ABSTRACT
El cáncer constituye un serio problema de salud a nivel mundial. Las estimaciones, en cuanto a incidencia y mortalidad, no son nada halagüeñas, en especial para los países subdesarrollados. Durante las últimas décadas se han realizado importantes contribuciones a la comprensión de la carcinogénesis humana, sobre todo desde la perspectiva ecológica y evolutiva. Los objetivos del presente trabajo se centran en: destacar las principales hipótesis que desde dicha perspectiva, tratan de explicar la etiología de los tumores malignos, así como adecuar las que, a la luz de los hallazgos recientes o cotejadas con datos empíricos, parecen más factibles. La hipótesis tradicionalmente aceptada se basa en la carcinogénesis en múltiples etapas y explica de manera satisfactoria algunos aspectos del proceso; aunque conlleva a falacias de lógica, como la conclusión que dos tercios de los cánceres humanos obedecen a la mala suerte. Por su parte, la hipótesis de la oncogénesis adaptativa parece adecuarse de manera más realística a las complejas relaciones ecológicas que se establecen entre las células malignas, las células normales y el microambiente celular; capaces de originar fenómenos tan inadmisibles, como la cooperación de células normales en la progresión tumoral o la adopción por parte de las células malignas de estrategias evolutivamente estables. De hecho, la oncogénesis adaptativa incluso puede ser extendida al nivel del macroambiente poblacional y social. Su conclusión definitiva no hace más que reiterar la importancia de la prevención como la medida más eficaz para reducir la carga global de enfermedad por cáncer(AU)
Cancer is a serious health problem worldwide. Estimates, in terms of incidence and mortality, are not at all promising especially for underdeveloped countries. During the last decades, important contributions have been made to the understanding of human carcinogenesis, especially from the ecological and evolutionary perspective. The objectives of this work are focused on: highlighting the main hypotheses that, from this perspective, try to explain the etiology of malignant tumors, as well as adapting those that, in the light of recent findings or collated with empirical data, seem more feasible. The traditionally accepted hypothesis is based on multi-stage carcinogenesis; and satisfactorily explains some aspects of the process; although it leads to logic fallacies, such as the conclusion that two thirds of human cancers obey to bad luck. On the other hand, the hypothesis of adaptive oncogenesis seems to adapt more realistically to the complex ecological relationships established between malignant cells, normal cells, and the cellular microenvironment; capable of originating such inadmissible phenomena, such as the cooperation of normal cells in tumor progression, or the adoption by malignant cells of evolutionarily stable strategies. In fact, adaptive oncogenesis can even be extended to the level of the population and social "macroenvironment". Its final conclusion does nothing but reiterate the importance of prevention as the most effective measure to reduce the global burden of cancer disease(AU)
Subject(s)
Humans , Social Environment , Carcinogenesis/immunology , Neoplasms/epidemiology , Hypothesis-TestingABSTRACT
El cáncer constituye un serio problema de salud a nivel mundial. Las estimaciones, en cuanto a incidencia y mortalidad, no son nada halagüeñas, en especial para los países subdesarrollados. Durante las últimas décadas se han realizado importantes contribuciones a la comprensión de la carcinogénesis humana, sobre todo desde la perspectiva ecológica y evolutiva. Los objetivos del presente trabajo se centran en: destacar las principales hipótesis que desde dicha perspectiva, tratan de explicar la etiología de los tumores malignos, así como adecuar las que, a la luz de los hallazgos recientes o cotejadas con datos empíricos, parecen más factibles. La hipótesis tradicionalmente aceptada se basa en la carcinogénesis en múltiples etapas y explica de manera satisfactoria algunos aspectos del proceso; aunque conlleva a falacias de lógica, como la conclusión que dos tercios de los cánceres humanos obedecen a la mala suerte. Por su parte, la hipótesis de la oncogénesis adaptativa parece adecuarse de manera más realística a las complejas relaciones ecológicas que se establecen entre las células malignas, las células normales y el microambiente celular; capaces de originar fenómenos tan inadmisibles, como la cooperación de células normales en la progresión tumoral o la adopción por parte de las células malignas de estrategias evolutivamente estables. De hecho, la oncogénesis adaptativa incluso puede ser extendida al nivel del macroambiente poblacional y social. Su conclusión definitiva no hace más que reiterar la importancia de la prevención como la medida más eficaz para reducir la carga global de enfermedad por cáncer(AU)
Cancer is a serious health problem worldwide. Estimates, in terms of incidence and mortality, are not at all promising especially for underdeveloped countries. During the last decades, important contributions have been made to the understanding of human carcinogenesis, especially from the ecological and evolutionary perspective. The objectives of this work are focused on: highlighting the main hypotheses that, from this perspective, try to explain the etiology of malignant tumors, as well as adapting those that, in the light of recent findings or collated with empirical data, seem more feasible. The traditionally accepted hypothesis is based on multi-stage carcinogenesis; and satisfactorily explains some aspects of the process; although it leads to logic fallacies, such as the conclusion that two thirds of human cancers obey to bad luck. On the other hand, the hypothesis of adaptive oncogenesis seems to adapt more realistically to the complex ecological relationships established between malignant cells, normal cells, and the cellular microenvironment; capable of originating such inadmissible phenomena, such as the cooperation of normal cells in tumor progression, or the adoption by malignant cells of evolutionarily stable strategies. In fact, adaptive oncogenesis can even be extended to the level of the population and social "macroenvironment". Its final conclusion does nothing but reiterate the importance of prevention as the most effective measure to reduce the global burden of cancer disease(AU)
Subject(s)
Humans , Male , Female , Social Environment , Carcinogenesis/immunology , Neoplasms/epidemiology , Hypothesis-TestingABSTRACT
PURPOSE: To evaluate the preliminary results of vaginal-cuff relapses (VCR) and complications of a short brachytherapy (BT) schedule in postoperative endometrial carcinoma. METHODS AND MATERIALS: From September 2011 to December 2014, 102 patients were treated with postoperative BT for endometrial carcinoma. Seventy-four patients received a single 7 Gy dose after external beam irradiation (Group 1), and 28 intermediate-risk patients received three daily fractions of 6 Gy (Group 2). The dose was prescribed at 5 mm from the applicator surface. Toxicity was prospectively evaluated after the objective late effects of normal tissues-subjective, objective, management, analytic scores for vagina and RTOG scores for rectum and bladder. STATISTICS: χ2 and Student's t tests. RESULTS: The mean followup was 28.85 months (9.6-58.5) in Group 1 and 31.19 months (7.7-62.3) in Group 2. No VCR was found during followup. Late toxicity: vagina toxicity was developed in 24.32% of the patients in Group 1 (G1-G2) and in 21.4% in Group 2 (G1-G2 but 1 G3). Rectal toxicity appeared in only 2.7% of patients in Group 1 (G1). Neither Group 1 nor Group 2 presented late bladder toxicity. No differences were found in late toxicity between Groups 1 and 2. CONCLUSIONS: The present short BT schedule was safe in relation to VCR and late toxicity for the followup period studied. These results are similar to those of two larger previous schedules performed in our center in relation to the same point of followup.
