Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A phase II study of vindesine in 41 evaluable patients demonstrated the drug to be active in heavily pretreated patients with breast cancer, non-Hodgkin's lymphoma, and other tumors. There were two partial responses in 11 patients with breast cancer (18%) and five partial responses and one complete response in 11 patients with non-Hodgkin's lymphoma (40%). Other responses were seen in small cell carcinoma of the lung, ovarian carcinoma, and Hodgkin's disease. Prior vinca exposure did not adversely affect the response rate. Neutropenia was dose-limiting. Neurotoxic effects occurred in 10% of the patients. A high incidence of local tissue reactions at the injection site (27%) could be reduced by a careful administration technique. Vindesine should be studied further in combination with other agents.
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PMID:Phase II trial of vindesine in the treatment of lymphomas, breast cancer, and other solid tumors. 744 18

Primary effusion lymphoma (PEL) is defined as a rare subtype of non-Hodgkin's B-cell lymphoma which is caused by Kaposi's sarcoma-associated herpesvirus (KSHV) in immunosuppressed patients. PEL is an aggressive lymphoma and is frequently resistant to conventional chemotherapies. Therefore, it is critical to investigate novel therapeutic options for PEL. Capsaicin is a pungent component of chili pepper and possesses unique pharmacological effects, such as pain relief, anti-microbial and anti-cancer properties. Here, we demonstrate that capsaicin markedly inhibited the growth of KSHV latently infected PEL cells by inhibiting ERK, p38 MAPK and expression hIL-6, which are known to contribute to PEL growth and survival. The underlying mechanism of action by capsaicin was through the inhibition of ERK and p38 MAPK phosphorylation and signaling that affected hIL-6 expression. As a result, capsaicin induced apoptosis in PEL cells in a caspase-9 dependent manner. In line with these results, ERK (U0126) and p38 MAPK (SB203580) specific signaling inhibitors suppressed hIL-6 expression and attenuated cell growth in PEL cells. Furthermore, the addition of hIL-6 neutralizing antibody to culture medium suppressed the growth of PEL cells. We also demonstrate that capsaicin suppressed PEL cell growth in the absence of nascent viral replication. Finally, we confirmed ex vivo treatment of capsaicin attenuated PEL development in SCID mice. Taken together, capsaicin could represent a lead compound for PEL therapy without the risk of de novo KSHV infection.
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PMID:Capsaicin Induces Apoptosis in KSHV-Positive Primary Effusion Lymphoma by Suppressing ERK and p38 MAPK Signaling and IL-6 Expression. 3083 76