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PubMed:25596284 JSONTXT

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sentences

Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-85 Sentence denotes ERBB3-independent activation of the PI3K pathway in EGFR-mutant lung adenocarcinomas.
TextSentencer_T2 86-260 Sentence denotes ERBB3, a member of the EGFR family of receptor tyrosine kinases, has been implicated in activation of the PI3K pathway in human lung adenocarcinomas driven by EGFR mutations.
TextSentencer_T3 261-465 Sentence denotes We investigated the contribution of ERBB3 to the initiation, progression, and therapeutic response of EGFR-induced lung adenocarcinomas using tetracycline- and tamoxifen-inducible transgenic mouse models.
TextSentencer_T4 466-623 Sentence denotes Deletion of Erbb3 at the time of induction of mutant EGFR had no effect on tumorigenesis, demonstrating that ERBB3 is not required to initiate tumorigenesis.
TextSentencer_T5 624-772 Sentence denotes Tumors that developed in the absence of ERBB3 remained sensitive to EGFR tyrosine kinase inhibitors and retained activation of the PI3K-AKT pathway.
TextSentencer_T6 773-882 Sentence denotes Interestingly, acute loss of Erbb3 suppressed further growth of established EGFR(L858R)-mediated lung tumors.
TextSentencer_T7 883-1141 Sentence denotes Four weeks after deletion of Erbb3, the tumors exhibited phosphorylation of EGFR, of the adaptor proteins GAB1 and GAB2, and of the downstream signaling molecules AKT and ERK, suggesting that alternative signaling pathways could compensate for loss of Erbb3.
TextSentencer_T8 1142-1335 Sentence denotes Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines.
TextSentencer_T9 1336-1606 Sentence denotes Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications.
T1 0-85 Sentence denotes ERBB3-independent activation of the PI3K pathway in EGFR-mutant lung adenocarcinomas.
T2 86-260 Sentence denotes ERBB3, a member of the EGFR family of receptor tyrosine kinases, has been implicated in activation of the PI3K pathway in human lung adenocarcinomas driven by EGFR mutations.
T3 261-465 Sentence denotes We investigated the contribution of ERBB3 to the initiation, progression, and therapeutic response of EGFR-induced lung adenocarcinomas using tetracycline- and tamoxifen-inducible transgenic mouse models.
T4 466-623 Sentence denotes Deletion of Erbb3 at the time of induction of mutant EGFR had no effect on tumorigenesis, demonstrating that ERBB3 is not required to initiate tumorigenesis.
T5 624-772 Sentence denotes Tumors that developed in the absence of ERBB3 remained sensitive to EGFR tyrosine kinase inhibitors and retained activation of the PI3K-AKT pathway.
T6 773-882 Sentence denotes Interestingly, acute loss of Erbb3 suppressed further growth of established EGFR(L858R)-mediated lung tumors.
T7 883-1141 Sentence denotes Four weeks after deletion of Erbb3, the tumors exhibited phosphorylation of EGFR, of the adaptor proteins GAB1 and GAB2, and of the downstream signaling molecules AKT and ERK, suggesting that alternative signaling pathways could compensate for loss of Erbb3.
T8 1142-1335 Sentence denotes Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines.
T9 1336-1606 Sentence denotes Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications.

DisGeNET5_variant_disease

Id Subject Object Predicate Lexical cue
25596284-5#81#86#geners121434568 854-859 geners121434568 denotes L858R
25596284-5#97#108#diseaseC0024121 870-881 diseaseC0024121 denotes lung tumors
81#86#geners12143456897#108#diseaseC0024121 25596284-5#81#86#geners121434568 25596284-5#97#108#diseaseC0024121 associated_with L858R,lung tumors

