Poly(I:C) increases the expression of mPGES-1 and COX-2 in rat primary microglia.
Belo Horizonte, Brazil. In J Neuroinflammation, Dec 2015
Protein levels of COX-2 and mPGES-1 were reduced by SB203580, SP600125, and SC514 (p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK), and IκB kinase (IKK) inhibitors, respectively), as well as by PD98059 and PD0325901 (mitogen-activated protein kinase kinase (MEK) inhibitors).
Low-grade epithelial ovarian cancer: a number of distinct clinical entities?
Edinburgh, United Kingdom. In Curr Opin Oncol, Sep 2015
A prospective study of the mitogen-activated protein kinase kinase inhibitor selumetinib (response rate 15%) and retrospective bevacizumab studies suggest that these may be more effective approaches.Limited retrospective clinical data and even more sparse molecular data suggest that similar distinctions may exist between low-grade endometrioid and mucinous ovarian cancers and their respective high-grade counterparts, but more research is required in order to clarify the biological differences and the implications that these have for management.
Long-term survival as a treatment benchmark in melanoma: latest results and clinical implications.
Salt Lake City, United States. In Ther Adv Med Oncol, May 2015
Fortunately, since the approval by the US Food and Drug Administration of agents targeting the cytotoxic T lymphocyte antigen-4 (CTLA-4) receptor, as well as those targeting B-raf and mitogen-activated protein kinase kinase (MEK) in the mitogen-activated protein kinase (MAPK) pathway for patients whose melanoma is 'driven' by a BRAF mutation, long-term survival of stage IV melanoma is increasing substantially.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma.
Boston, United States. In Nat Med, 2012
Here, leveraging an inducible mouse model of NRAS-mutant melanoma, we show that pharmacological inhibition of mitogen-activated protein kinase kinase (MEK) activates apoptosis but not cell-cycle arrest, which is in contrast to complete genetic neuroblastoma RAS homolog (NRAS) extinction, which triggers both of these effects.