María Torres-Durán1, Alberto Ruano-Ravina2, Isaura Parente-Lamelas3, José Abal-Arca3, Virginia Leiro-Fernández1, Carmen Montero-Martínez4, Carolina Pena5, Olalla Castro-Añón6, Antonio Golpe-Gómez7, Francisco J González-Barcala8, Cristina Martínez9, Rosirys Guzmán-Taveras9, Mariano Provencio10, María José Mejuto-Martí11, Alberto Fernández-Villar1, Juan Miguel Barros-Dios12. 1. Service of Pneumology, University Hospital Complex of Vigo, Vigo, Spain. 2. Department of Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain; CIBER de Epidemiología y Salud Pública, CIBERESP Madrid, Spain. Electronic address: alberto.ruano@usc.es. 3. Service of Pneumology, Ourense Hospital Complex, Ourense, Spain. 4. Service of Pneumology, University Hospital Complex of A Coruña, A Coruña, Spain. 5. Service of Oncology, Pontevedra Hospital Complex, Pontevedra, Spain. 6. Service of Pneumology, Hospital Lucus Augusta, Lugo, Spain. 7. Service of Pneumology, Santiago de Compostela University Clinic Hospital, Santiago de Compostela, Spain. 8. Service of Pneumology, Santiago de Compostela University Clinic Hospital, Santiago de Compostela, Spain; CIBER de Enfermedades Respiratorias, CIBERES, Madrid, Spain. 9. National Institute of Silicosis, University Hospital of Asturias, Oviedo, Spain. 10. Service of Oncology, Puerta de Hierro University Hospital, Madrid, Spain. 11. Service of Pneumology, Arquitecto Marcide Hospital, Ferrol, Spain. 12. Department of Preventive Medicine and Public Health, University of Santiago de Compostela, Santiago de Compostela, Spain; CIBER de Epidemiología y Salud Pública, CIBERESP Madrid, Spain; Service of Preventive Medicine, University Hospital Complex of Santiago de Compostela, Santiago de Compostela, Spain.
Abstract
BACKGROUND: Never-smokers comprise up to 25% of all lung cancer cases. They could have different molecular pathways for lung cancer induction compared with smokers. Alpha-1 antitrypsin (AAT) deficiency is a hereditary trait whose main characteristic is early onset of lung emphysema. Our aim is to know if AAT-deficient carriers have a higher risk of lung cancer in a study performed exclusively in never-smokers. METHODS: We designed a multicentre hospital-based case-control study, which included incident never-smoking lung cancer cases. Controls were never-smokers attending nonmajor surgery at the participating hospitals. Controls were frequency matched on age and gender with cases. We determined AAT variants (alleles S and Z) through polymerase chain reaction. RESULTS: Two hundred and twelve cases and 318 controls were included. PiSS individuals showed a lung cancer risk of 4.64 (95% confidence interval: 1.08-19.92) compared with those with normal genotype (PiMM). When the analysis was restricted to women, the risk for PiSS increased to 7.58 (95% confidence interval: 1.40-40.87). This risk for homozygous SS was even higher for individuals exposed to environmental tobacco smoke (greater than 20 years). The presence of other alleles did not show any effect on lung cancer risk. CONCLUSIONS: Never smoking SS homozygous individuals pose an increased risk of lung cancer. The risk is higher for individuals exposed to environmental tobacco smoke.
BACKGROUND: Never-smokers comprise up to 25% of all lung cancer cases. They could have different molecular pathways for lung cancer induction compared with smokers. Alpha-1 antitrypsin (AAT) deficiency is a hereditary trait whose main characteristic is early onset of lung emphysema. Our aim is to know if AAT-deficient carriers have a higher risk of lung cancer in a study performed exclusively in never-smokers. METHODS: We designed a multicentre hospital-based case-control study, which included incident never-smoking lung cancer cases. Controls were never-smokers attending nonmajor surgery at the participating hospitals. Controls were frequency matched on age and gender with cases. We determined AAT variants (alleles S and Z) through polymerase chain reaction. RESULTS: Two hundred and twelve cases and 318 controls were included. PiSS individuals showed a lung cancer risk of 4.64 (95% confidence interval: 1.08-19.92) compared with those with normal genotype (PiMM). When the analysis was restricted to women, the risk for PiSS increased to 7.58 (95% confidence interval: 1.40-40.87). This risk for homozygous SS was even higher for individuals exposed to environmental tobacco smoke (greater than 20 years). The presence of other alleles did not show any effect on lung cancer risk. CONCLUSIONS: Never smoking SS homozygous individuals pose an increased risk of lung cancer. The risk is higher for individuals exposed to environmental tobacco smoke.
Authors: Francesco Carraro; Jason D Williams; Mercedes Linares-Moreau; Chiara Parise; Weibin Liang; Heinz Amenitsch; Christian Doonan; C Oliver Kappe; Paolo Falcaro Journal: Angew Chem Int Ed Engl Date: 2020-03-17 Impact factor: 15.336
Authors: Ana Casal-Mouriño; Alberto Ruano-Ravina; María Torres-Durán; Isaura Parente-Lamelas; Mariano Provencio-Pulla; Olalla Castro-Añón; Iria Vidal-García; José Abal-Arca; María Piñeiro-Lamas; Alberto Fernández-Villar; Luis Valdés-Cuadrado; Juan Miguel Barros-Dios; Mónica Pérez-Ríos Journal: Sci Rep Date: 2020-12-03 Impact factor: 4.379
Authors: Simona De Vita; Maria Giovanna Chini; Gabriella Saviano; Claudia Finamore; Carmen Festa; Gianluigi Lauro; Simona De Marino; Roberto Russo; Carmen Avagliano; Agostino Casapullo; Antonio Calignano; Giuseppe Bifulco; Maria Iorizzi Journal: Biomolecules Date: 2021-10-09
Authors: Ramón Antonio Tubío-Pérez; María Torres-Durán; María Esmeralda García-Rodríguez; Cristina Candal-Pedreira; Julia Rey-Brandariz; Mónica Pérez-Ríos; Juan Barros-Dios; Alberto Fernández-Villar; Alberto Ruano-Raviña Journal: BMC Cancer Date: 2022-01-19 Impact factor: 4.430