Dysregulation of EGFR in Lung Cancer

From early studies into EGFR function, and the identification of ErbB transforming genes in the avian erythroblastosis virus, there was a clear consensus that aberrant EGFR activity likely contributes to the etiology of a large subset of cancers (1). Focusing on lung cancer in particular, there had been early suggestions that abnormal EGFR gene regulation was a common phenomenon in non-small cell lung cancer (NSCLC), with approximately 50% of such cancers exhibiting EGFR over-expression at the protein level (35,36), with more recent studies placing the number at around 62% (37). In addition, frequent amplifications of the chromosomal 7p12 region, in which the EGFR locus is contained, had been documented (38).

The clinical outlook for lung cancer is bleak. Worldwide, deaths due to the disease account for a third of all cancer-related deaths, making it the deadliest of all cancers. Lung cancer encompasses a number of diseases of diverse histological subtypes, the etiologies of which are somewhat varied. There are two broad classifications; small cell lung cancer (SCLC), representing only 20% of all cases and non-small cell lung cancer (NSCLC), which accounts for the remaining 80% (39).

NSCLC originates from the lung epithelia and can be further divided based on histology into adenocarcinoma, bronchoalveolar, squamous, anaplastic, and large cell carcinoma. Most patients present with advanced metastatic disease, with a median survival after diagnosis of 4-5 months, if no treatment is given (40). Combination chemotherapy is often administered with very limited efficacy, providing limited overall survival benefit to patients. The need for targeted therapeutics against specific oncogenic determinants, such as EGFR, has been clearly apparent.

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