Future treatment for non-AIDS-defining cancers in HIV-infected patients

Abstract

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