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Most endocrine cancers are highly dependent on growth factor receptor activation. However, their overexpression of the downstream target, phospho-p70S6K (pp70S6K), a major player of mTOR, presents a barrier to the development of potent mTOR-directed therapeutic regimens against these tumors. Here we show that targeting FGFR2, and its downstream signaling components, effectively inhibits all four subtypes of endocrine cancers (thyroid, prostate, endometrial and pancreatic), a finding that is not dependent on the co-expression of FGFR2 and pp70S6K. FGFR2 inhibition leads to a marked reduction in HSP70, a chaperone essential for HSP90 stability and function, and significantly impairs the function of the HSP90 chaperone machinery, resulting in a marked reduction in the expression of multiple oncogenic signaling proteins and in the growth of the endocrine cancers. Indeed, treatment with FGFR inhibitor AZ3146 effectively blocks the proliferation of endocrine cancers with little to no cytotoxicity to normal cells. Importantly, the combination of the HSP90 inhibitor 17-AAG and FGFR inhibitor AZ3146 has an inhibitory effect on the growth of endocrine cancers that is even more effective than 17-AAG alone.Comparison of the transport behavior of body surface area-normalized aminoglycoside doses in critically ill patients.
Aminoglycosides are frequently used in critically ill patients. Recommendations are available on the optimal dosing of aminoglycosides; however, there is little evidence in the literature for the transport and pharmacokinetics of large total aminoglycoside doses. The objective was to assess the comparative pharmacokinetics of different dose-normalized aminoglycoside regimens to determine a relationship between the pharmacokinetics of the aminoglycoside and the body surface area. A prospective observational study. A 12-bed critical care unit in a teaching hospital. Twenty-six critically ill patients on continuous renal replacement therapy or undergoing intermittent hemod


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