Cited 101 times in
Next-generation epidermal growth factor receptor tyrosine kinase inhibitors in epidermal growth factor receptor -mutant non-small cell lung cancer
DC Field | Value | Language |
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dc.contributor.author | 조병철 | - |
dc.date.accessioned | 2017-02-24T07:41:04Z | - |
dc.date.available | 2017-02-24T07:41:04Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 0169-5002 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/146488 | - |
dc.description.abstract | Since the discovery of sensitizing EGFR mutations as a predictive marker of sensitivity to EGFR tyrosine kinase inhibitors (TKIs), the field of targeted therapy in non-small cell lung cancer (NSCLC) has been revolutionized. Patients harbouring these sensitizing mutations treated with EGFR TKI have derived significant clinical outcome when compared with standard platinum based chemotherapy doublets. However disease progression invariably occurs at a median of about 9-13 months from initiation treatment, if acquired resistance commonly due to the development of EGFR T790M mutation. A novel class of "third generation" EGFR TKIs have been developed that is sensitising and T790M mutant-specific whilst sparing WT EGFR, representing a significant breakthrough in the treatment in NSCLC patients with acquired resistance harboring these genotypes. Early phase clinical data suggest the third generation EGFR TKIs such as osimertinib, rociletinib, and HM61713 are highly efficacious and well tolerated. Another promising class of EGFR TKI such as AZD3759 has been designed to penetrate blood brain barrier to treat brain metastases and leptomeningeal disease and has showed promising responses in patients with brain metastases. Acquired resistance to third generation EGFR TKIs has been reported including EGFR C797S. Given its non-invasive nature, plasma ctDNA is being explored as a possible approach to detect T790M mutation and to also inform on novel molecular mechansims of tertiary resistance to third generation EGFR TKIs. An understanding of the mechanisms of acquired resistance to the third-generation EGFR TKIs will greatly aid in the development of the next generation of EGFR TKIs. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.format.extent | 59~68 | - |
dc.language | English | - |
dc.publisher | Elsevier Scientific Publishers | - |
dc.relation.isPartOf | LUNG CANCER | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Antineoplastic Agents/pharmacology | - |
dc.subject.MESH | Antineoplastic Agents/therapeutic use* | - |
dc.subject.MESH | Antineoplastic Combined Chemotherapy Protocols/therapeutic use | - |
dc.subject.MESH | Blood-Brain Barrier/drug effects | - |
dc.subject.MESH | Blood-Brain Barrier/metabolism | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/drug therapy* | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/genetics* | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/mortality | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/pathology | - |
dc.subject.MESH | Clinical Trials as Topic | - |
dc.subject.MESH | Drug Discovery | - |
dc.subject.MESH | Drug Evaluation, Preclinical | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Lung Neoplasms/drug therapy* | - |
dc.subject.MESH | Lung Neoplasms/genetics* | - |
dc.subject.MESH | Lung Neoplasms/mortality | - |
dc.subject.MESH | Lung Neoplasms/pathology | - |
dc.subject.MESH | Molecular Targeted Therapy | - |
dc.subject.MESH | Mutation* | - |
dc.subject.MESH | Protein Kinase Inhibitors/pharmacology | - |
dc.subject.MESH | Protein Kinase Inhibitors/therapeutic use* | - |
dc.subject.MESH | Receptor, Epidermal Growth Factor/antagonists & inhibitors | - |
dc.subject.MESH | Receptor, Epidermal Growth Factor/genetics* | - |
dc.subject.MESH | Treatment Outcome | - |
dc.title | Next-generation epidermal growth factor receptor tyrosine kinase inhibitors in epidermal growth factor receptor -mutant non-small cell lung cancer | - |
dc.type | Article | - |
dc.publisher.location | Ireland | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Internal Medicine | - |
dc.contributor.googleauthor | Chee-Seng Tan | - |
dc.contributor.googleauthor | Byoung-Chul Cho | - |
dc.contributor.googleauthor | Ross A. Soo | - |
dc.identifier.doi | 10.1016/j.lungcan.2016.01.003 | - |
dc.contributor.localId | A03822 | - |
dc.relation.journalcode | J02174 | - |
dc.identifier.eissn | 1872-8332 | - |
dc.identifier.pmid | 26898616 | - |
dc.identifier.url | http://www.sciencedirect.com/science/article/pii/S0169500216300034 | - |
dc.subject.keyword | Epidermal growth factor receptor mutations | - |
dc.subject.keyword | HM61713 | - |
dc.subject.keyword | Non-small cell lung cancer | - |
dc.subject.keyword | Osimertinib | - |
dc.subject.keyword | Rociletinib | - |
dc.subject.keyword | Tyrosine kinase inhibitor | - |
dc.contributor.alternativeName | Cho, Byoung Chul | - |
dc.contributor.affiliatedAuthor | Cho, Byoung Chul | - |
dc.citation.volume | 93 | - |
dc.citation.startPage | 59 | - |
dc.citation.endPage | 68 | - |
dc.identifier.bibliographicCitation | LUNG CANCER, Vol.93 : 59-68, 2016 | - |
dc.date.modified | 2017-02-24 | - |
dc.identifier.rimsid | 45128 | - |
dc.type.rims | ART | - |
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