Abstract

Arsenicalism has been observed throughout the world and has become an urgent public health concern. The authors explored the mechanism of carcinogenesis of inorganic arsenic in patients with arsenicalism from coal-burning pollution. The 68 subjects were divided into 3 groups--carcinoma, precarcinoma, and common-on the basis of pathological diagnosis. The expressions of proliferating cell nuclear antigen (PCNA), mutant-type P53, and B-cell lymphoma/leukemia-2 (BCL-2) proteins were detected by immunohistochemical staining. PCNA, P53, and BCL-2 proteins were overexpressed. The proteins' overexpressions correlated with the pathological changes seen in each pathological study group (i.e., common < precarcinoma < carcinoma). Statistical correlation was observed between P53 and BCL-2, and between PCNA and BCL-2. The authors concluded that cell proliferation, antiapoptosis, and up-regulation of the mutant-type P53 gene played vital roles in the pathological development of arsenicalism.

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