Alternative explanations of the differing behaviour of ovarian and testicular teratomas

There are several aspects of the biology of teratomas which may be important in the aetiology of malignant versus non-malignant forms. Firstly, the ages when malignant teratomas form in the ovary (children) and testis (adult) follow by a similar span of years the time of oogenesis (fetus) and spermatogenesis (onset at puberty) and, specifically, follow by less than a decade the periods of active mitosis and meiosis during which interconnection of germ cells by intercellular bridges occurs. Secondly, ovarian teratomas may be viewed as parthenogenically activated oocytes, while testicular teratocarcinomas may represent post-meiotic fusion events more comparable to fertilisation; the malignant potential in the latter case could relate to fundamental differences in male and femal germ plasm. Thirdly,, the fact that malignant teratomas are easily produced by transplanting early embryos to extrauterine sites, while there is loss of malignancy with differentiation within a tumour or when malignant cells are injected into pre-implantation embryos and contribute cells to a variety of normal tissues, suggests that the malignant potential of teratomas has to do with gene control rather than mutational events.