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乳腺癌中的转化生长因子-β:过多,过晚。

Transforming growth factor-beta in breast cancer: too much, too late.

作者信息

Barcellos-Hoff Mary Helen, Akhurst Rosemary J

机构信息

New York University Langone School of Medicine, New York, NY 10016, USA.

出版信息

Breast Cancer Res. 2009;11(1):202. doi: 10.1186/bcr2224. Epub 2009 Feb 26.

DOI:10.1186/bcr2224
PMID:19291273
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2687712/
Abstract

The contribution of transforming growth factor (TGF)beta to breast cancer has been studied from a myriad perspectives since seminal studies more than two decades ago. Although the action of TGFbeta as a canonical tumor suppressor in breast is without a doubt, there is compelling evidence that TGFbeta is frequently subverted in a malignant plexus that drives breast cancer. New knowledge that TGFbeta regulates the DNA damage response, which underlies cancer therapy, reveals another facet of TGFbeta biology that impedes cancer control. Too much TGFbeta, too late in cancer progression is the fundamental motivation for pharmaceutical inhibition.

摘要

自二十多年前的开创性研究以来,人们从无数角度研究了转化生长因子(TGF)β对乳腺癌的作用。尽管TGFβ在乳腺中作为典型的肿瘤抑制因子的作用是毫无疑问的,但有令人信服的证据表明,TGFβ在驱动乳腺癌的恶性网络中经常被颠覆。TGFβ调节DNA损伤反应这一癌症治疗基础的新知识,揭示了TGFβ生物学阻碍癌症控制的另一个方面。在癌症进展过程中TGFβ过多、过晚是药物抑制的根本动机。

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本文引用的文献

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17-Beta-estradiol inhibits transforming growth factor-beta signaling and function in breast cancer cells via activation of extracellular signal-regulated kinase through the G protein-coupled receptor 30.17-β-雌二醇通过G蛋白偶联受体30激活细胞外信号调节激酶,抑制乳腺癌细胞中的转化生长因子-β信号传导及功能。
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The epithelial-mesenchymal transition generates cells with properties of stem cells.上皮-间质转化产生具有干细胞特性的细胞。
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TGFbeta primes breast tumors for lung metastasis seeding through angiopoietin-like 4.转化生长因子β通过血管生成素样蛋白4使乳腺肿瘤易于发生肺转移播散。
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Concordant epigenetic silencing of transforming growth factor-beta signaling pathway genes occurs early in breast carcinogenesis.转化生长因子-β信号通路基因的一致性表观遗传沉默在乳腺癌发生早期就会出现。
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Modulation of tumor induction and progression of oncogenic K-ras-positive tumors in the presence of TGF- b1 haploinsufficiency.在TGF-β1单倍体不足情况下对致癌性K-ras阳性肿瘤的肿瘤诱导和进展的调节
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TGFbeta-1 dependent fast stimulation of ATM and p53 phosphorylation following exposure to ionizing radiation does not involve TGFbeta-receptor I signalling.暴露于电离辐射后,转化生长因子β-1(TGFbeta-1)依赖性快速刺激ATM和p53磷酸化不涉及转化生长因子β受体I信号传导。
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