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PubMed:18199556 JSONTXT 8 Projects

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Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-141 Sentence denotes Inhibition of Hsp90 down-regulates mutant epidermal growth factor receptor (EGFR) expression and sensitizes EGFR mutant tumors to paclitaxel.
T1 0-141 Sentence denotes Inhibition of Hsp90 down-regulates mutant epidermal growth factor receptor (EGFR) expression and sensitizes EGFR mutant tumors to paclitaxel.
TextSentencer_T2 142-340 Sentence denotes Mutations in the kinase domain of the epidermal growth factor receptor (EGFR) are found in a subset of patients with lung cancer and correlate with response to EGFR tyrosine kinase inhibitors (TKI).
T2 142-340 Sentence denotes Mutations in the kinase domain of the epidermal growth factor receptor (EGFR) are found in a subset of patients with lung cancer and correlate with response to EGFR tyrosine kinase inhibitors (TKI).
TextSentencer_T3 341-460 Sentence denotes Resistance to these agents invariably develops, and current treatment strategies have limited efficacy in this setting.
T3 341-460 Sentence denotes Resistance to these agents invariably develops, and current treatment strategies have limited efficacy in this setting.
TextSentencer_T4 461-679 Sentence denotes Hsp90 inhibitors, such as 17-allylamino-17-demethoxygeldanamycin (17-AAG), induce the degradation of EGFR and other Hsp90 interacting proteins and may thus have utility in tumors dependent upon sensitive Hsp90 clients.
T4 461-679 Sentence denotes Hsp90 inhibitors, such as 17-allylamino-17-demethoxygeldanamycin (17-AAG), induce the degradation of EGFR and other Hsp90 interacting proteins and may thus have utility in tumors dependent upon sensitive Hsp90 clients.
TextSentencer_T5 680-826 Sentence denotes We find that the EGFR mutations found most commonly in patients with lung adenocarcinoma who respond to EGFR TKIs are potently degraded by 17-AAG.
T5 680-826 Sentence denotes We find that the EGFR mutations found most commonly in patients with lung adenocarcinoma who respond to EGFR TKIs are potently degraded by 17-AAG.
TextSentencer_T6 827-998 Sentence denotes Although the expression of wild-type EGFR was also down-regulated by 17-AAG, its degradation required higher concentrations of drug and a longer duration of drug exposure.
T6 827-998 Sentence denotes Although the expression of wild-type EGFR was also down-regulated by 17-AAG, its degradation required higher concentrations of drug and a longer duration of drug exposure.
TextSentencer_T7 999-1126 Sentence denotes In animal models, a single dose of 17-AAG was sufficient to induce degradation of mutant EGFR and inhibit downstream signaling.
T7 999-1126 Sentence denotes In animal models, a single dose of 17-AAG was sufficient to induce degradation of mutant EGFR and inhibit downstream signaling.
TextSentencer_T8 1127-1293 Sentence denotes 17-AAG treatment, at its maximal tolerated dose, caused a significant delay in H3255 (L858R EGFR) xenograft growth but was less effective than the EGFR TKI gefitinib.
T8 1127-1293 Sentence denotes 17-AAG treatment, at its maximal tolerated dose, caused a significant delay in H3255 (L858R EGFR) xenograft growth but was less effective than the EGFR TKI gefitinib.
TextSentencer_T9 1294-1477 Sentence denotes 17-AAG alone delayed, but did not completely inhibit, the growth of H1650 and H1975 xenografts, two EGFR mutant models which show intermediate and high levels of gefitinib resistance.
T9 1294-1477 Sentence denotes 17-AAG alone delayed, but did not completely inhibit, the growth of H1650 and H1975 xenografts, two EGFR mutant models which show intermediate and high levels of gefitinib resistance.
TextSentencer_T10 1478-1609 Sentence denotes 17-AAG could be safely coadministered with paclitaxel, and the combination was significantly more effective than either drug alone.
T10 1478-1609 Sentence denotes 17-AAG could be safely coadministered with paclitaxel, and the combination was significantly more effective than either drug alone.
TextSentencer_T11 1610-1860 Sentence denotes These data suggest that Hsp90 inhibition in combination with chemotherapy may represent an effective treatment strategy for patients whose tumors express EGFR kinase domain mutations, including those with de novo and acquired resistance to EGFR TKIs.
T11 1610-1860 Sentence denotes These data suggest that Hsp90 inhibition in combination with chemotherapy may represent an effective treatment strategy for patients whose tumors express EGFR kinase domain mutations, including those with de novo and acquired resistance to EGFR TKIs.