If you are interested in learning more about Angiotensin Receptor Blockers and what seems the likely mechanism of action you might be interested in a couple of review papers that I have written:
Smith, G.R. and S. Missailidis, Cancer, inflammation and the AT1 and AT2 receptors. J Inflamm (Lond), 2004. 1(1): p. 3.
Smith G.R. and S. Missailidis, Learning from cancer: The adaptive growth, wound and immune responses. Gene Therapy and Molecular Biology, 2009. 13(A): p. 158-185
I have been pushing for research into the huge potential for these drugs since 2004 and any help in spreading the message would be appreciated.
I am happy to answer questions.
Best regards, Gary.
Just as a point of clairification - Lisinopril is an ACE inhibitor drug.
I certainly do agree with you that some Angiotensin Receptor Blockers do GREAT things.
I asked my doctor put me on this one (Telmisartan) for obvious reasons.
I request that you consider changing my ARB medication from Benicar 20 mg to Telmisartan (brand names Micardis, Kinzal, Pritor) for the reasons of PCa advantages.
I would request the Generic. According to NIH-NLN Pub MED there have been over 16,000 hits on the search "Telmisartan PSA".
I know nothing about it value as a Angiotensin II blocker.My Rx Pharm no is CVS 555555555. Please Email a reply if possible. I am on my way to see the Urologist/Oncoligist today.
Oncol Rep. 2008 Aug;20(2):295-300.
is a potent target for prevention and treatment in human prostate cancer.
Funao K, Matsuyama M, Kawahito Y, Sano H, Chargui J, Touraine JL, Nakatani T, Yoshimura R.
Department of Urology, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan.
Angiotensin II receptor blockers (ARBs) are widely used as hypertensive therapeutic agent. Recent studies have reported that ARBs have the potential to inhibit the growth of prostate cancer (PC) cells. Moreover, it was recently reported that Telmisartan
(a kind of ARB) has peroxisome proliferator-activated receptor (PPAR)-gamma activation. We previously reported that PPAR-gamma ligand induces growth arrest of PC cells through apoptosis. In this study, we evaluated the effects of the Telmisartan and other ARBs on cell proliferation in several PC cell lines. We used normal prostate stromal cell (NPC), human hormone-refractory PC (PC3), androgen-independent PC (DU-145) and androgen-dependent PC (LNCaP) cell lines. Effects of Telmisartan and other ARBs (Candesartan, Valsartan, Irbesartan and Losartan) on PC cell growth were examined by MTT assay. Flow cytometry and Hoechst staining were used to determine whether or not ARBs induce apoptosis. [b]Telmisartan caused marked inhibition of PC cells in concentration-dependent and time-dependent manner. PC cells with treatment of 100 microM Telmisartan induced early apoptosis and DNA fragmentation.
[/b]However, NPC with treatment of 100 microM Telmisartan did not induce apoptosis or DNA fragmentation. Furthermore, other ARBs had no effect on cell proliferation in the PC cells and NPC. [b]Telmisartan may mediate potent antiproliferative effects against PC cells through PPAR-gamma.
Thus, Telmisartan is a potent target for prevention and treatment in PC.[/b]
PMID: 18636189 [PubMed - indexed for MEDLINE]
Regarding ONE ACE inhibitor I also demanded this specific ACE inhibitor captopril from my doctor.
Prostate. 2004 Jan 1;58(1):50-6.
Association between captopril,
other antihypertensive drugs and risk of prostate cancer.
Ronquist G, Rodríguez LA, Ruigómez A, Johansson S, Wallander MA, Frithz G, Svärdsudd K.
Department of Medical Sciences, Clinical Chemistry, University Hospital, Uppsala, Sweden.
BACKGROUND: There has been some debate on the existence of an association between hypertension, antihypertensive medications and cancer risk. METHODS: We performed a nested case-control study to assess the association between the risk of prostate cancer and the use of the angiotensin converting enzyme (ACE)-inhibitor captopri
l, and other antihypertensive drugs. We used data from the General Practice Research Database in UK.
RESULTS: We found an incidence rate of prostate cancer of 1.61 per 1,000 person-years among male patients aged 50-79 years old.
