Aims:The primary objective of this study was to estimate the clinicopathological and molecular profile of lung cancer patients along with the evaluation of their clinical characteristics at a tertiary care hospital in Northern India.Subjects and Methods:A total of 421 patients with lung cancer histology who were treated at Max Super Speciality Hospitals were included in the study. The study protocol conforms to the ethical guidelines of the 1975 Declaration of Helsinki and permission was obtained from the Ethics Committee before the start of the study. Clinical characteristics and molecular profiling data were collected from the patient's medical records.Results:There were 330 (78.4%) men and 91 (21.6%) women with a median age of 62 years (range: 30–93 years). Of the 421 patients, 388 (92.2%) patients had the nonsmall cell lung cancer (NSCLC) histology whereas 33 (7.8%) patients were of SCLC histology. Histology and gender had a significant association with NSCLC and SCLC (P < 0.05). Epidermal growth factor receptor (EGFR) and echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase (EML4-ALK) fusion gene testing was done in 120 and 93 patients, respectively. Of the 120 patients, 24 (20%) cases were positive for EGFR mutations whereas EML4-ALK fusion gene was present in 8 (8.6%) out of 93 patients.Conclusions:Our study confirms the importance of molecular testing in the NSCLC patient subgroup with an aim to identify the exact molecular targets that can benefit from the newer generation of targeted therapies.
Non-small cell lung cancer (NSCLC) accounts for the majority of primary lung cancer cases worldwide. The activating mutations of epidermal growth factor receptor (EGFR) have been demonstrated to associate with the development of NSCLC, with T790M mutation being the most common. Over the years, EGFR tyrosine kinase inhibitors (TKIs) were developed to target EGFR-related mutations. However, patients with activating EGFR mutations who are initially responsive to EGFR-TKIs eventually develop acquired resistance after a median progression-free survival of 10-16 months, followed by disease progression. Recently, the third-generation EGFR inhibitors have emerged as potential therapeutics to block the growth of EGFR T790M-positive tumors. This article reviews the emerging data regarding EGFR mutations and clinical evidence on third-generation agents against EGFR T790M mutation in the treatment of patients with advanced NSCLC. It also reviews the role of repeat biopsy in improving the success rates of treatment of EGFR T790M-derived drug-resistant NSCLC.
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