RESUMEN
The intestinal microbiota, composed of a large population of microorganisms, is often considered a "forgotten organ" in human health and diseases. Increasing evidence indicates that dysbiosis of the intestinal microbiota is closely related to colorectal cancer (CRC). The roles for intestinal microorganisms that initiated and facilitated the CRC process are becoming increasingly clear. Hypothesis models have been proposed to illustrate the complex relationship between the intestinal microbiota and CRC. Recent studies have identified Streptococcus bovis, enterotoxigenic Bacteroides fragilis, Fusobacterium nucleatum, Enterococcus faecalis, Escherichia coli, and Peptostreptococcus anaerobius as CRC candidate pathogens. In this review, we summarized the mechanisms involved in microbiota-related colorectal carcinogenesis, including inflammation, pathogenic bacteria, and their virulence factors, genotoxins, oxidative stress, bacterial metabolites, and biofilm. We also described the clinical values of intestinal microbiota and novel strategies for preventing and treating CRC.
Asunto(s)
Adenocarcinoma/microbiología , Neoplasias Colorrectales/microbiología , Microbioma Gastrointestinal , Adenocarcinoma/etiología , Adenocarcinoma/prevención & control , Adenocarcinoma/terapia , Animales , Bacterias/aislamiento & purificación , Bacterias/metabolismo , Bacterias/patogenicidad , Biodiversidad , Biopelículas , Carcinogénesis , Transformación Celular Neoplásica , Neoplasias Colorrectales/etiología , Neoplasias Colorrectales/prevención & control , Neoplasias Colorrectales/terapia , Dieta , Genes APC , Humanos , Inflamación , Ratones , Modelos Biológicos , Mutágenos/metabolismo , Síndromes Neoplásicos Hereditarios/genética , Síndromes Neoplásicos Hereditarios/microbiología , Estrés Oxidativo , Ratas , VirulenciaRESUMEN
OBJECTIVE: The purpose of this study was the clinical and pathological characterisation of a new autosomal dominant gastric polyposis syndrome, gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS). METHODS: Case series were examined, documenting GAPPS in three families from Australia, the USA and Canada. The affected families were identified through referral to centralised clinical genetics centres. RESULTS: The report identifies the clinical and pathological features of this syndrome, including the predominant dysplastic fundic gland polyp histology, the exclusive involvement of the gastric body and fundus, the apparent inverse association with current Helicobacter pylori infection and the autosomal dominant mode of inheritance. CONCLUSIONS: GAPPS is a unique gastric polyposis syndrome with a significant risk of gastric adenocarcinoma. It is characterised by the autosomal dominant transmission of fundic gland polyposis, including areas of dysplasia or intestinal-type gastric adenocarcinoma, restricted to the proximal stomach, and with no evidence of colorectal or duodenal polyposis or other heritable gastrointestinal cancer syndromes.
Asunto(s)
Adenocarcinoma/diagnóstico , Síndromes Neoplásicos Hereditarios/diagnóstico , Pólipos/diagnóstico , Neoplasias Gástricas/diagnóstico , Adenocarcinoma/genética , Adenocarcinoma/microbiología , Adenocarcinoma/patología , Adolescente , Adulto , Anciano , Niño , Femenino , Genes Dominantes , Infecciones por Helicobacter/complicaciones , Helicobacter pylori/aislamiento & purificación , Humanos , Masculino , Persona de Mediana Edad , Síndromes Neoplásicos Hereditarios/genética , Síndromes Neoplásicos Hereditarios/microbiología , Síndromes Neoplásicos Hereditarios/patología , Linaje , Pólipos/genética , Pólipos/patología , Neoplasias Gástricas/genética , Neoplasias Gástricas/microbiología , Neoplasias Gástricas/patologíaRESUMEN
The dose response of the enhanced reactivation (ER) of herpes simplex virus type 1 has been studied in UV-irradiated normal human skin fibroblasts and fibroblasts from the following hereditary cancer-prone syndromes: retinoblastoma, aniridia, polyposis coli, neurofibromatosis type 1 and 2, dysplastic nevus syndrome, Von Hippel-Lindau syndrome, multiple endocrine neoplasia type 2, and Bloom's syndrome. Surprisingly, much higher levels of ER were observed in all these genetically heterogeneous hereditary disorders than in normal human skin fibroblasts. These results suggest that loss of one allele of putative tumor suppressor genes may activate cellular processes that result in the induction of the ER response, and they support our previous observation suggesting that ER may somehow be related to the process of carcinogenesis (P. J. Abrahams et al., Cancer Res., 48: 6054-6057, 1988).