We investigated 18 AIDS hearts (5 with and 13 without cardiomyopathy) by using immunocytochemistry and computerized image analysis regarding the roles of HIV-1 proteins and tumor necrosis factor ligands in HIV cardiomyopathy (HIVCM). HIVCM and cardiomyocyte apoptosis were significantly related to each other and to the expression by inflammatory cells of gp120 and tumor necrosis factor-␣. In HIVCM heart, active caspase 9, a component of the mitochondrion-controlled apoptotic pathway, and the elements of the death receptor-mediated pathway, tumor necrosis factor-␣ and Fas ligand, were expressed strongly on macrophages and weakly on cardiomyocytes. HIVCM showed significantly greater macrophage infiltration and cardiomyocyte apoptosis rate compared with non-HIVCM. HIV-1 entered cultured neonatal rat ventricular myocytes by macropinocytosis but did not replicate. HIV-1-or gp120-induced apoptosis of rat myocytes through a mitochondrion-controlled pathway, which was inhibited by heparin, AOP-RANTES, or pertussis toxin, suggesting that cardiomyocyte apoptosis is induced by signaling through chemokine receptors. In conclusion, in patients with HIVCM, cardiomyocytes die through both mitochondrion-and death receptor-controlled apoptotic pathways.

Epithelial ovarian cancer is typically found in its advanced stages, where a combination of surgical debulking and platinum/taxane-based chemotherapy is recommended. Although over 70%–80% of patients achieve remission, a significant proportion develop recurrence of their disease. Additional cytotoxic chemotherapy, as well as surgery, is typically used to manage disease recurrence. Therapies that target specific pathways in cancer cells are rapidly developing in the laboratory and are increasingly being studied in patients with ovarian cancer. We review the current status of novel therapies in the management of epithelial ovarian cancer.