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人类免疫缺陷病毒相关卡波西肉瘤的发病机制。

Pathogenesis of HIV-related Kaposi's sarcoma.

作者信息

Miles S A

机构信息

University of California, Los Angeles.

出版信息

Curr Opin Oncol. 1994 Sep;6(5):497-502. doi: 10.1097/00001622-199409000-00009.

DOI:10.1097/00001622-199409000-00009
PMID:7827153
Abstract

Infection with HIV-1 is associated with a 7000-fold increase in the incidence of Kaposi's sarcoma (KS). Some studies suggest that the risk of KS in HIV infection is increased with certain sexual practices and that a sexually transmitted agent could be involved. Exposure to this agent apparently alters both the morphology and growth regulation of the KS progenitor cells. These changes include the expression of the different cytokine receptors and the acquisition of autocrine growth loops. Perturbations of multiple cytokines during HIV infection, including oncostatin-M, interleukin-1 beta, and tumor necrosis factor-alpha, alter the subsequent growth of KS. These studies suggest that control of cytokine perturbations or the underlying HIV-1 infection could result in a significant reduction in the growth rate of AIDS-related KS.

摘要

感染人类免疫缺陷病毒1型(HIV-1)会使卡波西肉瘤(KS)的发病率增加7000倍。一些研究表明,HIV感染中KS的风险会因某些性行为而增加,并且可能涉及一种性传播因子。接触这种因子显然会改变KS祖细胞的形态和生长调节。这些变化包括不同细胞因子受体的表达以及自分泌生长环的形成。HIV感染期间多种细胞因子的紊乱,包括抑瘤素-M、白细胞介素-1β和肿瘤坏死因子-α,会改变KS随后的生长。这些研究表明,控制细胞因子紊乱或潜在的HIV-1感染可能会使艾滋病相关KS的生长速率显著降低。

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