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肝脏肿瘤与宿主防御

Liver tumors and host defense.

作者信息

Tabor E

机构信息

Division of Transfusion Transmitted Diseases, Food and Drug Administration, Bethesda, Maryland 20852-1448, USA.

出版信息

Semin Liver Dis. 1997;17(4):351-5. doi: 10.1055/s-2007-1007212.

Abstract

Complex molecular and cellular mechanisms exist to protect cells against tumor formation and to protect the entire organism against further development and spread of established tumors. The p53 tumor suppressor gene controls the cell cycle through at least two mechanisms, namely, mitotic arrest and apoptosis. Human hepatocellular carcinomas (HCCs) are often found to have mutant p53, or sometimes may have dysfunctional p53 as a result of its being bound by viral or cellular proteins. Another mechanism of host response is the production of transforming growth factor beta 1, which acts on receptors in normal hepatocytes to cause inhibition of DNA synthesis; abnormalities of transforming growth factor beta 1 have been documented in HCCs, but their biologic significance is unclear. Other host defense mechanisms include cellular responses to the tumor and the proliferation of substances with anticoagulant properties.

摘要

存在复杂的分子和细胞机制来保护细胞免受肿瘤形成,并保护整个机体免受已形成肿瘤的进一步发展和扩散。p53肿瘤抑制基因通过至少两种机制控制细胞周期,即有丝分裂停滞和细胞凋亡。人类肝细胞癌(HCC)常常发现有p53突变,或者有时可能由于其被病毒或细胞蛋白结合而导致p53功能失调。宿主反应的另一种机制是转化生长因子β1的产生,它作用于正常肝细胞中的受体以抑制DNA合成;在HCC中已记录到转化生长因子β1异常,但其生物学意义尚不清楚。其他宿主防御机制包括细胞对肿瘤的反应以及具有抗凝血特性物质的增殖。

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