Mechanisms for pituitary tumorigenesis: the plastic pituitary
Shlomo Melmed
Shlomo Melmed
Published December 1, 2003
Citation Information: J Clin Invest. 2003;112(11):1603-1618. https://doi.org/10.1172/JCI20401.
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Category: Science in Medicine

Mechanisms for pituitary tumorigenesis: the plastic pituitary

Abstract

The anterior pituitary gland integrates the repertoire of hormonal signals controlling thyroid, adrenal, reproductive, and growth functions. The gland responds to complex central and peripheral signals by trophic hormone secretion and by undergoing reversible plastic changes in cell growth leading to hyperplasia, involution, or benign adenomas arising from functional pituitary cells. Discussed herein are the mechanisms underlying hereditary pituitary hypoplasia, reversible pituitary hyperplasia, excess hormone production, and tumor initiation and promotion associated with normal and abnormal pituitary differentiation in health and disease.

Authors

Shlomo Melmed

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Figure 6

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Securin function and aneuploidy. Normal mitosis (left): PTTG acts as a m...
Securin function and aneuploidy. Normal mitosis (left): PTTG acts as a mammalian securin that maintains sister chromatid adherence during mitosis. Sister chromatids are bound with cohesions, and PTTG inactivates separin, an enzyme that regulates cohesin degradation. At the end of metaphase, securin degradation by an anaphase-promoting complex releases tonic separin inhibition, which in turn mediates cohesin degradation, thus releasing sister chromatids for equal separation into daughter cells. PTTG overexpression (right) may disrupt equal sister chromatid separation and result in aneuploidy. Adapted with permission from Brain Pathology (143).