DisGeNET5_gene_disease

Id Subject Object Predicate Lexical cue
25596284-0#36#40#gene5290 755-759 gene5290 denotes PI3K
25596284-0#36#40#gene5291 755-759 gene5291 denotes PI3K
25596284-0#36#40#gene5293 755-759 gene5293 denotes PI3K
25596284-0#36#40#gene5294 755-759 gene5294 denotes PI3K
25596284-0#0#5#gene2065 297-302 gene2065 denotes ERBB3
25596284-0#52#56#gene1956 802-853 gene1956 denotes Erbb3 suppressed further growth of established EGFR
25596284-0#69#84#diseaseC0001418 1072-1605 diseaseC0001418 denotes at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications
25596284-0#69#84#diseaseC0001418 1072-1605 diseaseC0001418 denotes at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications
25596284-3#12#17#gene2065 478-483 gene2065 denotes Erbb3
25596284-3#53#57#gene1956 519-523 gene1956 denotes EGFR
25596284-3#109#114#gene2065 575-580 gene2065 denotes ERBB3
25596284-3#75#88#diseaseC0596263 541-554 diseaseC0596263 denotes tumorigenesis
25596284-3#143#156#diseaseC0596263 609-622 diseaseC0596263 denotes tumorigenesis
25596284-3#75#88#diseaseC0596263 541-554 diseaseC0596263 denotes tumorigenesis
25596284-3#143#156#diseaseC0596263 609-622 diseaseC0596263 denotes tumorigenesis
25596284-5#29#34#gene2065 802-807 gene2065 denotes Erbb3
25596284-5#76#80#gene1956 849-853 gene1956 denotes EGFR
25596284-5#97#108#diseaseC0024121 870-881 diseaseC0024121 denotes lung tumors
36#40#gene529069#84#diseaseC0001418 25596284-0#36#40#gene5290 25596284-0#69#84#diseaseC0001418 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
36#40#gene529069#84#diseaseC0001418 25596284-0#36#40#gene5290 25596284-0#69#84#diseaseC0001418 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
36#40#gene529169#84#diseaseC0001418 25596284-0#36#40#gene5291 25596284-0#69#84#diseaseC0001418 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
36#40#gene529169#84#diseaseC0001418 25596284-0#36#40#gene5291 25596284-0#69#84#diseaseC0001418 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
36#40#gene529369#84#diseaseC0001418 25596284-0#36#40#gene5293 25596284-0#69#84#diseaseC0001418 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
36#40#gene529369#84#diseaseC0001418 25596284-0#36#40#gene5293 25596284-0#69#84#diseaseC0001418 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
36#40#gene529469#84#diseaseC0001418 25596284-0#36#40#gene5294 25596284-0#69#84#diseaseC0001418 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
36#40#gene529469#84#diseaseC0001418 25596284-0#36#40#gene5294 25596284-0#69#84#diseaseC0001418 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
0#5#gene206569#84#diseaseC0001418 25596284-0#0#5#gene2065 25596284-0#69#84#diseaseC0001418 associated_with ERBB3,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
0#5#gene206569#84#diseaseC0001418 25596284-0#0#5#gene2065 25596284-0#69#84#diseaseC0001418 associated_with ERBB3,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
52#56#gene195669#84#diseaseC0001418 25596284-0#52#56#gene1956 25596284-0#69#84#diseaseC0001418 associated_with Erbb3 suppressed further growth of established EGFR,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
52#56#gene195669#84#diseaseC0001418 25596284-0#52#56#gene1956 25596284-0#69#84#diseaseC0001418 associated_with Erbb3 suppressed further growth of established EGFR,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
12#17#gene206575#88#diseaseC0596263 25596284-3#12#17#gene2065 25596284-3#75#88#diseaseC0596263 associated_with Erbb3,tumorigenesis
12#17#gene2065143#156#diseaseC0596263 25596284-3#12#17#gene2065 25596284-3#143#156#diseaseC0596263 associated_with Erbb3,tumorigenesis
12#17#gene206575#88#diseaseC0596263 25596284-3#12#17#gene2065 25596284-3#75#88#diseaseC0596263 associated_with Erbb3,tumorigenesis
12#17#gene2065143#156#diseaseC0596263 25596284-3#12#17#gene2065 25596284-3#143#156#diseaseC0596263 associated_with Erbb3,tumorigenesis
53#57#gene195675#88#diseaseC0596263 25596284-3#53#57#gene1956 25596284-3#75#88#diseaseC0596263 associated_with EGFR,tumorigenesis
53#57#gene1956143#156#diseaseC0596263 25596284-3#53#57#gene1956 25596284-3#143#156#diseaseC0596263 associated_with EGFR,tumorigenesis
53#57#gene195675#88#diseaseC0596263 25596284-3#53#57#gene1956 25596284-3#75#88#diseaseC0596263 associated_with EGFR,tumorigenesis
53#57#gene1956143#156#diseaseC0596263 25596284-3#53#57#gene1956 25596284-3#143#156#diseaseC0596263 associated_with EGFR,tumorigenesis
109#114#gene206575#88#diseaseC0596263 25596284-3#109#114#gene2065 25596284-3#75#88#diseaseC0596263 associated_with ERBB3,tumorigenesis
109#114#gene2065143#156#diseaseC0596263 25596284-3#109#114#gene2065 25596284-3#143#156#diseaseC0596263 associated_with ERBB3,tumorigenesis
109#114#gene206575#88#diseaseC0596263 25596284-3#109#114#gene2065 25596284-3#75#88#diseaseC0596263 associated_with ERBB3,tumorigenesis
109#114#gene2065143#156#diseaseC0596263 25596284-3#109#114#gene2065 25596284-3#143#156#diseaseC0596263 associated_with ERBB3,tumorigenesis
29#34#gene206597#108#diseaseC0024121 25596284-5#29#34#gene2065 25596284-5#97#108#diseaseC0024121 associated_with Erbb3,lung tumors
76#80#gene195697#108#diseaseC0024121 25596284-5#76#80#gene1956 25596284-5#97#108#diseaseC0024121 associated_with EGFR,lung tumors

DisGeNet-2017-sample

Id Subject Object Predicate Lexical cue
T966 755-759 gene:5290 denotes PI3K
T967 1072-1605 disease:C0001418 denotes at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications
R1 T966 T967 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
R2 T966 T967 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
R3 T966 T967 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"
R4 T966 T967 associated_with PI3K,"at alternative signaling pathways could compensate for loss of Erbb3. Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines. Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications"

UBERON-AE

Id Subject Object Predicate Lexical cue
PD-UBERON-AE-B_T1 64-68 http://purl.obolibrary.org/obo/UBERON_0002048 denotes lung
PD-UBERON-AE-B_T2 214-218 http://purl.obolibrary.org/obo/UBERON_0002048 denotes lung
PD-UBERON-AE-B_T3 376-380 http://purl.obolibrary.org/obo/UBERON_0002048 denotes lung
PD-UBERON-AE-B_T4 870-874 http://purl.obolibrary.org/obo/UBERON_0002048 denotes lung

performance-test

Id Subject Object Predicate Lexical cue
PD-UBERON-AE-B_T1 64-68 http://purl.obolibrary.org/obo/UBERON_0002048 denotes lung
PD-UBERON-AE-B_T2 214-218 http://purl.obolibrary.org/obo/UBERON_0002048 denotes lung
PD-UBERON-AE-B_T3 376-380 http://purl.obolibrary.org/obo/UBERON_0002048 denotes lung
PD-UBERON-AE-B_T4 870-874 http://purl.obolibrary.org/obo/UBERON_0002048 denotes lung