Genetics of Colorectal Cancer [electronic resource] /
Potter, John D.editor.
Lindor, Noralane M.editor.
The last 20 years have seen a remarkable increase in knowledge of the etiology of colorectal cancer. At least three aspects are much clearer. First, known environmental agents and behaviors have been identified that increase risk (for example, diets high in meat, obesity, and smoking ) or decrease risk (for example, diets high in plant foods, aspirin, and physical activity) of colorectal cancer. Second, germline mutations in specific genes have been identified for the major inherited syndromes involving colorectal cancer (FAP, Lynch Syndrome, Juvenile Polyposis, MYH-Associated Polyposis, Li-Fraumeni Syndrome) as have variants of genes that modify the risk associated with the known environmental agents. Third, the specific tissue, cellular, and molecular disturbances that characterize the progression to different subtypes of colorectal cancer have been recently described. Genetics of Colorectal Cancer provides the most up-to-date information in each of these areas.
Description based upon print version of record.
Includes bibliographical references and index.
Epidemiology and Models of Colorectal Cancer -- Colorectal Cancer: Epidemiology -- Mouse Models of Intestinal Cancer -- Pathways to Colorectal Cancer -- The Chromosomal-Instability Pathway and APC Gene Mutation in Colorectal Cancer -- DNA Methylation in Colorectal Cancer: Multiple Facets of Tumorigenesis -- Pathways and Pathology -- Germline Susceptibility – Mendelian and Other Syndromes -- Familial Adenomatous Polyposis -- DNA Mismatch Repair and Lynch Syndrome -- Additional Syndromes with Hereditary Predisposition to Colorectal Cancer -- Familial Colorectal Cancer Type X -- Families with Serrated Neoplasia of the Colon -- Peutz–Jeghers Syndrome -- Juvenile Polyposis -- BLM Mutation and Colorectal Cancer Susceptibility -- The Role of p53 in Colorectal Cancer -- Chromosomes 8q24 and 9p24: Associations with Colorectal Cancer -- Germline Susceptibility – Gene-Environment Interactions -- Genetic Variability in Folate-Mediated One-Carbon Metabolism and Risk of Colorectal Neoplasia -- Genetic Variability in NSAID Targets and NSAID-Metabolizing Enzymes and Colorectal Neoplasia -- The Role of Chemical Carcinogens and Their Biotransformation in Colorectal Cancer -- Calcium and Vitamin D.
The last 20 years have seen a remarkable increase in knowledge of the etiology of colorectal cancer. At least three aspects are much clearer. First, known environmental agents and behaviors have been identified that increase risk (for example, diets high in meat, obesity, and smoking ) or decrease risk (for example, diets high in plant foods, aspirin, and physical activity) of colorectal cancer. Second, germline mutations in specific genes have been identified for the major inherited syndromes involving colorectal cancer (FAP, Lynch Syndrome, Juvenile Polyposis, MYH-Associated Polyposis, Li-Fraumeni Syndrome) as have variants of genes that modify the risk associated with the known environmental agents. Third, the specific tissue, cellular, and molecular disturbances that characterize the progression to different subtypes of colorectal cancer have been recently described. Genetics of Colorectal Cancer provides the most up-to-date information in each of these areas.
Oncology  .
Gastroenterology .
Epidemiology.
Cancer research.
Human genetics.
Oncology.
Gastroenterology.
Epidemiology.
Cancer Research.
Human Genetics.