Effects of calcium channel blockers on cellular apoptosis

Mason, R. Preston

doi:10.1002/(sici)1097-0142(19990515)85:10<2093::aid-cncr1>3.0.co;2-e

Cited by 43 publications

(22 citation statements)

References 80 publications

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“…Calcium channel blockers have been associated with apoptosis. The association however, is complex because both increased and decreased intracellular levels of calcium have been associated with apoptosis (11,12). Calcium-channel blockers alter calcium transport at the cellular level and increase calcium release into the cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

“…Laboratory studies suggest that calcium channel blockers induce regression and inhibition of vascular wall growth (13) and also inhibit angiogenic growth factors (14) through increased apoptosis. Calcium channel blockers have also been associated with inhibition of tumor growth and metastases (12,15). It has been hypothesized that increased sympathetic activity may stimulate androgen-mediated prostatic growth and thereby promote PCa (16).…”

Section: Discussionmentioning

confidence: 99%

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Inverse Association between Prostate Cancer and the Use of Calcium Channel Blockers

Debes

Roberts²,

Jacobson

et al. 2004

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Calcium channel blockers block calcium signal-mediated apoptosis. It is hypothesized that the use of these drugs may be associated with the development of cancer. This study investigated the association between daily use of calcium channel blockers and prostate cancer in a community-based cohort of men who participated in a longitudinal study of lower urinary tract symptoms. Study subjects were men ages 40 to 79 years by January 1, 1990, and were randomly selected from Olmsted County in Minnesota. At baseline, participants underwent an interview to determine all medications taken on a daily basis, including calcium channel blockers and to elicit a family history of prostate cancer. During followup, all men with a histological diagnosis of prostate cancer were identified through patient self-report and by a review of the complete medical record. Over 12,668 person years of follow-up, 15 (6.8%) of 220 calcium channel blocker users and 120 (10.5%) of 1142 nonusers developed prostate cancer (P ‫؍‬ 0.09; odds ratio, 0.62; 95% confidence interval, 0.36 -1.10). With adjustment for age and family history of prostate cancer, the risk (odds ratio, 95% confidence interval) of prostate cancer was 0.55 (0.31-0.97) in calcium channel blocker users compared with nonusers. In analyses stratified by family history of prostate cancer, the risk of prostate cancer was 0.45 (0.23-0.88) in men without a family history and 2.64 (0.82-8.47) in men with a family history of prostate cancer (P ‫؍‬ 0.006). These findings suggest an association between prostate cancer and daily use of calcium channel blockers that varies by family history of prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Inverse Association between Prostate Cancer and the Use of Calcium Channel Blockers

Debes

Roberts²,

Jacobson

et al. 2004

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…The constellation of factors in metabolic syndrome, namely glucose intolerance and insulin resistance, central obesity, dyslipidemia, and hypertension, are also well-documented risk factors for cardiovascular disease and diabetes Zambon et al, 2005). As most of these components have suggestive links to the development of cancer, the possible association of metabolic factors in the aggregate with cancer risk has been speculated (Hamet, 1997;Mason, 1999;Yu and Rohan, 2000;Calle and Thun, 2004;Cowey and Hardy, 2006;Barb et al, 2007;Giovannucci, 2007;Hsing et al, 2007;Hsu et al, 2007;Watanabe et al, 2007;Xue and Michels, 2007). Epidemiologic evidence for this link is, however, limited (Russo et al, 2008), and most has been targeted at specific sites of cancer (Trevisan et al, 2001;Colangelo et al, 2002;Furberg et al, 2004;Laukkanen et al, 2004;Ahmed et al, 2006;Bowers et al, 2006;Lund Haheim et al, 2006;Sturmer et al, 2006;Tande et al, 2006;Beebe-Dimmer et al, 2007;Chiu et al, 2007;Cust et al, 2007;Tuohimaa et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Impact of metabolic factors on subsequent cancer risk: results from a large-scale population-based cohort study in Japan

Inoue

Noda

Kurahashi

et al. 2009

European Journal of Cancer Prevention

258

363

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The impact of metabolic factors, which are major risk factors for cardiovascular disease, on total cancer risk has not been clarified. We prospectively examined whether metabolic factors and their aggregates predict the subsequent occurrence of total and major sites of cancer in the Japan Public Health Center-based Prospective Study. A total of 27 724 participants (9548 men and 18 176 women) aged 40-69 years participating in a questionnaire and health checkup survey in 1993-1995 were followed for total cancer incidence through 2004. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated for metabolic factors and for two criteria of their aggregates (three or more than three factors and two or more than two additional factors in addition to being overweight) with a Cox proportional hazards model to control for potential confounding factors. In both sexes, the presence of metabolic factors in the aggregate did not predict subsequent occurrence of cancer as a whole. By site, a significant increase in risk was observed for male liver cancer [HR = 1.73, CI = 1.03-2.91 (three or more than three factors); HR = 1.99, CI = 1.11-3.58 (two or more than two additional factors in addition to being overweight)], and female pancreatic cancer [HR = 1.99, CI = 1.00-3.96 (two or more than two additional factors in addition to being overweight)]. For other sites, positive associations were observed only for specific metabolic factors, that is, high triglycerides and male colon cancer (HR = 1.71, CI = 1.11-2.62), and obesity and female breast cancer (HR = 1.75, CI = 1.21-2.55). Metabolic factors in the aggregate may have little impact on total cancer risk in the Japanese population, although the association between specific components and specific cancers suggests an etiologic link between them.

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“…In vitro studies have shown that intracellular calcium is involved in regulating apoptosis, whereas calcium antagonists inhibit apoptosis [93,94]. However, a review by Mason demonstrates that the effects of CCBs on apoptosis are complicated and the evidence is inconsistent [95].…”

Section: Biological Mechanismsmentioning

confidence: 99%

Commonly used diabetes and cardiovascular medications and cancer recurrence and cancer-specific mortality: a review of the literature

Boudreau

Park

et al. 2014

Expert Opinion on Drug Safety

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Metformin and aspirin were associated with a reduced risk of cancer recurrence and cancer-specific mortality. The evidence for statins and antihypertensive medications on cancer survival was inconsistent. There were few studies to suggest that any of the medication classes of interest were associated with negative effects on cancer survival. Methodological shortcomings within observational studies, such as confounding, distinguishing between use of medications pre-cancer versus post-cancer diagnosis/treatment, misclassification of exposures/outcomes, informative censoring and competing risks, must be considered. New observational studies addressing these limitations are essential. Some clinical trials are underway to further investigate the beneficial effects of these drugs and completed trials have confirmed results demonstrated in observational studies.

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Effects of calcium channel blockers on cellular apoptosis

Cited by 43 publications

References 80 publications

Inverse Association between Prostate Cancer and the Use of Calcium Channel Blockers

Inverse Association between Prostate Cancer and the Use of Calcium Channel Blockers

Impact of metabolic factors on subsequent cancer risk: results from a large-scale population-based cohort study in Japan

Commonly used diabetes and cardiovascular medications and cancer recurrence and cancer-specific mortality: a review of the literature

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