A chromosomal hypothesis of oncogenesis.
A chromosomal theory of cancer is advanced, based on accrued knowledge of nonrandom chromosome changes in human cancer. Proposed here is that the key cytogenetic event in oncogenesis involves chromosome rearrangement. Through breakage, chromosomes are rearranged. The rearrangement may be a translocation, inversion, insertion, or deletion. This removes one segment of a chromosome (segment A) from continuity with another segment (segment B). Segment A initially plays a role in embryogenesis and then normally is suppressed by segment B. When segment A is no longer suppressed through rearrangement by segment B, its malignant potential becomes evident. The nature of segment A is unique to each cell and tissue type. Segment A, which may be a proto-oncogene, is responsible, when derepressed, for cell proliferation, i.e., neoplasia. This general hypothesis of oncogenesis is consistent with current views and facts.
D002455:Cell Division; D002869:Chromosome Aberrations; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000139:chemically induced / Q000235:genetics*; D009381:Neoplasms, Radiation-Induced; D009857:Oncogenes; D000090063:Proto-Oncogene Mas; D014178:Translocation, Genetic