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RAF kinases are attractive cancer drug targets. Pre-clinical studies with cell lines and tumor xenographs bearing B-RAF mutations indicate that RAF kinase inhibitors are effective in decreasing cell proliferation. PLX4032, which has higher affinity for B-RAF than wild-type B-RAF, inhibits cancer progression in several animal models. The compound has demonstrated efficacy in Phase I clinical trials in the treatment of melanoma patients. Sorafenib has a lower affinity for B-RAF than C-RAF and is ineffective as monotherapy in the treatment of melanoma. RAF kinase inhibitor treatment of cancers with wild-type or activated mutant RAS co-expressed with wild-type B-RAF may be deleterious owing to up-regulation of RAF kinase signaling. Deciphering the mechanisms of RAS-RAF-MEK-ERK signaling continues to be an important and challenging task.

RAF kinases are attractive cancer drug targets. Pre-clinical studies with cell lines and tumor xenographs bearing B-RAF mutations indicate that RAF kinase inhibitors are effective in decreasing cell proliferation. PLX4032, which has higher affinity for B-RAF than wild-type B-RAF, inhibits cancer progression in several animal models. The compound has demonstrated efficacy in Phase I clinical<ref>PMID:20472680</ref> trials in the treatment of melanoma patients. Sorafenib has a lower affinity for B-RAF than C-RAF and is ineffective as monotherapy in the treatment of melanoma. RAF kinase inhibitor treatment of cancers with wild-type or activated mutant RAS co-expressed with wild-type B-RAF may be deleterious owing to up-regulation of RAF kinase signaling. Deciphering the mechanisms of RAS-RAF-MEK-ERK signaling continues to be an important and challenging task.

Sandbox Reserved 707: Difference between revisions

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Revision as of 18:36, 5 January 2013 view source Gilles A. Dupouy (talk \| contribs) 114 edits No edit summary ← Older edit		Revision as of 18:37, 5 January 2013 view source Gilles A. Dupouy (talk \| contribs) 114 edits No edit summary Newer edit →
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	RAF kinases are attractive cancer drug targets. Pre-clinical studies with cell lines and tumor xenographs bearing B-RAF mutations indicate that RAF kinase inhibitors are effective in decreasing cell proliferation. PLX4032, which has higher affinity for B-RAF than wild-type B-RAF, inhibits cancer progression in several animal models. The compound has demonstrated efficacy in Phase I clinical trials in the treatment of melanoma patients. Sorafenib has a lower affinity for B-RAF than C-RAF and is ineffective as monotherapy in the treatment of melanoma. RAF kinase inhibitor treatment of cancers with wild-type or activated mutant RAS co-expressed with wild-type B-RAF may be deleterious owing to up-regulation of RAF kinase signaling. Deciphering the mechanisms of RAS-RAF-MEK-ERK signaling continues to be an important and challenging task.		RAF kinases are attractive cancer drug targets. Pre-clinical studies with cell lines and tumor xenographs bearing B-RAF mutations indicate that RAF kinase inhibitors are effective in decreasing cell proliferation. PLX4032, which has higher affinity for B-RAF than wild-type B-RAF, inhibits cancer progression in several animal models. The compound has demonstrated efficacy in Phase I clinical<ref>PMID:20472680</ref> trials in the treatment of melanoma patients. Sorafenib has a lower affinity for B-RAF than C-RAF and is ineffective as monotherapy in the treatment of melanoma. RAF kinase inhibitor treatment of cancers with wild-type or activated mutant RAS co-expressed with wild-type B-RAF may be deleterious owing to up-regulation of RAF kinase signaling. Deciphering the mechanisms of RAS-RAF-MEK-ERK signaling continues to be an important and challenging task.