Shared risk factors for cancer and atherosclerosis—a review of the epidemiological evidence

Hansen, Ebba Holme

doi:10.1016/0165-1110(90)90004-u

Cited by 84 publications

(23 citation statements)

References 97 publications

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“…24 -27 Moreover, epidemiological studies have demonstrated that arsenic, ionizing radiation, and vinyl chloride monomer may induce various cancers and vascular diseases, including angiosarcoma and atherosclerotic plaques. 28 These findings suggest that somatic mutation and cell proliferation may play important roles in the dual effects on carcinogenesis and atherosclerosis. In support of arsenic-induced cell proliferation, researchers have demonstrated that sodium arsenite may induce increased mRNA transcripts of growth factors, including granulocyte-macrophage colony-stimulating factor, transforming growth factor-␣, and the inflammatory cytokine tumor necrosis factor-␣.…”

Section: Discussionmentioning

confidence: 99%

Biological Gradient Between Long-Term Arsenic Exposure and Carotid Atherosclerosis

et al. 2002

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Background-Long-term exposure to ingested arsenic has been documented to induce peripheral vascular disease, ischemic heart disease, and cerebral infarction in a dose-response relationship. This study further examined the biological gradient between ingested inorganic arsenic and carotid atherosclerosis. Methods and Results-We studied 199 male and 264 female adult residents from the southwestern area of endemic arseniasis in Taiwan. The extent of carotid atherosclerosis was assessed by duplex ultrasonography. Diabetes mellitus was determined by oral glucose tolerance test, hypertension by mercury sphygmomanometers, and serum lipid profiles by autoanalyzers. Information regarding the consumption of high-arsenic artesian well water, cigarette smoking, and alcohol consumption was obtained through standardized questionnaire interviews. Logistic regression analysis was used to estimate the odds ratio and its 95% CI of carotid atherosclerosis for various risk factors. Three indices of long-term exposure to ingested arsenic, including the duration of consuming artesian well water, the average arsenic concentration in consumed artesian well water, and cumulative arsenic exposure, were all significantly associated with prevalence of carotid atherosclerosis in a dose-response relationship. The biological gradient remained significant after adjustment for age, sex, hypertension, diabetes mellitus, cigarette smoking, alcohol consumption, waist-to-hip ratio, and serum levels of total cholesterol and LDL cholesterol. The multivariate-adjusted odds ratio was 3.1 (95% CI 1.3 to 7.4) for those who had a cumulative arsenic exposure of Ն20 mg/L-years compared with those without exposure to arsenic from drinking artesian well water. Conclusions-Carotid atherosclerosis is associated with ingested inorganic arsenic, showing a significant biological

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Section: Discussionmentioning

confidence: 99%

Biological Gradient Between Long-Term Arsenic Exposure and Carotid Atherosclerosis

et al. 2002

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“…The epidemiological evidence for shared risk factors for cancer and atherosclerosis has been reviewed [42]. Exposure to carcinogenic environmental agents is associated with an increased risk of atherosclerosis.…”

Section: Agentmentioning

confidence: 99%

Humic acid induced genotoxicity in human peripheral blood lymphocytes using comet and sister chromatid exchange assay

Hseu

Chen

et al. 2008

Journal of Hazardous Materials

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“…Mutant cells might have a selective advantage over their sister cells in their ability either to replicate or to survive [Benditt and Benditt, 1973;Bridges et al, 1990;Hansen, 1990;Penn, 1990;Wakabayashi, 1990]. In accordance with the clonal hypothesis, a complex series of independent molecular events would have to occur in plaque cells, such as the accumulation of damage in crucial regions of DNA.…”

Section: Monoclonal Hypothesis Of Atherosclerosismentioning

confidence: 89%

Genetic instability and atherosclerosis: can somatic mutations account for the development of cardiovascular diseases?

Andreassi

Botto

Colombo

et al. 2000

Environ. Mol. Mutagen.

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Several observations suggest that cancer and atherosclerosis may entail fundamentally common biological mechanisms. The accumulation of lipids and the proliferation of smooth muscle cells (SMCs) are the main histological features of sclerotic plaque formation. The most prominent theory concerning the pathophysiological mechanisms of atherosclerotic plaque formation is the “inflammatory response to injury” hypothesis, which states that SMC proliferation is an inflammation‐fibroproliferative reaction to different insults to the artery wall. However, recent evidence suggests that alterations at the DNA level may contribute significantly to the development of the disease. In accordance with these findings, the “monoclonal” hypothesis of atherosclerosis has been suggested. This hypothesis proposes that atherosclerosis begins as a mutation or viral infection, transforming a single, isolated smooth muscle cell into the progenitor of a proliferative clone, as seen in carcinogenesis. Studies of DNA damage in atherosclerotic tissues are lacking. Biological evidence for the hypothesis that cancer and atherosclerosis may share pathological mechanisms is discussed, emphasizing the need to perform studies investigating the involvement of somatic mutations in heart diseases. Environ. Mol. Mutagen. 35:265–269, 2000 © 2000 Wiley‐Liss, Inc.

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Shared risk factors for cancer and atherosclerosis—a review of the epidemiological evidence

Cited by 84 publications

References 97 publications

Biological Gradient Between Long-Term Arsenic Exposure and Carotid Atherosclerosis

Biological Gradient Between Long-Term Arsenic Exposure and Carotid Atherosclerosis

Humic acid induced genotoxicity in human peripheral blood lymphocytes using comet and sister chromatid exchange assay

Genetic instability and atherosclerosis: can somatic mutations account for the development of cardiovascular diseases?

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