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• W2014564738 endingPage "15" @default.
• W2014564738 startingPage "5" @default.
• W2014564738 abstract "Approximately 20 % of human breast cancers (BC) overexpress HER2 protein, and HER2-positivity is associated with a worse prognosis. Although HER2-targeted therapies have significantly improved outcomes for HER2-positive BC patients, resistance to trastuzumab-based therapy remains a clinical problem. In order to better understand resistance to HER2-targeted therapies in HER2-positive BC, it is necessary to examine HER family signalling as a whole. An extensive literature search was carried out to critically assess the current knowledge of HER family signalling in HER2-positive BC and response to HER2-targeted therapy. Known mechanisms of trastuzumab resistance include reduced receptor-antibody binding (MUC4, p95HER2), increased signalling through alternative HER family receptor tyrosine kinases (RTK), altered intracellular signalling involving loss of PTEN, reduced p27kip1, or increased PI3K/AKT activity and altered signalling via non-HER family RTKs such as IGF1R. Emerging strategies to circumvent resistance to HER2-targeted therapies in HER2-positive BC include co-targeting HER2/PI3K, pan-HER family inhibition, and novel therapies such as T-DM1. There is evidence that immunity plays a key role in the efficacy of HER-targeted therapy, and efforts are being made to exploit the immune system in order to improve the efficacy of current anti-HER therapies. With our rapidly expanding understanding of HER2 signalling mechanisms along with the repertoire of HER family and other targeted therapies, it is likely that the near future holds further dramatic improvements to the prognosis of women with HER2-positive BC." @default.
• W2014564738 created "2016-06-24" @default.
• W2014564738 creator A5011649305 @default.
• W2014564738 creator A5029977513 @default.
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• W2014564738 creator A5053110781 @default.
• W2014564738 creator A5066488338 @default.
• W2014564738 creator A5090856144 @default.
• W2014564738 date "2014-12-27" @default.
• W2014564738 modified "2023-10-18" @default.
• W2014564738 title "HER2-family signalling mechanisms, clinical implications and targeting in breast cancer" @default.
• W2014564738 cites W155933052 @default.
• W2014564738 cites W1597931794 @default.
• W2014564738 cites W1968590850 @default.
• W2014564738 cites W1971267920 @default.
• W2014564738 cites W1971738718 @default.
• W2014564738 cites W1978941237 @default.
• W2014564738 cites W1979563875 @default.
• W2014564738 cites W1982729445 @default.
• W2014564738 cites W1985620074 @default.
• W2014564738 cites W1992847318 @default.
• W2014564738 cites W1996539011 @default.
• W2014564738 cites W2003396164 @default.
• W2014564738 cites W2005448278 @default.
• W2014564738 cites W2008560339 @default.
• W2014564738 cites W2011435623 @default.
• W2014564738 cites W2014457594 @default.
• W2014564738 cites W2020372547 @default.
• W2014564738 cites W2023681515 @default.
• W2014564738 cites W2023685040 @default.
• W2014564738 cites W2023980114 @default.
• W2014564738 cites W2024651005 @default.
• W2014564738 cites W2039628288 @default.
• W2014564738 cites W2040142253 @default.
• W2014564738 cites W2043765412 @default.
• W2014564738 cites W2050216284 @default.
• W2014564738 cites W2051289826 @default.
• W2014564738 cites W2053600405 @default.
• W2014564738 cites W2063391304 @default.
• W2014564738 cites W2065545617 @default.
• W2014564738 cites W2065725840 @default.
• W2014564738 cites W2066368614 @default.
• W2014564738 cites W2066471812 @default.
• W2014564738 cites W2068326740 @default.
• W2014564738 cites W2069526613 @default.
• W2014564738 cites W2071786690 @default.
• W2014564738 cites W2075901113 @default.
• W2014564738 cites W2087861588 @default.
• W2014564738 cites W2088145034 @default.
• W2014564738 cites W2089288294 @default.
• W2014564738 cites W2092159470 @default.
• W2014564738 cites W2095659509 @default.
• W2014564738 cites W2095949683 @default.
• W2014564738 cites W2096283457 @default.
• W2014564738 cites W2096362504 @default.
• W2014564738 cites W2102148658 @default.
• W2014564738 cites W2103498669 @default.
• W2014564738 cites W2103808574 @default.
• W2014564738 cites W2104239861 @default.
• W2014564738 cites W2104289405 @default.
• W2014564738 cites W2105871790 @default.
• W2014564738 cites W2106036365 @default.
• W2014564738 cites W2107426197 @default.
• W2014564738 cites W2108070374 @default.
• W2014564738 cites W2112499354 @default.
• W2014564738 cites W2113170011 @default.
• W2014564738 cites W2114101532 @default.
• W2014564738 cites W2114195503 @default.
• W2014564738 cites W2115175735 @default.
• W2014564738 cites W2116424772 @default.
• W2014564738 cites W2117115931 @default.
• W2014564738 cites W2125239609 @default.
• W2014564738 cites W2125457274 @default.
• W2014564738 cites W2127735232 @default.
• W2014564738 cites W2132537022 @default.
• W2014564738 cites W2134878729 @default.
• W2014564738 cites W2136269815 @default.
• W2014564738 cites W2136775492 @default.
• W2014564738 cites W2139444209 @default.
• W2014564738 cites W2147641755 @default.
• W2014564738 cites W2148181778 @default.
• W2014564738 cites W2152811375 @default.
• W2014564738 cites W2154834163 @default.
• W2014564738 cites W2155794195 @default.
• W2014564738 cites W2157771579 @default.
• W2014564738 cites W2159967578 @default.
• W2014564738 cites W2164190676 @default.
• W2014564738 cites W2165404212 @default.
• W2014564738 cites W2168814163 @default.
• W2014564738 cites W2169430911 @default.
• W2014564738 cites W2169450835 @default.
• W2014564738 cites W2170241131 @default.
• W2014564738 cites W2171584014 @default.
• W2014564738 cites W2341945705 @default.
• W2014564738 cites W2591201173 @default.
• W2014564738 cites W3011091910 @default.
• W2014564738 cites W4234411800 @default.
• W2014564738 doi "https://doi.org/10.1007/s10549-014-3250-x" @default.

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