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Review
. 2005 Oct;28(1):37-41.
doi: 10.1385/ENDO:28:1:037.

Recent progress in studies of pituitary tumor pathogenesis

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Review

Recent progress in studies of pituitary tumor pathogenesis

Takeo Minematsu et al. Endocrine. 2005 Oct.

Abstract

The mechanisms of tumorigenesis of the human pituitary have been elucidated to a limited extent. Classically, pituitary tumor formation was shown to be induced by thyroidectomy and estrogen administration. Molecular biological and immunohistochemical studies have revealed several aspects of pituitary tumorigenesis. Translineage cell differentiation has been shown to be induced by the aberrant expression of transcription factors and co-factors, such as Pit-1, Prop-1, and estrogen receptor. Defects or overexpression of cell cycle regulators, such as CDK inhibitors, PTTG, and GADD45gamma, result in the abnormal proliferation of pituitary cells. Recently, epigenetic regulation has been suggested to be related to pituitary tumor formation. This article presents a review and update of recent progress in studies of the development and differentiation of pituitary tumors.

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References

    1. Endocr J. 1993 Feb;40(1):133-9 - PubMed
    1. Cell. 1996 May 31;85(5):707-20 - PubMed
    1. Mol Endocrinol. 2005 Jan;19(1):138-47 - PubMed
    1. Cell. 1988 Nov 4;55(3):505-18 - PubMed
    1. Endocrinology. 2003 Oct;144(10):4626-36 - PubMed

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