Mapping of translocation breakpoints on the short arm of chromosome 19 in acute leukemias by in situ hybridization.
Non-random translocation involving the short arm of chromosome 19 are frequently observed in acute leukemias. Recent studies have shown that the 19p13 genes E2A and LYLl, both of which encode helix-loop-helix proteins, lie at two different translocation breakpoints in acute lymphoblastic leukemias (ALL). The E2A gene is involved by the t(1;19)(q23;p13) in acute pre-B-cell leukemias and the LYL1 gene is structurally altered by a t(7;19)(q34;p13) in T-cell ALL. To assess the role of these genes in other leukemia-associated translocations we mapped their locations with respect to the t(11;19)(q23;p13) and t(4;19)(q21;p13) translocation breakpoints carried by T-ALL cell lines SUP-T13 and SUP-T8a, respectively. In situ hybridization studies indicated that the E2A and LYL1 genes are physically distinct from the t(4;19) and t(11;19) breakpoints. Using these and other 19p13 translocation breakpoints as landmarks, we established a partial physical map of 19p: 19pter-E2A-INSR-LYL1-[t(4;19)]-19cen. These data should help guide molecular studies to further characterize 19p13 breakpoints and mapping of genes in this chromosomal region.
Saltman
D L
DL
Department of Pathology, Stanford University School of Medicine, California.
Mellentin
J D
JD
Smith
S D
SD
Cleary
M L
ML
D000208:Acute Disease; D002874:Chromosome Mapping; D002888:Chromosomes, Human, Pair 19; D015342:DNA Probes; D004268:DNA-Binding Proteins / Q000235:genetics; D006801:Humans; D007621:Karyotyping; D015458:Leukemia, T-Cell / Q000235:genetics*; D009693:Nucleic Acid Hybridization; D011972:Receptor, Insulin / Q000235:genetics; D014178:Translocation, Genetic; D014407:Tumor Cells, Cultured
D015342:DNA Probes; D004268:DNA-Binding Proteins; D011972:Receptor, Insulin