16 12/08, 25D 16 7/09, ph1 11/08, ph2 12/08, ph3 7/09, NoIR's, sunscreen
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Dr Trevor Marshall
Foundation Staff
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Posted: Sun Dec 20th, 2009 15:41 |
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Phil,
Different sources have different expectations. The one that seems to be most reliable is an expectation of 10 % to 30% of autoimmune disease patients will die from cancer within a decade. This is also in line with the overall cancer death-rate in CFS patients.
I break this down to a year-by year average expectation of 1% to 3%. For our current reporting cohort size of 700+ this would lead to an expectation of 7 to 21 cases a year.
We are well below that Whether total cancers or just metastasizing cancers (the ones which lead to death) are considered in the total...
One of the biggest problems this cohort faces is that they are pushed (by oncologists) to accept treatments for a non-metastasizing tumor regardless of whether those treatments will exacerbate their underlying inflammatory disease, and thus eventually fuel the metastasis. We need to work on getting together enough case histories so that MP cohort members don't panic when Doc considers a potential "cancer" diagnosis.
We have been walking around for decades without the probing and testing and imaging that Doc has available these days. We should not be surprised if all this new technology finds tumors, some of which may have been there for years... The key is to focus on whether they present a future danger of spreading (metastasis)...
..Trevor..
Last edited on Sun Dec 20th, 2009 18:43 by Dr Trevor Marshall
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Bane
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Posted: Sun Dec 20th, 2009 16:44 |
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http://www.ncbi.nlm.nih.gov/pubmed/18677709
http://www3.interscience.wiley.com/cgi-bin/fulltext/121359256/PDFSTART
Last edited on Sun Dec 20th, 2009 18:40 by Bane
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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Joyful
Foundation Staff
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Posted: Sun Dec 20th, 2009 18:37 |
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Bane, your link is to a pay-to-view article. 
Would you care to summarize here?
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Bane
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Posted: Sun Dec 20th, 2009 18:57 |
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Joyful wrote: Bane, your link is to a pay-to-view article.
Would you care to summarize here?
"To investigate the effect of Ang-III on human prostate cancer cells, we applied it in LNCaP (androgen-dependent) and DU145 (androgen-independent) cells. As shown in Figure 2A,B, Ang-III treatment increased both prostate cancer cells in a dose-dependent manner. Because earlier reports indicated that Ang-III can bind to theAT1 receptor,which is predominantly for Ang-II (Fig. 1) [16], we investigated the effect of an AT1 receptor blocker on cell proliferation induced by Ang-III. Olmesartan is a selective blocker of the AT1 receptor and is widely used as anti-hypertensive agent. As shown in Figure 2A,B, olmesartan significantly suppressed the cell growth induced by Ang-III treatment in prostate cancer cells."
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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jrfoutin
Research Team
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Posted: Sun Dec 20th, 2009 23:09 |
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"75 to 85% survival rate at 5 years. Interesting data in and of itself.
"One of the problems with studies like this is that they clump all the drugs into one class - for example - 'ARBs' - without realizing that each of the ARB drugs is a little bit different.."
Along with lumping ARBs together, there is no discussion of atypical dose for any ARB. The study assumption for the full ARB set they lump is standard ARB dose, right?
The MP cohort daily ARB intake has always been on the line. With a void annual 7-21 cohort cancer record to date, might it be appropriate already--specific to study strength--to state more Benicar (typical MP dose levels with extra when needed) is simply not leading to cancer?
Thank you Dr Marshall and others for excellent discussion and links--Janet
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Sarcoidosis 125D61, MP10/05 ModP2 12/05 Ph2 6/06 Ph3 10/06, NoIRs limited outings covered, 2/08 25D6.2, 10/08 25D6.9
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Bane
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Posted: Fri Dec 25th, 2009 19:08 |
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Dr Trevor Marshall wrote: Phil,
Different sources have different expectations. The one that seems to be most reliable is an expectation of 10 % to 30% of autoimmune disease patients will die from cancer within a decade. This is also in line with the overall cancer death-rate in CFS patients.
I break this down to a year-by year average expectation of 1% to 3%. For our current reporting cohort size of 700+ this would lead to an expectation of 7 to 21 cases a year.
We are well below that Whether total cancers or just metastasizing cancers (the ones which lead to death) are considered in the total...
One of the biggest problems this cohort faces is that they are pushed (by oncologists) to accept treatments for a non-metastasizing tumor regardless of whether those treatments will exacerbate their underlying inflammatory disease, and thus eventually fuel the metastasis. We need to work on getting together enough case histories so that MP cohort members don't panic when Doc considers a potential "cancer" diagnosis.
We have been walking around for decades without the probing and testing and imaging that Doc has available these days. We should not be surprised if all this new technology finds tumors, some of which may have been there for years... The key is to focus on whether they present a future danger of spreading (metastasis)...
..Trevor..
Immunological Similarities between Cancer and Chronic Fatigue Syndrome: The Common Link to Fatigue?
http://www.ncbi.nlm.nih.gov/pubmed/20032425
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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Bane
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Posted: Mon Feb 8th, 2010 16:13 |
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Blocking Angiotensin II Type 1 Receptor Triggers Apoptotic Cell Death in Human Pancreatic Cancer Cells.
http://www.ncbi.nlm.nih.gov/pubmed/20118823
Angiotensin II regulates the expression of monocyte chemoattractant protein-1 in pancreatic cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/19816747
Inhibition of angiotensin II receptor 1 limits tumor-associated angiogenesis and attenuates growth of murine melanoma.
http://www.ncbi.nlm.nih.gov/pubmed/19771429
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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Bane
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Posted: Sun Feb 28th, 2010 22:30 |
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Association of ACE inhibitors and angiotensin receptor blockers with keratinocyte cancer prevention in the randomized VATTC trial.
http://jnci.oxfordjournals.org/cgi/content/full/100/17/1223
"Among a high-risk group of veterans, users of ACE inhibitors or ARBs had a lower incidence of keratinocyte cancers than nonusers. The more pronounced reduction among those who initiated use during the study may indicate an immediate effect."
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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