On a mechanism for isochromatid 17q in a subset of Ph+ chronic myeloid leukemia patients.
A mechanism for converting human chromatid 17 into its isoforms-isochromatid 17q and isochromosome X17q--is discussed. The frequency of these isoforms in a subset of Ph+ chronic myeloid leukemia patients is traceable to singularities of the nuclear envelope of myeloid cells. When statistically interpreted, loss of tumor suppressor gene (p53) seems less significant than additive retention of genes on the q arm of 17, at least regarding evolution of clones carrying both Ph and X17q markers.
Matioli
G T
GT
USC Medical School, Los Angeles, CA 90033, USA.
D002842:Chromatids / Q000235:genetics*; D002874:Chromosome Mapping; D002886:Chromosomes, Human, Pair 17; D006801:Humans; D018404:Isochromosomes; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000145:classification / Q000235:genetics*; D008957:Models, Genetic