Translocation (5;10)(q22;q24) in a case of acute lymphoblastic leukemia.
The activation of genes important to acute lymphoblastic leukemia (ALL) may be evidenced by somatically acquired chromosomal translocations found recurrently in different patient subgroups. It is for this reason that research efforts have focused on the molecular dissection of recurring chromosomal rearrangements. However, even though a large number of leukemia-causing genes have been identified, the genetic basis of many ALL cases remains unknown. We and others have reasoned that novel translocations found in the leukemic cells of ALL patients may mark the location of more frequent gene rearrangements that are otherwise hidden submicroscopically within normal or complex karyotypes. Towards this end, we here describe the first reported association of a t(5;10)(q22;q24) with adult ALL. Fluorescence in situ hybridization (FISH) and Southern blot hybridization studies have eliminated likely involvement of the candidate genes APC and MCC on chromosome 5, and PAX2, TLX1, and NFKB2 on chromosome 10. Results further suggest that the breakpoint on chromosome 5 lies centromeric of APC and the chromosome 10 breakpoint is centromeric of PAX2. The genomic regions disrupted by this t(5;10)(q22;q24) have not previously been associated with leukemia.
Cancer Genetics Research Group, Department of Pathology, Christchurch School of Medicine & Health Sciences, PO Box 4345, University of Otago, Christchurch, New Zealand.
Sheryl M
SM
Gough
Suzanne M
SM
Benjes
Margaret
M
McDonald
David
D
Heaton
Peter
P
Ganly
Christine M
CM
Morris
D001854:Bone Marrow Cells / Q000473:pathology; D002871:Chromosome Banding; D002874:Chromosome Mapping; D002879:Chromosomes, Human, Pair 10; D002895:Chromosomes, Human, Pair 5; D006801:Humans; D008297:Male; D008677:Metaphase; D008875:Middle Aged; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000473:pathology; D014178:Translocation, Genetic