Non-random chromosome changes in human cancer.
Chromosome changes in human cancer cells appear to evolve by non-random losses and/or gains of particular homologues or groups. It is probable that some of the apparent losses or gains actually represent formation of new chromosome structures, which are then classified as markers or are misclassified as normal homologues. In many cancers these changes appear to continue at a high rate throughout the life of the cancer (so that in some cancers almost every cell will exhibit a different karyotype). In other cancers the rate of change may be slow or arrested so that all cells will have the same abnormal karyotype. One very common step in karyotype evolution is doubling of the entire chromosome complement (2n → 4n or more commonly, S → 2S where S is the stemline number). The 2S cells tend to replace the original stemline. Homologues which have larger amounts of concentrated blocks of heterochromatin (i.e. late replicating DNA) seem more apt to be lost.
D001943:Breast Neoplasms / Q000235:genetics; D002460:Cell Line; D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D003110:Colonic Neoplasms / Q000235:genetics; D005260:Female; D006570:Heterochromatin; D006689:Hodgkin Disease / Q000235:genetics; D006801:Humans; D007621:Karyotyping; D008175:Lung Neoplasms / Q000235:genetics; D016403:Lymphoma, Large B-Cell, Diffuse / Q000235:genetics; D008297:Male; D008545:Melanoma / Q000235:genetics; D009369:Neoplasms / Q000235:genetics*; D010051:Ovarian Neoplasms / Q000235:genetics; D011123:Polyploidy; D013274:Stomach Neoplasms / Q000235:genetics
D006570:Heterochromatin