Abstract

The causation of cervical cancer is conveniently discussed by using themes emergent from a great volume of field studies and by using the manner in which this evidence has been exploited in the clinic and laboratory. Epidemiology themes dwell on the strong correlation of disease incidence with sexual behaviour of both male and female, sufficient to regard cervical cancer as a type of venereal disease and an equally strong correlation with socio-economic class. Mortality rises when the male partner resides in the lower social classes. Laboratory and clinical studies have defined the tissue at risk and a few studies attempt definition of reasons for such risk. The accent in these studies is on a derangement of the cell filament system seen as grades of unusual keratinization. The vast bulk of laboratory studies is devoted to a definition of the carcinogen. The venereal nature of the epidemiological evidence renders a transmissible agent as most suspect. Viruses have been a popular subject because of this demonstrable capacity to transform cells in vitro and in vivo. Our own studies have concentrated on a component of the sperm as carcinogen or cocarcinogen. A new approach to carcinogenesis, relying on study of energy flow through the cell, is discussed in terms of its close relationship to events in the transforming and transformed cervical cell.

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