Patients with a history of benign prostatic hyperplasia and/or prostatism carried a two-fold greater risk of prostate cancer than those without such antecedents. None of the other studied co-morbidities were associated with prostate cancer. We found that users of captopril had a relative risk of 0.7 (95% CI: 0.4-1.2) to develope prostate cancer
. None of the other studied individual ACE-inhibitors shared a similar effect with the one observed for captopril.
CONCLUSIONS: No clear association was apparent between the use of antihypertensive drugs and prostate cancer. However, specific focus on users of captopril showed a lower risk of subsequent prostate cancer.
Further research is needed to explore this association. Copyright 2003 Wiley-Liss, Inc.
PMID: 14673952 [PubMed - indexed for MEDLINE]
Scand J Urol Nephrol. 2009;43(1):32-6.
may reduce biochemical (prostate-specific antigen) failure following radical prostatectomy for clinically localized prostate cancer.
Ronquist G, Frithz G, Wang YH, Lindeborg T.
Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden. firstname.lastname@example.org
OBJECTIVE: A prior report suggested that individuals medicated with captopril showed a decreased incidence of prostate cancer. This study therefore investigated whether captopril given postoperatively had any preventive effect on biochemical recurrence for patients treated with radical prostatectomy. MATERIAL AND METHODS: Data were prospectively reviewed for 62 men subjected to radical retropubic prostatectomy due to biopsy-confirmed, clinically localized prostate cancer and comparisons were made between two groups, those receiving captopril postoperatively (12.5 mg twice daily; captopril group, n=32) and those not receiving any captopril (control group, n=30). One surgeon carried out the surgery.
RESULTS: The two groups were comparable as regards age at surgery, prostate volume, preoperative prostate-specific antigen values, pathological stage, Gleason score, organ-confined disease, occurrence of positive surgical margins and extraprostatic extension. The incidence of biochemical failure was three out of 32 patients in the captopril group and 10 out of 30 in the control group (p=0.034) during a mean observational time of 29 months.
CONCLUSIONS: A lower rate of biochemical recurrence was observed in men subjected to radical prostatectomy treated with captopril postoperatively than in those not receiving captopril.
These results were based on only 32 observations; a larger study may show no evidence of an association.
PMID: 18932051 [PubMed - indexed for MEDLINE]
Ann N Y Acad Sci. 2008 Sep;1138:65-72.
Captopril as a potential inhibitor of lung tumor growth and metastasis.
Attoub S, Gaben AM, Al-Salam S, Al Sultan MA, John A, Nicholls MG, Mester J, Petroianu G.
Department of Pharmacology, Faculty of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates. email@example.com
Lung cancer is the most common form of cancer in the world, and 90% of patients die from their disease.
The angiotensin converting enzyme (ACE) inhibitors are used widely as antihypertensive agents, and it has been suggested that they decrease the risk of some cancers, although available data are conflicting. Accordingly, we investigated the anticancer activity of the ACE inhibitor, captopril
, in athymic mice injected with highly tumorigenic LNM35 human lung cells as xenografts. Using this model, we demonstrated that daily IP administration of captopril (2.8 mg/mouse) for 3 weeks resulted in a remarkable reduction of tumor growth (58%, P < 0.01)
and lymph node metastasis (50%, P= 0.088).
There were no undesirable effects of captopril treatment on animal behavior and body weight. In order to determine the mechanism by which captopril inhibited tumor growth, we investigated the impact of this drug on cell proliferation, apoptosis, and angiogenesis. Immunohistochemical analysis demonstrated that captopril treatment significantly reduced the number of proliferating cells (Ki-67) in the tumor samples but was not associated with inhibition of tumor angiogenesis (CD31). Using cell viability and fluorescent activated cell sorting analysis tests, we demonstrated that captopril inhibited the viability of LNM35 cells by inducing apoptosis, providing insight about the mechanisms underlying its antitumorigenic activities.
In view of these experimental findings, we conclude that captopril could be a promising option for the treatment of lung cancer.
PMID: 18837885 [PubMed - indexed for MEDLINE]