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Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-88 Sentence denotes Inductive mechanisms limiting response to anti-epidermal growth factor receptor therapy.
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.
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.
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.
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.
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.
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.
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.
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.