"The combination of arsenic, interferon-alpha, and zidovudine restores an ""immunocompetent-like"" cytokine expression profile in patients with adult T-cell leukemia lymphoma."
"The combination of arsenic, interferon-alpha, and zidovudine restores an ""immunocompetent-like"" cytokine expression profile in patients with adult T-cell leukemia lymphoma."
"The combination of arsenic, interferon-alpha, and zidovudine restores an ""immunocompetent-like"" cytokine expression profile in patients with adult T-cell leukemia lymphoma."
"The combination of arsenic, interferon-alpha, and zidovudine restores an ""immunocompetent-like"" cytokine expression profile in patients with adult T-cell leukemia lymphoma."
"The combination of arsenic, interferon-alpha, and zidovudine restores an ""immunocompetent-like"" cytokine expression profile in patients with adult T-cell leukemia lymphoma."
<b>Purpose:</b> Although expression of CD30 is reported in a subset of adult T-cell leukemia/lymphoma cases, its clinicopathologic significance is poorly understood.
Human T-cell leukemia virus type I oncoprotein Tax represses Smad-dependent transforming growth factor beta signaling through interaction with CREB-binding protein/p300.
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.
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.
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.
Human T cell leukemia virus type 1 (HTLV-1) causes two major diseases: adult T-cell leukemia-lymphoma and tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM).
Adult T-cell leukemia (ATL), which is abundant with Fas (Apo-1/CD95), has the characteristic feature of high tumor burden, suggesting that ATL cells probably prolong their lives as a result of escape from apoptosis.