The segregation of cancer-causing genes in human populations.
Cancer can arise through genetic damage of a variety of sorts, including recessive and dominant mutations, large chromosomal rearrangements, and the inability of cells to repair damaged DNA. Many of these events can be studied by standard methods of genetic analysis and thereby furnish the means to localize the gene to a specific region in the human genome. However, conventional methods of segregation analysis cannot provide the molecular and cellular understanding of the process of gene action essential to informed intervention. Here, recent advances in molecular biology, immunology and biochemistry hold promise of providing the understanding of how normal cells control their replication and why cancer cells do not. Heretofore these techniques have been largely restricted to modest-sized studies, but the requisite assays have now reached a level of development that makes practicable large clinical and population-based studies. Collectively, through these rapidly evolving techniques, we may eventually achieve the acquisition of new methods of prevention, diagnosis and therapy, and a better awareness of the events that order the lives of our cells.
Schull
W J
WJ
University of Texas Health Science Center, Genetics Center, Houston 77225.
D005190:Family; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D009154:Mutation / Q000235:genetics; D009369:Neoplasms / Q000235:genetics*