Southern Africa has the highest HIV incidence worldwide. Thus far there is no cure; however, the lives of individuals infected with the virus can be prolonged through the use of Highly Active AntiRetroviral Therapy (HAART). According to the United Nations Programme on HIV and AIDS (UNAIDS) fact sheet for 2015, 2 out of 3 new HIV infections are in the Sub-Saharan African region, with approximately 25.8 million people living with HIV and 1.4 million new infections in 2014. In 2004, South Africa introduced ART (Anti-retroviral Therapy) free of charge in the public healthcare sector, and today South Africa has the largest treatment programme in the world approximately 2.4 million people have received the life-saving treatment which has significantly increased their life expectancy. Shaheen Mowla* Department of Pathology, Faculty of Health Sciences, University of Cape Town, South Africa Shaheen Mowla Clinics in Oncology General Oncology Remedy Publications LLC., | http://clinicsinoncology.com/ 2017 | Volume 2 | Article 1366 2 novel targeted agents for these two subtypes [8]. Despite undergoing therapy, about 40% of HIV negative DLBCL patients suffer from relapsed or refractory disease under current the chemotherapeutic regimens (R-CHOP-rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone) [9]. The majority of them succumb to their disease. The poor response is largely attributed to how genetically and molecularly heterogeneous the disease is [10]. Among DLBCL patients who are HIV positive, response to standard therapy is even more heterogeneous. Currently, the genetic causes of HIVDLBCL are unknown. Additionally, the contribution of Epstein Barr Virus (EBV) co-infection, which is common in HIV-DLBCLs, is also unknown and current studies in our laboratory are focusing on exploring the genetic and molecular subgroups of HIV-DLBCL patients within our population. While HIV uninfected patients with BL generally respond well to existing therapy, the response in HIV infected patients remains poor, and in some settings, there is report of no improvement at all [1113]. The pathogenesis of BL is strongly related to the overexpression of c-MYC resulting from translocation of the c-MYC gene to the highly active immunoglobulin (IGH) locus in B cells. The common treatment approach for BL is surgical resection if necessary, followed by chemotherapy. Different combinations of chemotherapeutic agents are used such as cyclophosphamidine, Vincristine, doxorubicin and dexamethasone; and in HIV positive patients this is administered after HAART [13,14]. Several case studies have shown that despite combination antiretroviral therapy, the outcome of HIV infected individuals with BL remains inferior compared to HIV-uninfected patients suffering from this cancer. Contrary to what is expected, some reports found that BL incidence among HIV infected individuals has not improved significantly despite the advent of HAART, and that the cancer develops in patients with relatively high CD4 counts [5]. The latter observation points to other enabling factors, aside from an immunocompromised state. Indeed, in recent years, our laboratory as well as others have shown that HIV-encoded proteins can contribute to oncogenesis by activating or enhancing oncogenic pathways in B cells. This is already shown in Kaposi sarcoma where the HIV Tat protein was found to cooperate with the Kaposi sarcoma herpes virus (KSHV) to enhance the development of the cancer [15].
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