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
Henrys 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 superfamilyof growth
and differentiation factors. They were first identifiedas
gonadal-derived regulators of pituitary FSH and were subsequently
assignedmultiple actions in a wide range of tissues. More recently,
theinhibin subunit was considered as a tumor suppressor basedon
functional studies employing transgenic mouse models. Thisreview
evaluates the functional and molecular evidence thatthe inhibin
subunit is a tumor suppressor in endocrine cancers.The evaluation
highlights the discrepant results from the humanand mouse studies, as
well as the differences between endocrinetumor types. In addition, we
examine the evidence that the activin-signalingpathway is tumor
suppressive and identify organ-specific differencesin the actions and
putative roles of this pathway in endocrinetumors. In summary, there
is a considerable body of evidenceto support the role of inhibins and
activins in endocrine-relatedtumors. Future studies will define the
mechanisms by which inhibinsand activins contribute to the process of
initiation, promotion,or progression of endocrine-related
cancers.
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