Chromosome imbalances in endometrial adenocarcinomas: a possible adaptation to abnormal metabolic pathways.
Chromosome studies of endometrial carcinomas show several recurrent trisomies or tetrasomies: 1 (long arm), 10, 2, 7, 12, 3 and possibly X (long arm). These chromosomes or chromosome segments carry the majority of the genes coding for enzymes of glucidic metabolism, citrate cycle, and initial steps of nucleotide synthesis. Their excess, which does not appear as a primary event in tumorigenesis, is interpreted as an adaptation of the cancer cells to abnormalities of metabolic pathways. The increase of gene copies, by chromosome duplication, would facilitate the synthesis of enzymes the activity of which is increased. If this view is correct and has a general value, it would mean that, in addition to primary chromosome changes, which may induce oncogene activation, most anomalies, which are obviously secondary, may reflect a disturbance of metabolic pathways coded by housekeeping genes.
D000230:Adenocarcinoma / Q000235:genetics* / Q000378:metabolism; D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D002877:Chromosomes, Human / Q000648:ultrastructure*; D002952:Citric Acid Cycle; D005260:Female; D006019:Glycolysis; D006801:Humans; D007621:Karyotyping; D009711:Nucleotides / Q000378:metabolism; D014594:Uterine Neoplasms / Q000235:genetics* / Q000378:metabolism
D009711:Nucleotides