Chronic disease in the workplace and environment: cancer

The quest for the etiology and prevention of cancer has stimulated a vast frontier of scientific investigations concerning the biochemical and genetic mechanisms that control cell differentiation and proliferation. The contribution of cancer epidemiology to cancer prevention is in identifying risk factors, providing clues for understanding etiologic mechanisms, and in developing the scientific rationale for the effective application of preventive measures. Carcinogenesis involves a complex interplay of environment and heredity. If there is a unifying principle, it is that carcinogenesis is a multistage process. A common oncogenic pathway involves molecular activation of transforming genes. Various links with this pathway may be triggered by environmental and host factors. Transformation of a normal cell to a cancer cell represents a self-perpetuating programming error. Normal cells may indeed harbor the seeds of transformation in the form of cancer genes. These cancer genes may be closely linked with the vital components of the genetic apparatus of a cell. The stage of initiation may involve the unveiling or derepression of cancer genes. However, it would be overly simplistic to assume that the activation of cellular oncogenes was the only aberration necessary and sufficient for malignant transformation. The proliferation of a clone of malignant cells involves the interaction of multiple factors. Promotional events are potentially reversible or modifiable. Herein lies a challenging path of research. Namely, through understanding of the dynamic events that affect tumor growth and host susceptibility, preventive strategies for reversing aberrant cellular proliferation will ultimately be developed and then subjected to rigorous experimental trial.(ABSTRACT TRUNCATED AT 250 WORDS)