Research article summary (published 29 Jun 2009):

[Small-molecule tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR)]

Full Abstract

Five years have passed since the activating mutation of the epidermal growth factor receptor (EGFR) gene was discovered. Patients with lung cancer harboring EGFR mutation respond remarkably well to small molecules, such as gefitinib or erlotinib, that specifically inhibit tyrosine kinase of the EGFR. Furthermore, recent evidence leads strong support to the idea that EGFR-tyrosine kinase inhibitors prolong survival of lung cancer patients with EGFR mutation. It has been also shown that secondary mutation of the EGFR gene and amplification of the MET gene are responsible for acquired resistance that emerges in virtually all cases treated with EGFR-TKI. Strategies to circumvent this resistance is currently in development. It is possible to personalize lung cancer therapy using the genetic information.

Author information

Author/s: Mitsudomi, Tetsuya (T);

Affiliation: Department of Thoracic Surgery, Aichi Cancer Center Hospital, Chikusa-ku, Nagoya, Japan.

Journal and publication information

Publication Type: English Abstract; Journal Article; Review

Journal: Gan to kagaku ryoho. Cancer & chemotherapy (Gan To Kagaku Ryoho), published in Japan. (Language: jpn)

Reference: 2009-Jul; vol 36 (issue 7) : pp 1058-62

Dates: Created 2009/07/21; Completed 2009/08/20;

PMID: 19620791, status: MEDLINE (last retrieval date: 8/21/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Female Genes, erbB-1 - genetics Humans Lung Neoplasms - drug therapy

Male Mutation Protein-Tyrosine Kinases - antagonists & inhibitors Receptor, Epidermal Growth Factor - antagonists & inhibitors

Associated Chemicals: Protein-Tyrosine Kinases (EC 2.7.1.112) ; Receptor, Epidermal Growth Factor (EC 2.7.1.112)

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