Mason R P
Cardiovascular and Pulmonary Research Institute, Department of Biochemistry, MCP Hahnemann University School of Medicine, Pittsburgh, Pennsylvania, USA.
Cancer. 1999 May 15;85(10):2093-102. doi: 10.1002/(sici)1097-0142(19990515)85:10<2093::aid-cncr1>3.0.co;2-e.
A small number of well-publicized, retrospective epidemiologic reports have suggested a causal relation between the use of calcium channel blockers (CCBs) for the treatment of hypertension and an increased risk for cancer. The biologic mechanism proposed to explain this possible relation is that CCBs interfere with apoptosis, an active cell death process required for the regulation of normal cell populations in the body. Because an elevation in cellular calcium (Ca2+) is thought to be involved in apoptosis, it has been argued that CCBs could inhibit apoptosis, leading directly to tumor promotion.
A comprehensive and critical review of the scientific literature was conducted specifically to evaluate the effects of pharmacologic CCBs on apoptosis and tumor development in various experimental models.
A review of the scientific literature revealed that CCBs have complex and often contradictory effects on cellular apoptosis. In various experimental models of cancer, CCBs did not promote neoplastic growth. By contrast, CCB treatment was associated with an inhibition of tumor growth in certain models of neoplasia and was also an effective adjuvant therapy in the treatment of certain drug-resistant tumors. Additional large epidemiologic studies have failed to support the hypothesis that CCB use is associated with an increased susceptibility for cancer.
A biologic link between the use of CCBs and increased human risk for cancer development as a result of modulating cellular apoptosis is not supported by the scientific literature.
少数广为宣传的回顾性流行病学报告表明，使用钙通道阻滞剂（CCB）治疗高血压与癌症风险增加之间存在因果关系。为解释这种可能的关系而提出的生物学机制是，CCB干扰细胞凋亡，而细胞凋亡是调节体内正常细胞群所需的主动细胞死亡过程。由于细胞内钙（Ca2+）升高被认为与细胞凋亡有关，因此有人认为CCB可抑制细胞凋亡，直接导致肿瘤促进。
对科学文献进行了全面且批判性的综述，专门评估药理学CCB对各种实验模型中细胞凋亡和肿瘤发展的影响。
对科学文献的综述显示，CCB对细胞凋亡具有复杂且往往相互矛盾的影响。在各种癌症实验模型中，CCB并未促进肿瘤生长。相比之下，在某些肿瘤模型中，CCB治疗与肿瘤生长抑制有关，并且在治疗某些耐药肿瘤时也是一种有效的辅助治疗方法。更多大型流行病学研究未能支持使用CCB与癌症易感性增加相关的假设。
科学文献不支持使用CCB与因调节细胞凋亡而增加人类患癌风险之间存在生物学联系。
