FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4361946695> ?p ?o ?g. }

• W4361946695 abstract "<div>AbstractPurpose:<p>While <i>FGFR1</i> amplification has been described in breast cancer, the optimal treatment approach for <i>FGFR1</i>-amplified (FGFR1⁺) metastatic breast cancer (MBC) remains undefined.</p><p><b>Experimental Design:</b> We evaluated clinical response to endocrine and targeted therapies in a cohort of patients with hormone receptor–positive (HR⁺)/HER2⁻ MBC and validated the functional role of <i>FGFR1</i>-amplification in mediating response/resistance to hormone therapy <i>in vitro</i>.</p>Results:<p>In the clinical cohort (<i>N</i> = 110), we identified that patients with FGFR1⁺ tumors were more likely to have progesterone receptor (PR)-negative disease (47% vs. 20%; <i>P</i> = 0.005), coexisting <i>TP53</i> mutations (41% vs. 21%; <i>P</i> = 0.05), and exhibited shorter time to progression with endocrine therapy alone and in combination with CDK4/6 inhibitor, but not with a mTOR inhibitor (everolimus), adjusting for key prognostic variables in multivariate analysis. Furthermore, mTOR-based therapy resulted in a sustained radiological and molecular response in an index case of FGFR1⁺ HR⁺/HER2⁻ MBC. In preclinical models, estrogen receptor–positive (ER⁺)/<i>FGFR1</i>-amplified CAMA1 human breast cancer cells were only partially sensitive to fulvestrant, palbociclib, and alpelisib, but highly sensitive to everolimus. In addition, transduction of an FGFR1 expression vector into ER⁺ T47D cells induced resistance to fulvestrant that could be overcome by added TORC1 inhibition, but not PI3K or CDK4/6 inhibition.</p>Conclusions:<p>Collectively, these findings suggest that while <i>FGFR1</i> amplification confers broad resistance to ER, PI3K, and CDK4/6 inhibitors, mTOR inhibitors might have a unique therapeutic role in the treatment of patients with ER⁺/FGFR1⁺ MBC.</p></div>" @default.
• W4361946695 created "2023-04-05" @default.
• W4361946695 creator A5003417891 @default.
• W4361946695 creator A5010429902 @default.
• W4361946695 creator A5012686198 @default.
• W4361946695 creator A5014302041 @default.
• W4361946695 creator A5017550097 @default.
• W4361946695 creator A5018738915 @default.
• W4361946695 creator A5019054377 @default.
• W4361946695 creator A5025351031 @default.
• W4361946695 creator A5028403057 @default.
• W4361946695 creator A5034256147 @default.
• W4361946695 creator A5034972183 @default.
• W4361946695 creator A5039802529 @default.
• W4361946695 creator A5043946489 @default.
• W4361946695 creator A5051072215 @default.
• W4361946695 creator A5052735318 @default.
• W4361946695 creator A5056275493 @default.
• W4361946695 creator A5062479121 @default.
• W4361946695 creator A5087308492 @default.
• W4361946695 creator A5087584954 @default.
• W4361946695 date "2023-03-31" @default.
• W4361946695 modified "2023-09-30" @default.
• W4361946695 title "Data from <i>FGFR1</i> Amplification Mediates Endocrine Resistance but Retains TORC Sensitivity in Metastatic Hormone Receptor–Positive (HR⁺) Breast Cancer" @default.
• W4361946695 doi "https://doi.org/10.1158/1078-0432.c.6529178" @default.
• W4361946695 hasPublicationYear "2023" @default.
• W4361946695 type Work @default.
• W4361946695 citedByCount "0" @default.
• W4361946695 crossrefType "posted-content" @default.
• W4361946695 hasAuthorship W4361946695A5003417891 @default.
• W4361946695 hasAuthorship W4361946695A5010429902 @default.
• W4361946695 hasAuthorship W4361946695A5012686198 @default.
• W4361946695 hasAuthorship W4361946695A5014302041 @default.
• W4361946695 hasAuthorship W4361946695A5017550097 @default.
• W4361946695 hasAuthorship W4361946695A5018738915 @default.
• W4361946695 hasAuthorship W4361946695A5019054377 @default.
• W4361946695 hasAuthorship W4361946695A5025351031 @default.
• W4361946695 hasAuthorship W4361946695A5028403057 @default.
• W4361946695 hasAuthorship W4361946695A5034256147 @default.
• W4361946695 hasAuthorship W4361946695A5034972183 @default.
• W4361946695 hasAuthorship W4361946695A5039802529 @default.
• W4361946695 hasAuthorship W4361946695A5043946489 @default.
• W4361946695 hasAuthorship W4361946695A5051072215 @default.
• W4361946695 hasAuthorship W4361946695A5052735318 @default.
• W4361946695 hasAuthorship W4361946695A5056275493 @default.
• W4361946695 hasAuthorship W4361946695A5062479121 @default.
• W4361946695 hasAuthorship W4361946695A5087308492 @default.
• W4361946695 hasAuthorship W4361946695A5087584954 @default.
• W4361946695 hasConcept C121608353 @default.
• W4361946695 hasConcept C126322002 @default.
• W4361946695 hasConcept C134018914 @default.
• W4361946695 hasConcept C530470458 @default.
• W4361946695 hasConcept C71924100 @default.
• W4361946695 hasConceptScore W4361946695C121608353 @default.
• W4361946695 hasConceptScore W4361946695C126322002 @default.
• W4361946695 hasConceptScore W4361946695C134018914 @default.
• W4361946695 hasConceptScore W4361946695C530470458 @default.
• W4361946695 hasConceptScore W4361946695C71924100 @default.
• W4361946695 hasLocation W43619466951 @default.
• W4361946695 hasOpenAccess W4361946695 @default.
• W4361946695 hasPrimaryLocation W43619466951 @default.
• W4361946695 hasRelatedWork W1966504330 @default.
• W4361946695 hasRelatedWork W1966775726 @default.
• W4361946695 hasRelatedWork W1974041167 @default.
• W4361946695 hasRelatedWork W1979139803 @default.
• W4361946695 hasRelatedWork W2030889776 @default.
• W4361946695 hasRelatedWork W2037631372 @default.
• W4361946695 hasRelatedWork W2040058909 @default.
• W4361946695 hasRelatedWork W2132898409 @default.
• W4361946695 hasRelatedWork W2748952813 @default.
• W4361946695 hasRelatedWork W4249176446 @default.
• W4361946695 isParatext "false" @default.
• W4361946695 isRetracted "false" @default.
• W4361946695 workType "article" @default.