ABSTRACT
El cáncer es la segunda causa de muerte en el mundo, según datos de la Organización Mundial de la Salud (OMS) en el año 2015 ocasionó 8,8 millones de muertes. Dentro de los factores de riesgo para el desarrollo de cáncer se encuentran el tabaquismo y el consumo de alcohol. En Chile el 33,6% de la población fuma y un 21,2 % de los jóvenes. El consumo de alcohol en la población chilena es de 74,5 % y en los jóvenes de un 12,2 %. Entre los factores fisiológicos que influyen en el desarrollo de cáncer, el factor genético juega un rol relevante, habiéndose demostrado que la presencia de polimorfismos genéticos alteran la capacidad del organismo de eliminar contaminantes y aumentan el riesgo de desarrollar cáncer. Lo mismo ocurre con polimorfismos que impiden la reparación de ADN debido a daños producidos por efecto de contaminantes ambientales como el humo de cigarrillo. El objetivo de esta revisión es analizar el estado del arte de la relación entre farmacogenética, tabaco y alcohol como factores de riesgo para el desarrollo de cáncer. Los resultados sugieren que la presencia de po limorfismos que alteran la función de enzimas de biotransformación fase I (CYP1A1, CYP1E1) y fase II (GST), además de polimorfismos en enzimas de reparación del ADN (ERCC1/ERCC2) aumentan el riesgo de cáncer inducido por el hábito tabáquico y alcohólico. Esta asociación es importante, si consideramos que en la población chilena el hábito de fumar y beber alcohol es altamente prevalente.
Cancer is the second leading cause of death in the world, causing 8.8 million deaths in 2015 according to the World Health Organization (WHO). Risk factors for cancer include smoking and alcohol con sumption. In Chile, 33.6% of the population and 21.2% of young people smokes. Alcohol consump tion in the Chilean population is 74.5% and 12.2% in young people. Among the physiological factors that influence the development of cancer, the genetic factor plays a relevant role. It has been shown that the presence of genetic polymorphisms that alter the ability of the body to eliminate contami nants increase the risk of developing cancer. The same applies to polymorphisms that prevent DNA repair due to damage caused by environmental pollutants such as cigarette smoke. The objective of this review is to analyze the state of the art of the relationship between pharmacogenetics, smoking, and alcohol consumption as risk factors for the development of cancer. In conclusion, the results suggest that the presence of polymorphisms that alter the function of biotransformation enzymes phase I (CYP1A1, CYP1E1) and phase II (GST), as well as polymorphisms in DNA repair enzymes (ERCC1 / ERCC2), increase the risk of cancer induced by smoking and alcohol consumption. This association is important considering that smoking and drinking alcohol are highly prevalent among the Chilean population.
Subject(s)
Humans , Alcohol Drinking/adverse effects , Inactivation, Metabolic/genetics , Genetic Predisposition to Disease , Tobacco Smoking/adverse effects , Neoplasms/etiology , Pharmacogenetics , Polymorphism, Genetic , Alcohol Drinking/genetics , Alcohol Drinking/metabolism , Genetic Markers , Risk Factors , Tobacco Smoking/genetics , Tobacco Smoking/metabolism , Neoplasms/metabolismABSTRACT
BACKGROUND: Gallbladder cancer (GBC) is the second leading cause of cancer death in women in Chile. Even after curative surgery, prognosis is grim. To evaluate acute and late toxicity and efficacy of adjuvant chemoradiation (CRT) after curatively resected GBC. MATERIALS AND METHODS: We retrospectively analyzed the cohort of patients diagnosed between January 1999 and December 2009, treated with adjuvant CRT at our institution. Treatment protocol considered external beam radiation (RT) (45–54 Gy) to tumor bed and regional lymph nodes with or without concurrent 5-fluorouracil (5-FU) (500 mg/m2/day by 120-hours continuous infusion on days 1–5 and 29–33). Data was obtained from medical records, mortality from death certificates. Survival was estimated by Kaplan– Meier curves. RESULTS: 46 patients with curatively resected GBC received adjuvant CRT. Median age was 57 years (range 33–76); 39 patients were female. After diagnosis, a second surgery was performed in 42 patients. Cholecystectomy with hepatic segmentectomy and lymphadenectomy was the curative surgery in 41 patients. All patients received RT with a planned dose of 45 Gy in 25 fractions, 11 patients received a boost to the tumor bed up to 54 Gy and 34 patients had concurrent 5-FU. Therapy was well tolerated. Five patients experienced grade 3 toxicities. No grade 4 or 5 toxicity was observed. No grade >2 late toxicity was observed. Three- and 5-year overall survival (OS) were 57% and 51%, respectively. CONCLUSIONS: Adjuvant chemoradiation is well tolerated and might impact favorably on survival in patients with curatively resected GBC.
Subject(s)
Adult , Aged , Chemoradiotherapy, Adjuvant , Chile , Cohort Studies , Female , Gallbladder Neoplasms/mortality , Gallbladder Neoplasms/therapy , Humans , Kaplan-Meier Estimate , Male , Middle Aged , Proportional Hazards Models , Retrospective StudiesABSTRACT
Background: Survival rates after curative surgery for gastric cancer are disappointing. Therefore adjuvant therapeutic strategies are required. Aim: To analyze survival and side effects of treatment among gastric cancer patients treated with adjuvant chemo radiotherapy after curative resection of gastric adenocarcinoma. Material and methods: Retrospective review of medical records of 74 patients aged 20 to 74 years, treated with complete resection of gastric adenocarcinoma followed by adjuvant chemo radiation. Survival analysis was based on the records and information from the National Mortality Registry. Results: Five years survival fluctuated from 50 percent among patients in stage IB to 25 percent among those is stage IV. Significant acute toxicity was observed in 23 patients (31 percent). No patients died due to acute toxicity. Eleven patients (16.4 percent) developed significant late toxicity, with two possible deaths related to treatment. Conclusions: Postoperative chemo radiotherapy is feasible in our experience. Continues infusion of 5-fluoruracil is recommended to reduce toxicity.
Subject(s)
Adult , Aged , Humans , Middle Aged , Young Adult , Adenocarcinoma/therapy , Stomach Neoplasms/therapy , Adenocarcinoma/mortality , Chemotherapy, Adjuvant/adverse effects , Disease-Free Survival , Neoplasm Staging , Radiotherapy, Adjuvant/adverse effects , Retrospective Studies , Stomach Neoplasms/mortality , Survival Analysis , Treatment Outcome , Young AdultABSTRACT
Se presentan los resultados de un protocolo prospectivo de tratamiento combinado de quimioterapia y cirugía conservadora para el osteosarcoma clásico en etapas I A a II B (Enneking). Se evaluaron 64 pacientes, 39 hombres y 25 mujeres, con edades en rango de 14-60 años. La mediana de seguimiento fue de 40 meses (mínimo 20 y máximo de 72). Todos los pacientes fueron tratados con: doxorrubicina, cisplatino, ifosfamida y mesna en tres ciclos preoperatorios y ciclos postoperatorios, realizándose cirugía conservadora de reemplazos protésicos, alo o autoinjertos. La sobrevida actuarial fue de 60,2 por ciento a los 72 meses de observación. Se describe la relación del diagnóstico tardío con la incidencia de metástasis y sobrevida. Se enfatiza el buen resultado funcional y se recomienda el uso del protocolo presentado