艾滋病毒感染患者非艾滋病定义癌症的未来治疗

HIV therapy Pub Date : 2009-07-06 DOI:10.2217/HIV.09.14
J. Deeken, L. Pantanowitz, B. Dezube
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引用次数: 1

摘要

ISSN 1758-4310 10.2217/HIV.09.14©2009未来医学有限公司HIV Ther。(2009) 3(4), 311-314与非裔美国人和其他族裔患者相比,罹患某些癌症的风险更高[7]。其他危险因素包括行为方面,如艾滋病毒患者吸烟和饮酒增加[8]。研究表明,艾滋病毒本身可能直接影响NADC的发展。例如,HIV Tat蛋白可能导致原癌基因的反激活[9]。HIV病毒内的其他基因可能抑制肿瘤抑制基因,包括p53。HIV感染可能导致微卫星基因不稳定和基因改变导致肿瘤发生。组织感染艾滋病毒可能使这些问题对环境致癌物的影响更加敏感。最后,HIV感染可引起内皮异常,包括促血管生成,这可能促进肿瘤生长和转移的发展[1]。关于HAART是否与发生NADCs的风险相关,一直存在相互矛盾的数据。一些研究表明,与未接受抗逆转录病毒治疗或仅接受单药或双药抗逆转录病毒治疗的患者相比,接受HAART治疗的患者发生NADC的风险降低[7]。其他研究表明,如果患者接受HAART治疗,特别是非核苷类逆转录酶抑制剂治疗,风险可能会增加[4]。最近在大型III期试验中,一项令人担忧的发现是,在研究期间,与服用安慰剂的患者相比,服用雷替韦韦(一种整合酶抑制剂,也称为Isentress[默克]和MK-0518)的患者发生NADC的风险更高[10]。显然,需要更多的研究来阐明抗逆转录病毒治疗的作用、免疫重建和发生NADCs的相对风险。编辑
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Future treatment for non-AIDS-defining cancers in HIV-infected patients
ISSN 1758-4310 10.2217/HIV.09.14 © 2009 Future Medicine Ltd HIV Ther. (2009) 3(4), 311–314 at higher risk for some cancers compared with African–Americans and patients of other ethnic groups [7]. Additional risk factors include behavioral aspects, such as an increased use of tobacco and alcohol in patients with HIV [8]. Research has demonstrated that HIV itself may have direct effects that contribute to the development of NADC. For example, the HIV Tat protein may cause transactivation of protooncogenes [9]. Other genes within the HIV virus may inhibit tumor suppressor genes, including p53. HIV infection may cause microsatellite gene instability and genetic alterations leading towards onco genesis. Tissue infection with HIV may make these t issues more sensitive to the effects of carcinogens from the environment. Finally, HIV infection can cause endothelial abnormalities including pro angiogenesis, which may enhance the development of tumor growth and metastasis [1]. There have been conflicting data regarding whether HAART is associated with the risk of developing NADCs. Some studies have demonstrated a decreased risk of developing a NADC while patients are on HAART, compared with patients who are not receiving antiretroviral therapy or are only on single agent or dual agent antiretroviral therapy [7]. Other studies have demonstrated a possible increased risk if patients are on HAART [4], and specifically if they are on a non-nucleoside reverse transcriptase inhibitorbased therapy [5]. A concerning, recent finding in the large Phase III trial that led to the approval of raltegravir (an integrase inhibitor also known as Isentress [Merck] and MK-0518) was that during the period of the study, patients on raltegravir had a higher risk of developing a NADC compared with those taking placebo [10]. Clearly more research is needed to elucidate the role of antiretroviral therapy, immune reconstitution and the relative risk of developing NADCs. Editorial
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