> top > docs > PubMed:17259562 > annotations

PubMed:17259562 JSONTXT

Annnotations TAB JSON ListView MergeView

DisGeNET

Id Subject Object Predicate Lexical cue
T0 98-130 gene:1956 denotes epidermal growth factor receptor
T1 186-198 disease:C0006826 denotes malignancies
R1 T0 T1 associated_with epidermal growth factor receptor,malignancies

PubmedHPO

Id Subject Object Predicate Lexical cue
T1 243-249 HP_0002664 denotes tumour
T2 1094-1107 HP_0003002 denotes breast cancer
T3 1094-1107 HP_0100013 denotes breast cancer
T4 1101-1107 HP_0002664 denotes cancer
T5 1160-1166 HP_0002664 denotes cancer
T6 1406-1412 HP_0002664 denotes tumour

DisGeNET5_gene_disease

Id Subject Object Predicate Lexical cue
17259562-5#181#185#gene1956 1054-1058 gene1956 denotes EGFR
17259562-5#221#234#diseaseC0006142 1094-1107 diseaseC0006142 denotes breast cancer
17259562-5#221#234#diseaseC0678222 1094-1107 diseaseC0678222 denotes breast cancer
181#185#gene1956221#234#diseaseC0006142 17259562-5#181#185#gene1956 17259562-5#221#234#diseaseC0006142 associated_with EGFR,breast cancer
181#185#gene1956221#234#diseaseC0678222 17259562-5#181#185#gene1956 17259562-5#221#234#diseaseC0678222 associated_with EGFR,breast cancer

DisGeNet-2017-sample

Id Subject Object Predicate Lexical cue
T325 1054-1058 gene:1956 denotes EGFR
T326 1094-1107 disease:C0006142 denotes breast cancer
R1 T325 T326 associated_with EGFR,breast cancer
R2 T325 T326 associated_with EGFR,breast cancer

sentences

Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-88 Sentence denotes Inductive mechanisms limiting response to anti-epidermal growth factor receptor therapy.
TextSentencer_T2 89-363 Sentence denotes Aberrant epidermal growth factor receptor (EGFR) signalling, a key feature of a variety of human malignancies, can drive a range of mechanisms underlying tumour growth and progression, including increased cell proliferation, angiogenesis, metastasis and decreased apoptosis.
TextSentencer_T3 364-545 Sentence denotes Anti-EGFR therapies, as monotherapies and in combination with chemotherapy, have proved effective in inhibiting these processes both in the clinical and in the preclinical settings.
TextSentencer_T4 546-735 Sentence denotes However, only a small cohort of patients have derived significant benefit from this therapy, with both de novo and acquired resistance to these agents evident in a number of recent studies.
TextSentencer_T5 736-872 Sentence denotes If we are to improve the effectiveness of such targeted therapies, then there is an urgent need to understand the resistance mechanisms.
TextSentencer_T6 873-1173 Sentence denotes Here, we describe both non-genomic and genomic mechanisms of resistance to the selective EGFR tyrosine kinase inhibitor gefitinib (IRESSA), which we have identified initially in an EGFR-positive tamoxifen-resistant MCF-7 breast cancer cell line, but more recently in other EGFR-positive cancer types.
TextSentencer_T7 1174-1508 Sentence denotes Importantly, we show that gefitinib, in common with anti-hormonal agents, is not a passive bystander in the cellular response to drug treatment, but plays an active role in promoting signalling pathways that serve to limit its anti-tumour activity and maintain the cellular cohort from which acquired resistance can ultimately evolve.
TextSentencer_T8 1509-1800 Sentence denotes These findings indicate that inductive signalling is an important determinant of response to EGFR-targeted therapies and deciphering such pathways may provide us with the opportunity to design more effective strategies to combat resistance mechanisms and improve response to initial therapy.
T1 0-88 Sentence denotes Inductive mechanisms limiting response to anti-epidermal growth factor receptor therapy.
T2 89-363 Sentence denotes Aberrant epidermal growth factor receptor (EGFR) signalling, a key feature of a variety of human malignancies, can drive a range of mechanisms underlying tumour growth and progression, including increased cell proliferation, angiogenesis, metastasis and decreased apoptosis.
T3 364-545 Sentence denotes Anti-EGFR therapies, as monotherapies and in combination with chemotherapy, have proved effective in inhibiting these processes both in the clinical and in the preclinical settings.
T4 546-735 Sentence denotes However, only a small cohort of patients have derived significant benefit from this therapy, with both de novo and acquired resistance to these agents evident in a number of recent studies.
T5 736-872 Sentence denotes If we are to improve the effectiveness of such targeted therapies, then there is an urgent need to understand the resistance mechanisms.
T6 873-1173 Sentence denotes Here, we describe both non-genomic and genomic mechanisms of resistance to the selective EGFR tyrosine kinase inhibitor gefitinib (IRESSA), which we have identified initially in an EGFR-positive tamoxifen-resistant MCF-7 breast cancer cell line, but more recently in other EGFR-positive cancer types.
T7 1174-1508 Sentence denotes Importantly, we show that gefitinib, in common with anti-hormonal agents, is not a passive bystander in the cellular response to drug treatment, but plays an active role in promoting signalling pathways that serve to limit its anti-tumour activity and maintain the cellular cohort from which acquired resistance can ultimately evolve.
T8 1509-1800 Sentence denotes These findings indicate that inductive signalling is an important determinant of response to EGFR-targeted therapies and deciphering such pathways may provide us with the opportunity to design more effective strategies to combat resistance mechanisms and improve response to initial therapy.

UBERON-AE

Id Subject Object Predicate Lexical cue
PD-UBERON-AE-B_T1 1094-1100 http://purl.obolibrary.org/obo/UBERON_0000310 denotes breast

performance-test

Id Subject Object Predicate Lexical cue
PD-UBERON-AE-B_T1 1094-1100 http://purl.obolibrary.org/obo/UBERON_0000310 denotes breast