Our current analysis suggests that VCAP-AMP-VECP regimen is a preferable front-line therapy in patients with aggressive ATL in intermediate- and high-risk groups.
Human T-cell leukemia virus type I tax protein induces the expression of anti-apoptotic gene Bcl-xL in human T-cells through nuclear factor-kappaB and c-AMP responsive element binding protein pathways.
Conditioned media from cultures of human T-cell lymphotropic virus type I-infected cell line (MT-2) as well as peripheral lymphocytes from a hypercalcemic ATLL patient stimulated cyclic AMP production in osteoblast-like rat osteogenic sarcoma cells (UMR 106) and bone resportion in organ cultures of fetal mouse calvaria.
Our observation of a human T cell leukemia cell (Molt 4) demonstrating low affinity thyroid-stimulating hormone (TSH) responses, as evidenced by generation of cyclic AMP, led us to test Molt 4 cells as a suitable partner for immortalizing high affinity TSH receptors present on human thyroid cells.