کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2197986 | 1550996 | 2007 | 8 صفحه PDF | دانلود رایگان |
Human hereditary tumor syndromes serve as an ideal model for studying molecular pathways regulating tumorigenesis. Multiple endocrine neoplasia type 1 (MEN1), a human familial tumor syndrome, results from mutations in the Men1 gene. Men1 encodes a novel tumor suppressor, menin, of unknown biochemical function. Recently, significant progress has been made in identifying menin as a regulator of gene transcription, cell proliferation, apoptosis, and genome stability, leading to a new model of understanding menin's tumor-suppressing function. These findings suggest that menin's diverse functions depend on its association with chromatin and its control over gene transcription. This knowledge will likely be translated into new strategies to improve therapeutic interventions against MEN1 and other related cancers.
Journal: Molecular and Cellular Endocrinology - Volumes 265–266, February 2007, Pages 34–41