کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8476526 | 1550815 | 2018 | 43 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Consider the context: Ras/ERK and PI3K/AKT/mTOR signaling outcomes are pituitary cell type-specific
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Conserved signaling pathways are critical regulators of pituitary homeostasis and, when dysregulated, contribute to adenoma formation. Pituitary adenomas are typically benign and rarely progress to malignant cancer. Pituitary and other neuroendocrine cell types often display non-proliferative responses to ERK and PI3K, in contrast to non-endocrine cell types which typically proliferate in response to ERK and PI3K activation. These differences likely contribute to the infrequent progression to malignancy in many endocrine tumors. In this review, we highlight the Ras/ERK and PI3K/AKT/mTOR signaling pathways in each pituitary cell type, as well as in other endocrine tissues. Furthermore, we provide evidence that a balance of ERK and PI3K signaling is required to maintain pituitary homeostasis. It is unlikely that one sole oncogene will be identified as being responsible for sporadic pituitary adenoma formation. This review emphasizes the necessity to consider endocrine cell-specific contexts and the interplay of signaling pathways to define the mechanisms underlying pituitary tumorigenesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 463, 5 March 2018, Pages 87-96
Journal: Molecular and Cellular Endocrinology - Volume 463, 5 March 2018, Pages 87-96
نویسندگان
Allyson K. Roof, Arthur MD,