Abstract
Endometriosis is generally regarded as a benign disease but it does
exhibit some characteristics reminiscent of malignancy. This raises
the possibility that, like malignant diseases, the development of
endometriosis may involve the acquisition of somatic genetic alterations
in genes that regulate cell growth and differentiation. Studies over
the past few years have substantiated this view with the identification
of a variety of genetic abnormalities usually only associated with
malignancies. Our own studies have shown that genetic alterations,
as shown by loss of heterozygosity, are relatively common in endometriosis
implying that tumour suppressor gene inactivation is likely to be
involved in the proliferation and maintenance of all endometriotic
implants. We have also shown by DNA fingerprinting that endometriotic
lesions found adjacent to ovarian cancers have a common lineage,
reinforcing the compelling histological and epidemiological data
that endometriosis is a precursor of endometrioid and clear cell
ovarian cancers. It is now well accepted that susceptibility to endometriosis
may also involve an inherited genetic component. Studies aimed at
identifying the predisposing genes are still in their infancy but
should eventually provide invaluable insights into the pathology
and aetiology of endometriosis.
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