Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Gefitinib

Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_2354-6

Definition

Gefitinib (Iressa) is an anticancer drug against epidermal growth factor receptor (EGFR) on cancer cells, which combines with the receptor (EGFR) and blocks survival signaling through the receptor in target cancer cells, resulting in cancer cell death.

Characteristics

Gefitinib in Cancer Therapy

Gefitinib Sensitivity

Although the target of gefitinib, EGFR, is widely expressed by epidermal cancer, e.g., cancers of lung, colorectal, breast, prostate, and skin, and other cancer types, e.g., cancers from bone, cartilage, fiber, muscle, fat, nerve, and blood vessels, etc., its action is limited. However, cancers with mutated EGFR tyrosine kinase (TK) gene or overactive EGFR are more sensitized to gefitinib, and it becomes very effective.

Mechanism of Action

Gefitinib selectively inhibits the EGFR tyrosine kinase domain by binding to the intracellular adenosine triphosphate (ATP)-binding site of the enzyme and blocks EGFR signaling. EGFR is a family of receptors which includes...

Keywords

Epidermal Growth Factor Receptor Epidermal Growth Factor Receptor Mutation Epidermal Growth Factor Receptor Gene Epidermal Growth Factor Receptor Signaling Epidermal Growth Factor Receptor Tyrosine Kinase 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

  1. Kim SM, Kwon OJ, Hong YK et al (2012) Activation of IL-6R/JAK1/STAT3 signaling induces de novo resistance to irreversible EGFR inhibitors in non–small cell lung cancer with T790M resistance mutation. Mol Cancer Ther 11:2254–2264CrossRefPubMedGoogle Scholar
  2. Ramalingam SS, Blackhall F, Krzakowski M et al (2012) Randomized phase II study of dacomitinib (PF-00299804), an irreversible pan-human epidermal growth factor receptor inhibitor, versus erlotinib in patients with advanced non-small-cell lung cancer. J Clin Oncol 30:3337–3344CrossRefPubMedGoogle Scholar
  3. Sen M, Joyce S, Panahandeh M, Li C, Thomas SM, Maxwell J, Wang L, Gooding WE, Johnson DE, Grandis JR (2012) Targeting Stat3 abrogates EGFR inhibitor resistance in cancer. Clin Cancer Res 18:4986–4996PubMedCentralCrossRefPubMedGoogle Scholar
  4. Wang D, Boerner SA, Winkler JD, LoRusso PM (2007) Clinical experience of MEK inhibitors in cancer therapy. Biochim Biophys Acta 1773:1248–1255CrossRefPubMedGoogle Scholar
  5. Wang X, Goldstein D, Crowe PJ, Yang JL (2013) S3I-201, a novel STAT3 inhibitor, inhibits growth of human soft tissue sarcoma cell lines. World J Cancer Res 1:61–68Google Scholar

See Also

  1. (2012) Phosphatidylinositol-3,4,5-trisphosphate. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 2866. doi: 10.1007/978-3-642-16483-5_4528Google Scholar
  2. (2012) Serine/Threonine Kinase. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 3384. doi: 10.1007/978-3-642-16483-5_5258Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2014

Authors and Affiliations

  1. 1.Adult Cancer Program, Lowy Cancer Research Centre, Prince of Wales Clinical School, Faculty of MedicineUniversity of New South WalesSydneyAustralia