Linkage of angiotensin I‐converting enzyme gene insertion/deletion polymorphism to the progression of human prostate cancer

Medeiros, Rui; Vasconcelos, André; Costa, Sandra; Pinto, Daniela; Lobo, Francisco; Morais, António; Oliveira, Jorge; Lopes, Carlos

doi:10.1002/path.1529

Cited by 76 publications

(62 citation statements)

References 56 publications

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“…27 We confirmed that the ACE genotype was not related to lung cancer 34 There is one study that investigated prostate cancer progression and observed more advanced tumors in DD carriers. 35 No significant relation was reported for ACE genotype and colorectal cancer risk.…”

Section: Discussionmentioning

confidence: 99%

Renin‐angiotensin system inhibitors, angiotensin I‐converting enzyme gene insertion/deletion polymorphism, and cancer

Knaap

Siemes

Coebergh

et al. 2008

Cancer

123

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BACKGROUND. Angiotensin I‐converting enzyme (ACE) inhibitors, angiotensin II antagonists, and the ACE insertion/deletion (I/D) gene polymorphism all influence serum angiotensin II action. Because angiotensin II levels have been associated with cancer, the objective of the current epidemiologic study was to investigate whether renin‐angiotensin system inhibitors and/or ACE genotypes were associated with an altered risk of colorectal, lung, breast, and prostate cancer. METHODS. Data were obtained from the Rotterdam Study, a population‐based, prospective cohort study with 7983 participants. Participants who had a history of 1 of the cancers of interest (n = 216) or who had a medication history <6 months (n = 88) were excluded, leaving 7679 participants, of whom the ACE genotypes could be assessed in 6670 individuals. The mean follow‐up was 9.6 years, during which 730 incident cancers occurred. The effect of medication, ACE I/D genotypes, and their interaction on cancer risk and progression was studied by using Cox proportional hazard models. RESULTS. Carriers of the high‐activity genotype DD had an increased risk of breast cancer compared with low‐activity II/ID genotype carriers (hazard ratio [HR], 1.47; 95% confidence interval [95% CI], 1.05–2.04), but no association was demonstrated for other cancers. DD carriers who were exposed to long‐term and high‐dose medication were at lower risk for cancer (HR, 0.28; 95% CI, 0.10–0.79). Short‐term, high‐dose users were at risk for colorectal cancer progression in the II/ID stratum (HR, 3.83; 95% CI, 1.67–8.79). CONCLUSIONS. Renin‐angiotensin system‐inhibiting drugs seemed to protect against cancer in individuals with the DD genotype, which was associated with high levels of ACE. Cancer 2008. © 2008 American Cancer Society.

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Section: Discussionmentioning

confidence: 99%

Renin‐angiotensin system inhibitors, angiotensin I‐converting enzyme gene insertion/deletion polymorphism, and cancer

Knaap

Siemes

Coebergh

et al. 2008

Cancer

123

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“…144 The role of ACE in cancer is further supported by the findings that ACE polymorphism has been found to be associated with several cancers, including prostate, gastric and breast cancer. [145][146][147] Thus, several studies support anti-cancer effects of ACEis through RAS-dependent and/or -independent mechanisms, and these inhibitors may help us understand interactions between components of RAS in tumorigenesis and design new anti-cancer agents.…”

Section: Anticancer Effect Of Aceismentioning

confidence: 99%

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

2009

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Since their inception, angiotensin-converting enzyme (ACE) inhibitors have been used as first-line therapy for the treatment of cardiovascular and renal diseases. They restore the balance between the vasoconstrictive salt-retentive and hypertrophy-causing peptide angiotensin II (Ang II) and bradykinin, a vasodilatory and natriuretic peptide. As ACE is a promiscuous enzyme, ACE inhibitors alter the metabolism of a number of other vasoactive substances. ACE inhibitors decrease systemic vascular resistance without increasing heart rate and promote natriuresis. They have been proven effective in the treatment of hypertension, and reduce mortality in congestive heart failure and left ventricular dysfunction after myocardial infarction. They inhibit ischemic events and stabilize plaques. Furthermore, they delay the progression of diabetic nephropathy and neuropathy and act as antioxidants. Ongoing studies have elucidated protective roles for them in both memory-related disorders and cancer. INTRODUCTIONIn recent years, stressful and fiercely competitive lifestyles and food habits have compounded the problems of hypertension. Long-standing and stressful, progressively rising hypertension can lead to many disorders, including myocardial infarction (MI), cerebrovascular events, congestive heart failure, peripheral arterial insufficiency, premature mortality 1 and renal dysfunction leading to glomerulosclerosis and kidney artery aneurysm. 2 A number of therapies are available, but angiotensin-converting enzyme (ACE) inhibitors have been the preferred first-line therapy for hypertension, congestive heart failure, left ventricular (LV) systolic dysfunction and MI. 3,4 ACE inhibitors (ACEis) have been in use for the past two decades, and the interest in them is still growing. Recently, the discovery of domain-selective ACEis and new members of the renin-angiotensin system (RAS) (that is, angiotensin-converting enzyme 2) have again fueled the interest of researchers. Some new studies have expanded the already impressive clinical profile of ACEis. This review traces some already known and new facets of ACE inhibition and introduces new advances in the designing of a new generation of ACEis.

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“…[29][30][31][32][33][34][35][36] Furthermore, the genetic background may alter the natural history of prostate cancer development. [37][38][39] Moreover, impaired ability to undergo apoptosis seems to be important in prostate cancer. 40 Polymorphisms in the promoter region of the FAS and FASL genes alter the transcriptional activity of these genes, this could be an important role in Fas/FasL pathway.…”

Section: Introductionmentioning

confidence: 99%

Association between FAS polymorphism and prostate cancer development

Lima

Morais

Lobo

et al. 2007

Prostate Cancer Prostatic Dis

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The role of FAS polymorphisms in prostate cancer has not been studied. Using the PCR-based restriction fragment-length polymorphism methodology, we evaluated FAS gene locus À670 genotypes in DNA from 904 men: 657 prostate cancer patients and 247 healthy controls. We found that carriers of AG or GG genotypes have a statistically significant protection (odds ratio (OR) ¼ 0.30; confidence interval (CI): 0.20-0.44 and OR ¼ 0.22; CI: 0.12-0.74, respectively) for disease with extra-capsular invasion. Taken together, a 72% protection was found for G allele carriers (OR ¼ 0.28; CI: 0.19-0.41). Fas exist as membrane-bound and soluble forms and with opposite roles. They derive from the same gene by alternative splicing. Membrane Fas receptors trigger apoptosis whereas, on the other hand, soluble Fas (sFas) bind to Fas ligand antagonizing Fas-Fas ligand apoptotic pathway. Our results suggest that G allele may reduce sFas levels preventing the apoptotic inhibition caused by the soluble form.

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Linkage of angiotensin I‐converting enzyme gene insertion/deletion polymorphism to the progression of human prostate cancer

Cited by 76 publications

References 56 publications

Renin‐angiotensin system inhibitors, angiotensin I‐converting enzyme gene insertion/deletion polymorphism, and cancer

Renin‐angiotensin system inhibitors, angiotensin I‐converting enzyme gene insertion/deletion polymorphism, and cancer

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

Association between FAS polymorphism and prostate cancer development

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