IMR Press / FBL / Volume 16 / Issue 5 / DOI: 10.2741/3815

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Kinase-driven pathways of EGFR in lung carcinomas: perspectives on targeting therapy
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1 Department of Pathology, Saitama Medical Center, Jichi Medical University, Saitama, Japan
2 Department of Pulmonary Medicine, Saitama Medical Center, Jichi Medical University, Saitama, Japan 1-847 Amanuma, Omiya, Saitama Saitama 330-8503 Japan
3 Department of Thoracic Surgery, Saitama Medical Center, Jichi Medical University, Saitama, Japan 1-847 Amanuma, Omiya, Saitama Saitama 330-8503 Japan

Academic Editor: Yoh Dobashi

Front. Biosci. (Landmark Ed) 2011, 16(5), 1714–1732; https://doi.org/10.2741/3815
Published: 1 January 2011
Abstract

Despite remarkable advances in oncology medicine, the prognosis of lung cancer patients has not greatly improved over the past few decades. To overcome the current limit, new classes of agents that specifically target particular cascades have been developed. Gefitinib and erlotinib, which are tyrosine kinase inhibitors specific for the epidermal growth factor receptor (EGFR), have provided hope for better survival. The relationship between the sensitivity to gefitinib and the tumors' EGFR mutations have allowed the selective and accelerated use of these therapies. However, their efficacy is still limited, predominantly due to side effects and drug resistance. Further development of rational clinical strategies will require greater clarification of the key signaling factors downstream of EGFR which are potential targets for cancer therapies. In this review, we describe the various observed abnormalities in EGFR, the mechanisms of activation of several critical signaling cascades in lung cancer. Summarizing the data gleaned from preclinical, and clinicopathological aspects, we discuss the molecular mechanisms that may underlie a possible successful response to the blockade of EGFR and/or its downstream signaling.

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