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肢端肥大症的分子发病机制。

Molecular pathogenesis of acromegaly.

作者信息

Drange M R, Melmed S

机构信息

Cedars-Sinai Research Institute, UCLA School of Medicine, USA.

出版信息

Pituitary. 1999 Jun;2(1):43-50. doi: 10.1023/a:1009917920589.

Abstract

Acromegaly is generally caused by growth hormone (GH) hypersecretion from a benign, monoclonal pituitary adenoma. As in other neoplastic conditions, pituitary tumor formation and dysregulated hormone secretion are most likely the ultimate result of a series of genetic alterations. A number of molecular and biochemical defects have been associated with pituitary tumorigenesis. Molecular events such as tumor suppressor gene inactivation and oncogene activation involved in pituitary tumor progression are examined. The role of hypothalamic regulatory hormones and hereditary syndromes involving acromegaly are also discussed.

摘要

肢端肥大症通常由良性单克隆垂体腺瘤分泌过多生长激素(GH)所致。与其他肿瘤情况一样,垂体肿瘤形成和激素分泌失调很可能是一系列基因改变的最终结果。许多分子和生化缺陷与垂体肿瘤发生有关。本文探讨了垂体肿瘤进展过程中涉及的肿瘤抑制基因失活和癌基因激活等分子事件。还讨论了下丘脑调节激素的作用以及与肢端肥大症相关的遗传综合征。

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