Metastasis is the main cause for lethality of prostate cancer, because conventional therapies like surgery and hormone treatment rarely work in this *** cell migration, invasion, adhesion as well as angiogenesis are n...
Metastasis is the main cause for lethality of prostate cancer, because conventional therapies like surgery and hormone treatment rarely work in this *** cell migration, invasion, adhesion as well as angiogenesis are necessary processes for ***474 is a specific PI3K (phosphatidylinositol 3-kinase) inhibitor developed for solid tumor therapy, which is under clinical trial *** the present report, antimetastatic activities of ZSTK474 were investigated in vitro.
Stel B (Stellettin B) was isolated from marine sponge Jaspis *** vitro antitumor activities were investigated on 39 human cancer cell lines (JFCR39).Stel B exhibited highly potent inhibition against the growth of a hu...
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Stel B (Stellettin B) was isolated from marine sponge Jaspis *** vitro antitumor activities were investigated on 39 human cancer cell lines (JFCR39).Stel B exhibited highly potent inhibition against the growth of a human glioblastoma cell line SF295, with a GI50 of *** contrast, Stel B showed very weak inhibitory activity on normal cell lines including HMEC, RPTEC, NHBE and PrEC, with GI50s higher than 10M, suggesting its low *** then focused on the antitumor activity of this compound on SF295 cells.
As accumulating evidences suggest close involvement of phosphatidylinositol 3-kinase (PI3K) in cancer, novel PI3K inhibitors such as ZSTK474, GDC-0941,NVP-BEZ235 and BKM-120 have been developed for cancer therapy.A hi...
As accumulating evidences suggest close involvement of phosphatidylinositol 3-kinase (PI3K) in cancer, novel PI3K inhibitors such as ZSTK474, GDC-0941,NVP-BEZ235 and BKM-120 have been developed for cancer therapy.A high frequency ofhotspot mutations known as E542K, E545K and H1047R in the PIK3CA gene, which encodes the catalytic subunit of PI3K, has been found in various types of human *** hotspot PIK3CA mutations also lead to resistance to therapeutics targeting epidermal growth factor receptor (EGFR), further suggesting that inhibition of hotspot mutant PIK3CA be required for a PI3K inhibitor as anticancer drug.
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