Introduction: The most widely used and reliable marker for the selection of patients candidates for treatment with tyrosine kinase inhibitors is the detection of mutations in exons 19 to 21 of the EGFR gene. The behavior of these mutations depends on the exposure factor and this has prognostic implications. Objective: To evaluate the epidemiological profile of EGFR mutations in lung adenocarcinoma in smokers and non-smokers exposed to wood smoke at INER. Material and methods: An observational, retrospective and cross-sectional study was conducted at INER, Mexico City. We included patients with a diagnosis of pulmonary adenocarcinoma in the period from June 2013 to December 2016. Qualitative variables (gender, occupation, biomass exposure, histological pattern of adenocarcinoma, degree of histological differentiation, clinical stage, presence of metastasis, Gene EGFR) and quantitative (age, smoking, exposure to wood smoke). The analysis was performed in terms of absolute and relative frequencies as well as measures of central tendency. Results: A total sample of 252 patients was analyzed, 58.33% female and 41.67%. Of the male sex. EGFR mutation was identified in 32.5%. It was found that the most frequently mutated exon in both sexes was the 19 with differences in histological pattern in relation to the exposition factor. Conclusion: The characterization of molecular profiles is an extremely useful tool in the presentation of therapeutic offers in non-small cell lung cancer. This is of interest since, like the histological pattern has a prognostic implication.
KEYWORDS
Pulmonary adenocarcinoma, EGFR, prognosis.
REFERENCES
Globocan 2008. Organización Mundial de la Salud. Fecha de consulta: 2018 agosto. Disponible en: https://www.iarc.fr/en/media-centre/iarcnews/2010/globocan2008.php
Duggan MA, Anderson WF, Altekruse S, Penberthy L, Sherman ME. The surveillance, epidemiology, and end results (SEER) program and pathology: toward strengthening the critical relationship. Am J Surgical Pathol 2016;40(12):e94-e102.
Aldaco-Sarvide F, Pérez-Pérez P, Cervantes-Sánchez G, Torrecillas-Torres L, Erazo-V AE. Mortalidad por cáncer en México 2000-2010: el recuento de los daños. Gaceta Mex Onc 2012;11(6):371-379.
Ruíz-Godoy L, Rizo-Ríos P, Sánchez-Cervantes F, Osornio-Vargas A, García-Cuellar C, Meneses-García A. Mortality due to lung cancer in Mexico. Lung Cancer 2007;58(2):184-190.
Iniesta-Serrano P. Carcinogénesis pulmonar. Rev Patol Respir 2007;10(1):50-54.
Gómez RC, de Castro CJ, González BM. Factores etiológicos del cáncer de pulmón: fumador activo, fumador pasivo, carcinógenos medioambientales y factores genéticos. Med Clin 2007;128(10):390-396. doi: 10.1157/13099973.
Peto R, Darby S, Deo H, Silcocks P, Whitley E, Doll R. Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of national statistics with two case-control studies. BMJ 2000;321(7257):323-329.
Kerr KM. Pulmonary adenocarcinomas: classification and reporting. Histopathology 2009:54(1):12-27. doi: 10.1111/j.1365-2559.2008.03176.x.
Spiro SG, Gould MK, Colice GL; American College of Chest Physicians. Initial evaluation of the patient with lung cancer: symptoms, signs, laboratory test, and paraneoplastic syndromes: ACCP evidenced-based clinical practice guidelines (2nd edition). Chest 2007;132(3 Suppl):149S-160S.
De Vita HS. Cancer: Principles and practice of oncology. 6th ed. Boston: Lippincott Williams & Wilkins Publishers; 2010.
Arrieta O, Guzmán-de Alba E, Alba-López LF, et al. Consenso Nacional de Diagnóstico y Tratamiento del Cáncer de Pulmón de Células no Pequeñas. Consenso de Cáncer de Pulmón. Rev Invest Clin 2013;65(Supl.1):s5-s84.
Franco-Marina F, Villalba-Caloca J. La epidemia de cáncer pulmonar en México. Rev Inst Nal Enf Resp Mex 2001;14(4):207-214.
Ruano-Ravina A, Pérez RM, Fernández-Villar A. Cribado de cáncer de pulmón con tomografía computarizada de baja dosis después del National Lung Screening Trial. El debate continúa abierto. Arch Bronconeumol 2013;49 (4):158-165.
Sierra JR, Cepero V, Giordano S. Molecular mechanisms of acquired resistance to tyrosine kinase targeted therapy. Mol Cancer 2010;9:75. doi: 10.1186/1476-4598-9-75.
Arora A, Scholar EM. Role of tyrosine kinase inhibitors in cancer therapy. J Pharmacol Exp Ther 2005;315(3):971-979.
Wheatley-Price P, Shepherd FA. Epidermal growth factor receptor inhibitors in the treatment of lung cancer: reality and hopes. Curr Opin Oncol 2008;20(2):162-175. doi: 10.1097/CCO.0b013e3282f335a3.
Rosell R, Taron M, Reguart N, Isla D, Moran T. Epidermal growth factor receptor activation: how exon 19 and 21 mutations changed our understanding of the pathway. Clin Cancer Res 2006;12(24):7222-7231.
Lynch TJ, Bell DW, Sordella R, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med 2004;350(21):2129-2139.
Yotsukura M, Yasuda H, Shigenobu T, et al. Clinical and pathological characteristics of EGFR mutation in operable early-stage lung adenocarcinoma. Lung Cancer 2017;109:45-51. doi: 10.1016/j.lungcan.2017.04.014.