DOI . ORG {
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Title[redir]:
Rationale for co-targeting IGF-1R and ALK in ALK fusion–positive lung cancer | Nature Medicine
Description:
Activation of the insulin-like growth factor 1 receptor may underlie clinical resistance to inhibition of the anaplastic lymphoma receptor kinase in lung cancer. Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising from the clinical observation of a patient with ALK fusion–positive lung cancer who had an exceptional response to an insulin-like growth factor 1 receptor (IGF-1R)-specific antibody, we define a therapeutic synergism between ALK and IGF-1R inhibitors. Similar to IGF-1R, ALK fusion proteins bind to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdown enhances the antitumor effects of ALK inhibitors. In models of ALK TKI resistance, the IGF-1R pathway is activated, and combined ALK and IGF-1R inhibition improves therapeutic efficacy. Consistent with this finding, the levels of IGF-1R and IRS-1 are increased in biopsy samples from patients progressing on crizotinib monotherapy. Collectively these data support a role for the IGF-1R–IRS-1 pathway in both ALK TKI–sensitive and ALK TKI–resistant states and provide a biological rationale for further clinical development of dual ALK and IGF-1R inhibitors.
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Keywords {🔍}
cancer, pubmed, article, google, scholar, alk, cas, lung, nature, central, department, data, resistance, usa, center, oncology, res, supported, igfr, inhibitors, cell, kinase, grant, medicine, chen, clinical, access, med, clin, hospital, university, cologne, york, content, receptor, sci, research, cookies, lovly, crizotinib, tyrosine, patients, cancers, gene, nonsmall, kölnbonn, germany, pathology, privacy, bos,
Topics {✒️}
nature portfolio permissions reprints sequence alignment/map format privacy policy prostate cancer research advertising nature index patient author information authors social media variable primary responses research excellence research hospital illumina bead-based data career development award small-cell lung cancer institutional subscriptions read research comprehensive mrna-based screen eu-framework programme curelung author correspondence alk-positive lung cancer dana-farber cancer institute alk-driven cancers revealed growth factor-ir pathway nonlinear mixed-effects modeling eml4-alk fusion oncogene fusion oncogene eml4-alk alk-rearranged lung cancers nucleolar protein gene alk tki–resistant states alk gene rearranged integrated oncology köln-bonn targeting igf-1r targeting oncogenic alk springerlink instant access permissions clinical development tumor-agnostic target igf-1r–irs-1 pathway tyrosine kinase fusions kinase gene genome sequencing data lung cancer grant targeting therapy european economic area therapeutic synergism harbor eml4-alk eml4-alk–positive victorian cancer biobank
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- ALK fusions in the pan-cancer setting: another tumor-agnostic target?
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headline:Rationale for co-targeting IGF-1R and ALK in ALK fusionâpositive lung cancer
description:Activation of the insulin-like growth factor 1 receptor may underlie clinical resistance to inhibition of the anaplastic lymphoma receptor kinase in lung cancer. Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising from the clinical observation of a patient with ALK fusionâpositive lung cancer who had an exceptional response to an insulin-like growth factor 1 receptor (IGF-1R)-specific antibody, we define a therapeutic synergism between ALK and IGF-1R inhibitors. Similar to IGF-1R, ALK fusion proteins bind to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdown enhances the antitumor effects of ALK inhibitors. In models of ALK TKI resistance, the IGF-1R pathway is activated, and combined ALK and IGF-1R inhibition improves therapeutic efficacy. Consistent with this finding, the levels of IGF-1R and IRS-1 are increased in biopsy samples from patients progressing on crizotinib monotherapy. Collectively these data support a role for the IGF-1RâIRS-1 pathway in both ALK TKIâsensitive and ALK TKIâresistant states and provide a biological rationale for further clinical development of dual ALK and IGF-1R inhibitors.
datePublished:2014-08-31T00:00:00Z
dateModified:2014-08-31T00:00:00Z
pageStart:1027
pageEnd:1034
sameAs:https://doi.org/10.1038/nm.3667
keywords:
Non-small-cell lung cancer
Biomedicine
general
Cancer Research
Metabolic Diseases
Infectious Diseases
Molecular Medicine
Neurosciences
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headline:Rationale for co-targeting IGF-1R and ALK in ALK fusionâpositive lung cancer
description:Activation of the insulin-like growth factor 1 receptor may underlie clinical resistance to inhibition of the anaplastic lymphoma receptor kinase in lung cancer. Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising from the clinical observation of a patient with ALK fusionâpositive lung cancer who had an exceptional response to an insulin-like growth factor 1 receptor (IGF-1R)-specific antibody, we define a therapeutic synergism between ALK and IGF-1R inhibitors. Similar to IGF-1R, ALK fusion proteins bind to the adaptor insulin receptor substrate 1 (IRS-1), and IRS-1 knockdown enhances the antitumor effects of ALK inhibitors. In models of ALK TKI resistance, the IGF-1R pathway is activated, and combined ALK and IGF-1R inhibition improves therapeutic efficacy. Consistent with this finding, the levels of IGF-1R and IRS-1 are increased in biopsy samples from patients progressing on crizotinib monotherapy. Collectively these data support a role for the IGF-1RâIRS-1 pathway in both ALK TKIâsensitive and ALK TKIâresistant states and provide a biological rationale for further clinical development of dual ALK and IGF-1R inhibitors.
datePublished:2014-08-31T00:00:00Z
dateModified:2014-08-31T00:00:00Z
pageStart:1027
pageEnd:1034
sameAs:https://doi.org/10.1038/nm.3667
keywords:
Non-small-cell lung cancer
Biomedicine
general
Cancer Research
Metabolic Diseases
Infectious Diseases
Molecular Medicine
Neurosciences
image:
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