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Mapping of translocation breakpoints on the short arm of chromosome 19 in acute leukemias by in situ hybridization
Author(s) -
Saltman David L.,
Mellentin Julia D.,
Smith Stephen D.,
Cleary Michael L.
Publication year - 1990
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.2870020402
Subject(s) - chromosomal translocation , breakpoint , biology , gene , chromosome , genetics , comparative genomic hybridization , microbiology and biotechnology
Non‐random translocations involving the short arm of chromosome 19 are frequently observed in acute leukemias. Recent studies have shown that the 19p13 genes E2A and LYL1 , 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), t(11;19)]‐19cen. These data should help guide molecular studies to further characterize 19p13 breakpoints and mapping of genes in this chromosomal region.