Are ABL and BCR imprinted? No definitive answers, but more questions.
The apparent nonrandom contribution of the paternally-derived chromosome 9 and the maternally-derived chromosome 22 to the leukemia-specific translocation t(9;22)(q34;q11) obtained by cytogenetic analysis suggested that the two genes affected by this rearrangement, namely ABL and BCR, are imprinted. The results of recent molecular genetic studies have challenged this notion, since it was shown that both the paternal as well as the maternal BCR- and ABL-alleles may be affected by the translocation event and that both genes may be expressed from both alleles. This paper offers possible explanations for the apparent contradictory results obtained through cytogenetic and molecular genetic means. Based on the few available data concerning their allelic methylation pattern, replication behavior and expression status, as well as by referring to similar problems encountered in other genes whose imprinting status had also remained elusive for a long time, I argue that it still remains likely that ABL and BCR are imprinted.
Haas
O A
OA
Children's Cancer Research Institute (CCRI), St Anna Children's Hospital, Vienna, Austria.
D000483:Alleles; D004261:DNA Replication; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D016313:Genes, abl; D006801:Humans; D007173:Imprinting, Psychological; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics*; D008297:Male; D008745:Methylation; D010677:Philadelphia Chromosome; D014178:Translocation, Genetic
D016044:Fusion Proteins, bcr-abl