Inhibin/activin and ovarian cancer.

in Endocrine-Related Cancer
Authors:
D M Robertson Prince Henry's Institute of Medical Research, PO 5152, Clayton, Victoria 3168, Australia. david.robertson@med.monash.edu.au

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H G Burger Prince Henry's Institute of Medical Research, PO 5152, Clayton, Victoria 3168, Australia. david.robertson@med.monash.edu.au

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P J Fuller Prince Henry's Institute of Medical Research, PO 5152, Clayton, Victoria 3168, Australia. david.robertson@med.monash.edu.au

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DOI:
https://doi.org/10.1677/erc.0.0110035
Volume/Issue:
Volume 11: Issue 1
Article Type:
Abstract
Page Range:
35–49
Online Publication Date:
Mar 2004
Free access

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Inhibin and activin are members of the transforming growth factor beta (TGFbeta) family of cytokines produced by the gonads, with a recognised role in regulating pituitary FSH secretion. Inhibin consists of two homologous subunits, alpha and either betaA or betaB (inhibin A and B). Activins are hetero- or homodimers of the beta-subunits. Inhibin and free alpha subunit are known products of two ovarian tumours (granulosa cell tumours and mucinous carcinomas). This observation has provided the basis for the development of a serum diagnostic test to monitor the occurrence and treatment of these cancers. Transgenic mice with an inhibin alpha subunit gene deletion develop stromal/granulosa cell tumours suggesting that the alpha subunit is a tumour suppressor gene. The role of inhibin and activin is reviewed in ovarian cancer both as a measure of proven clinical utility in diagnosis and management and also as a factor in the pathogenesis of these tumours. In order to place these findings into perspective the biology of inhibin/activin and of other members of the TGFbeta superfamily is also discussed.

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Print ISSN:
1351-0088
Online ISSN:
1479-6821
Page(s):
15
Print Publication Date:
01 Jan 2004
Online Publication Date:
Mar 2004