Abstract
Recently, epidermal growth factor receptor (EGFR) was a key molecule in investigation of lung cancer, and it was a target for a new therapeutic strategy, based on molecular analyses. In this review, we have summarized some issues considering the role of EGFR in lung cancer, its coding gene, and its promoter gene polymorphisms (SNPs) -216G/T and -191C/A in non-small-cell lung cancer (NSCLC). The position of the SNPs indicates their significant role in EGFR regulation. The accumulation of knowledge regarding SNPs lately suggests their significant and important role in the onset of carcinogenesis, the prediction of the onset of metastases, the response to therapy with TKI inhibitors, and the onset of toxic effects of the applied therapy. Based on this, we suggest further studies of the relationship of clinical significance to SNPs in patients with lung tumors.
Highlights
Epidermal growth factor receptor (EGFR) was a key molecule in investigation of lung cancer, and it was a target for a new therapeutic strategy, based on molecular analyses
We have summarized some issues considering the role of epidermal growth factor receptor (EGFR) in lung cancer, its coding gene, and its promoter gene polymorphisms (SNPs) -216G/T and -191C/A in non-small-cell lung cancer (NSCLC)
In NSCLC with overexpressed EGFR, the inhibition of the receptor signaling has been introduced as a targeted treatment, with tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib, rendered optimal in carriers of EGFR-activating mutations [21, 28, 29]
Summary
Many scientific reports referred to lung cancer as “the leading cause of death” worldwide [1,2,3,4,5,6]. Classical chemotherapy has been a major option for this type of tumor for many years, but the mortality remained high For this incurable disease, the hope seems to lie in preventive medicine, i.e., various education strategies about risk factors, introduction of new programs for early cancer screening and early diagnostics, and providing equal chances for proper treatment to all patients [6, 8]. The recent development of new techniques and methods has increased the knowledge of molecular mechanisms during carcinogenesis [13,14,15] These mechanisms, including increased gene amplification and protein expression, abnormal cell activation, allelic disbalance, and epigenetic mechanisms [13,14,15,16,17,18,19,20], might be just the top of the iceberg for all undiscovered interactions and signaling networks that are present in cancer cells. Studies in animal transgenic mice have shown that during carcinogenesis, one of the important molecules is epidermal growth factor receptor (EGFR) [13, 20]
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