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Being one of the leading causes of cancer deaths worldwide and their resistance to conventional treatment methods, made gastrointestinal stromal tumors (GISTs) one of the hot topics in medical research areas in the past decade. To investigate molecular alterations underlying the tumor is of great importance to be able to develop new, targeted treatment options. In this study, GIST samples obtained from 40 Turkish patients were analyzed for actionable epidermal growth factor receptor (EGFR) mutations that are related to treatment regimes in non small cell lung cancer (NSCLC) to understand whether EGFR expression is altered in GISTs. Established alterations in EGFR can make the use of tyrosine kinase inhibitors possible, which are currently used in cancer therapy, especially in NSCLC. Our results indicated that EGFR mutations are rare in GISTs. Further research is needed to sequence whole coding regions of the gene to investigate new actionable mutations in EGFR in an increased sample size.

Being one of the leading causes of cancer deaths worldwide and their resistance to conventional treatment methods, made gastrointestinal stromal tumors (GISTs) one of the hot topics in medical research areas in the past decade. To investigate molecular alterations underlying the tumor is of great importance to be able to develop new, targeted treatment options. In this study, GIST samples obtained from 40 Turkish patients were analyzed for actionable epidermal growth factor receptor (EGFR) mutations that are related to treatment regimes in non small cell lung cancer (NSCLC) to understand whether EGFR expression is altered in GISTs. Established alterations in EGFR can make the use of tyrosine kinase inhibitors possible, which are currently used in cancer therapy, especially in NSCLC. Our results indicated that EGFR mutations are rare in GISTs. Further research is needed to sequence whole coding regions of the gene to investigate new actionable mutations in EGFR in an increased sample size. [ABSTRACT FROM AUTHOR]

Purpose: Mutations in the epidermal growth factor receptor (EGFR) gene have been identified as potential targets for the treatment and prognostic factors for non-small cell lung cancer (NSCLC). We assessed the correlation between fluorodeoxyglucose (FDG) uptake and EGFR mutations, as well as their prognostic implications. Methods: A total of 163 patients with pathologically confirmed NSCLC were enrolled (99 males and 64 females; median age, 60 years). All patients underwent FDG positron emission tomography before treatment, and genetic studies of EGFR mutations were performed. The maximum standardized uptake value (SUVmax) of the primary lung cancer was measured and normalized with regard to liver uptake. The SUVmax between the wild-type and EGFR mutant groups was compared. Survival was evaluated according to SUVmax and EGFR mutation status. Results: EGFR mutations were found in 57 patients (60.8 %). The SUVmax tended to be higher in wild-type than mutant tumors, but was not significantly different (11.1 ± 5.7 vs. 9.8 ± 4.4, P = 0.103). The SUVmax was significantly lower in patients with an exon 19 mutation than in those with either an exon 21 mutation or wild type ( P = 0.003 and 0.009, respectively). The EGFR mutation showed prolonged overall survival (OS) compared to wild-type tumors ( P = 0.004). There was no significant difference in survival according to SUVmax. Both OS and progression-free survival of patients with a mutation in exon 19 were significant longer than in patients with wild-type tumors. Conclusion: In patients with NSCLC, a mutation in exon 19 was associated with a lower SUVmax and is a reliable predictor for good survival. [ABSTRACT FROM AUTHOR]

Background: Epidermal growth factor receptor ( EGFR ) gene was the major causative gene of lung cancer and also the specific treatment target. It is necessary to analyze the genotype and phenotype characters of patients., Methods: We investigated 1,034 lung cancer patients in this study. The collected clinicopathological parameters included gender, age at diagnosis, smoking status, pathological TNM stage, tumor morphology and location, visceral pleural invasion as well as histological type., Results: Almost 50% participants had EGFR mutations. L858R in exon 21 was the most common type. Concomitant mutation, 19 del and L858R, were detected in 20 patients. Compared to patients with exon 19 del or L858R mutations solely, they were inclined to have small size adenocarcinomas which occurred in bilateral and invaded the visceral pleura. The tyrosine kinases inhibitors (TKIs)-resistant mutation, insertions in exon 20, was detected in 11 patients., Conclusions: The summarized clinicopathological features will help clinicians to implement the feasible treatment plan., Competing Interests: Conflicts of Interest: The authors have no conflicts of interest to declare.

Background: Erlotinib is a standard first-line therapy for patients who have metastatic nonsmall cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutations. The recommended dose of 150 mg daily is the maximum tolerated dose (MTD). Few clinical data are available regarding its efficacy at doses less than the MTD., Methods: An institutional database was queried for patients with advanced NSCLC who were positive for EGFR L858R mutations or exon 19 deletions and had received treatment with erlotinib. The treatment course, including the erlotinib dose at initiation of treatment, at 4 months into therapy, and at disease progression, was retrospectively studied. Progression-free survival (PFS) was compared between patients who received the MTD (150 mg) and those who received reduced-dose erlotinib (≤100 mg)., Results: In total, 198 eligible patients were identified. Thirty-one patients (16%) were initiated on reduced-dose erlotinib; they were older (P = .001) and had lower performance status (P = .01) compared with those who were initiated on erlotinib at the MTD. The response rate to reduced-dose erlotinib was 77%. The median PFS of patients initiated on reduced-dose erlotinib was 9.6 months versus 11.4 months for those initiated at the MTD, a difference that was not statistically significant (hazard ratio, 0.81; 95% confidence interval, 0.54-1.21; P = .30). There was a nonsignificant trend toward higher rates of progression within the central nervous system with reduced-dose erlotinib., Conclusions: At doses below the MTD, erlotinib treatment results in a high response rate and a prolonged median PFS. Review of the literature indicates that 15 of 30 small-molecule inhibitors that are approved or in late-stage development for cancer therapy have recommended doses below the MTD. When the toxicities of MTD dosing are a concern, an investigation of small-molecule inhibitors at doses below the MTD is warranted. Cancer 2016;122:3456-63. © 2016 American Cancer Society., (© 2016 American Cancer Society.)