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Endocrine Reviews 22 (6): 836-858
Copyright © 2001 by The Endocrine Society

Activins and Inhibins in Endocrine and Other Tumors

Gail P. Risbridger, Jacqueline F. Schmitt and David M. Robertson

Centre for Urological Research, Institute of Reproduction and Development, Monash University (G.P.R., J.F.S.), Melbourne, Prince Henry’s Institute of Medical Research (D.M.R.), Clayton, Victoria 3168, Australia

Correspondence: Address all correspondence and requests for reprints to: Dr. Gail P. Risbridger, Associate Professor, Director, Center for Urological Research, Monash Institute of Reproduction and Development, Monash Medical Center, 246 Clayton Road, Clayton, Victoria 3168, Australia. E-mail: gail.risbridger{at}med.monash.edu.au

Inhibin and activin are members of the TGFß superfamily of growth and differentiation factors. They were first identified as gonadal-derived regulators of pituitary FSH and were subsequently assigned multiple actions in a wide range of tissues. More recently, the inhibin {alpha} subunit was considered as a tumor suppressor based on functional studies employing transgenic mouse models. This review evaluates the functional and molecular evidence that the inhibin {alpha} subunit is a tumor suppressor in endocrine cancers. The evaluation highlights the discrepant results from the human and mouse studies, as well as the differences between endocrine tumor types. In addition, we examine the evidence that the activin-signaling pathway is tumor suppressive and identify organ-specific differences in the actions and putative roles of this pathway in endocrine tumors. In summary, there is a considerable body of evidence to support the role of inhibins and activins in endocrine-related tumors. Future studies will define the mechanisms by which inhibins and activins contribute to the process of initiation, promotion, or progression of endocrine-related cancers.




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