) The development of antiviral and antibiotic therapy has prolonged survival in those infected with Human Immunodeficiency Virus (HIV). At least in America, the number of infectious complications are fewer and hospital admissions have dropped, however, earlier accomplishments in therapeutics (nucleoside analogues) which resulted in longer, immunosuppressed survival, are likely part of the reason for an upsurge in AIDS associated cancers. No one knows if today's advances may set the stage for future neoplasms. HIV associated malignancies are an entirely new set of tumors which behave much more aggressively than their histologic counterparts seen in the HIV negative community. An oncologist trained only in the latter will be poorly prepared to manage AIDS malignancy patients. The interplay between HIV, cellular factors and other viruses is just starting to be appreciated. We outline a training program which will take promising young physicians, train them intensively in the clinical aspects of AIDS and associated malignancies and provide scientific mentorship with varied expertise in tumor immunology and molecular biology. Trainees will have the advantage of exposure to nearly all of the manifestations of retroviral malignancies while they develop their basic research project. Our institution is able to meet all of the prerequisites of AIDS oncology training; a large and varied patient population, novel clinical trials, and strong basic science mentors.
| Beaupre, Darrin M; Cepero, Enrique; Obeng, Esther A et al. (2004) R115777 induces Ras-independent apoptosis of myeloma cells via multiple intrinsic pathways. Mol Cancer Ther 3:179-86 |
| Hayward, Richard L; Macpherson, Janet S; Cummings, Jeff et al. (2004) Enhanced oxaliplatin-induced apoptosis following antisense Bcl-xl down-regulation is p53 and Bax dependent: Genetic evidence for specificity of the antisense effect. Mol Cancer Ther 3:169-78 |
| Beaupre, Darrin M; McCafferty-Grad, Jennifer; Bahlis, Nizar J et al. (2003) Farnesyl transferase inhibitors enhance death receptor signals and induce apoptosis in multiple myeloma cells. Leuk Lymphoma 44:2123-34 |
