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The impact of epidermal-growth-factor-receptor mutations in response to lung-cancer therapy

Nature Clinical Practice Oncology volume 1, pages 2–3 (2004)Cite this article

Non-small-cell lung cancer (NSCLC) is the leading cause of cancer death in the US. Despite treatment advances in the past decade, most NSCLC patients still die from this disease. During this time, understanding of the biology of NSCLC has increased and rational molecular targets for therapeutic approaches have been discovered. One target extensively studied is the epidermal-growth-factor receptor (EGFR). In lung cancers, EGFR is frequently overexpressed, and activation of EGFR in cancer cells leads to several downstream signaling effects that regulate proliferation, invasion, metastasis and apoptosis. A large number of clinical trials have tested drugs that inhibit EGFR.

Particular attention has focused on EGFR-specific tyrosine kinase inhibitors (TKIs) in lung and other cancers, and these have shown clinical benefit in a subset of patients with occasional dramatic responses. Two reports galvanized the translational research community by showing that lung-cancer patients who responded to the TKI gefitinib had EGFR mutations.1,2 These findings sparked an exciting meeting within 2 months of their initial publication, sponsored by the International Association for the Study of Lung Cancer (IASLC). Groups from around the world presented new work supporting these findings.

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Acknowledgements

Grant Support: Lung Cancer SPORE P50CA70907

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Authors and Affiliations

  1. Director of Hamon Center for Therapeutic Oncology Research and a Professor in the Departments of Internal Medicine and Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX, USA

    John D Minna

  2. Chief of Hematology and Oncology at the Dallas Veterans Affairs Medical Center, TX, USA

    Jonathan E Dowell

Authors
  1. Jonathan E Dowell
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  2. John D Minna
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Correspondence to John D Minna.

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Competing interests

Jonathan E Dowell declared that he has financial interests that include consulting fees for Celgene, GlaxoSmithKline, and Aventis.

John D Minna declared that he has financial interests that include unrestricted research grant from Bristol Myers Squibb; consulting fees for Eli Lilly, Celera; clinical trial research support from AstraZeneca to the National Cancer Institute, US.

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Dowell, J., Minna, J. The impact of epidermal-growth-factor-receptor mutations in response to lung-cancer therapy. Nat Rev Clin Oncol 1, 2–3 (2004). https://doi.org/10.1038/ncponc0007

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