The Investigation of EGFR mutation and ALK gene rearrangement rates in lung adenocarcinoma patients in Mardin EGFR Mutation and ALK Gene Rearrangement Rates in Mardin
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Abstract
Objective: Non-Small Cell Lung Cancer (NSCLC) is a heterogeneous group of tumors comprising different histologic subtypes and genetic mutations. Important mutations are EGFR (Epidermal Growth Factor Receptor), ALK (Anaplastic Lymphoma Kinase) rearrangement and ROS 1 rearrangement. This study aimed to determine the mutation rates of lung adenocarcinoma patients admitted to Mardin State Hospital Oncology clinic and to review the literature on the term mutually exclusivity.
Materials and Methods: The records of patients admitted to Mardin State Hospital Medical Oncology Clinic between 2014-2018 were retrospectively analyzed. The descriptive statistics for continuous variables mean/median; for categorical variables, frequency (n) and percentage (%) were shown.
Results: There were 39 lung adenocarcinoma patients (30.2%) among 130 lung cancer patients. The median age of female patients was 49.31 (27-74), while the median age of male patients was 58.87 (43-78). There were 6 EGFR mutant (15.4%) patients and 2 (5.1%) patients with ALK rearrangement. There were no ROS-1 positive patients.
Conclusion: This study indicates that EGFR mutation rates may be very low in Turkey compared to the literature and ALK rates may be close to the literature. To determine the actual mutation rates and factors affecting genetic alterations in Turkey, there are needed to further studies.
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Accepted 2019-11-22
Published 2019-11-27
References
Novello S, Barlesi F, Califano R, Cufer T, Ekman S, Levra MG, et al. Metastatic non-small-cell lung cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Annals of Oncology. 2016;27(suppl_5):v1-v27.
Gaughan EM, Costa DB. Genotype-driven therapies for non-small cell lung cancer: focus on EGFR, KRAS and ALK gene abnormalities. Therapeutic advances in medical oncology. 2011;3(3):113-25.
Kerr KM, Bubendorf L, Edelman MJ, Marchetti A, Mok T, Novello S, et al. Second ESMO consensus conference on lung cancer: pathology and molecular biomarkers for non-small-cell lung cancer. Annals of Oncology. 2014;25(9):1681-90.
Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S, et al. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature. 2007;448(7153):561-6.
Takeuchi K, Choi YL, Soda M, Inamura K, Togashi Y, Hatano S, et al. Multiplex reverse transcription-PCR screening for EML4-ALK fusion transcripts. Clin Cancer Res. 2008;14(20):6618-24.
Shaw AT, Yeap BY, Mino-Kenudson M, Digumarthy SR, Costa DB, Heist RS, et al. Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK. J Clin Oncol. 2009;27(26):4247-53.
Koivunen JP, Mermel C, Zejnullahu K, Murphy C, Lifshits E, Holmes AJ, et al. EML4-ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancer. Clin Cancer Res. 2008;14(13):4275-83.
Wong DW, Leung EL, So KK, Tam IY, Sihoe AD, Cheng LC, et al. The EML4-ALK fusion gene is involved in various histologic types of lung cancers from nonsmokers with wild-type EGFR and KRAS. Cancer. 2009;115(8):1723-33.
Gainor JF, Varghese AM, Ou S-HI, Kabraji S, Awad MM, Katayama R, et al. ALK rearrangements are mutually exclusive with mutations in EGFR or KRAS: an analysis of 1,683 patients with non–small cell lung cancer. Clinical Cancer Research. 2013;19(15):4273-81.
Won J, Keam B, Koh J, Cho H, Jeon Y, Kim T, et al. Concomitant ALK translocation and EGFR mutation in lung cancer: a comparison of direct sequencing and sensitive assays and the impact on responsiveness to tyrosine kinase inhibitor. Annals of Oncology. 2015;26(2):348-54.
Yang J-J, Zhang X-C, Su J, Xu C-R, Zhou Q, Tian H-X, et al. Lung cancers with concomitant EGFR mutations and ALK rearrangements: diverse responses to EGFR-TKI and crizotinib in relation to diverse receptors phosphorylation. Clinical Cancer Research. 2014;20(5):1383-92.
Lee JK, Kim TM, Koh Y, Lee SH, Kim DW, Jeon YK, et al. Differential sensitivities to tyrosine kinase inhibitors in NSCLC harboring EGFR mutation and ALK translocation. Lung Cancer. 2012;77(2):460-3.
Takahashi T, Sonobe M, Kobayashi M, Yoshizawa A, Menju T, Nakayama E, et al. Clinicopathologic features of non-small-cell lung cancer with EML4-ALK fusion gene. Ann Surg Oncol. 2010;17(3):889-97.
Sequist LV, Heist RS, Shaw AT, Fidias P, Rosovsky R, Temel JS, et al. Implementing multiplexed genotyping of non-small-cell lung cancers into routine clinical practice. Ann Oncol. 2011;22(12):2616-24.
Kris M, Johnson B, Kwiatkowski D, Iafrate A, Wistuba I, Aronson S, et al., editors. Identification of driver mutations in tumor specimens from 1,000 patients with lung adenocarcinoma: The NCI's Lung Cancer Mutation Consortium (LCMC). ASCO Annual Meeting Proceedings; 2011.
Zhao F, Xu M, Lei H, Zhou Z, Wang L, Li P, et al. Clinicopathological Characteristics of Patients with Non-Small-Cell Lung Cancer Who Harbor EML4-ALK Fusion Gene: A Meta-Analysis. PloS one. 2015;10(2).
Wang Y, Wang S, Xu S, Qu J, Liu B. Clinicopathologic Features of Patients with Non-Small Cell Lung Cancer Harboring the EML4-ALK Fusion Gene: A Meta-Analysis. PloS one. 2014;9(10):e110617.
Cicek T, Ozturk A, Yılmaz A, Aktas Z, Demirag F, Akyurek N. Adequacy of EBUS‐TBNA specimen for mutation analysis of lung cancer. The clinical respiratory journal. 2019;13(2):92-7.