Open AccessGenetic analysis of the 15;17 chromosome translocation associated with acute promyelocytic leukemia.
Author(s) -
Denise Sheer,
Lynne R. Hiorns,
Karina Stanley,
Peter N. Goodfellow,
Dallas M. Swallow,
S. Povey,
Nora Heisterkamp,
John Groffen,
John Stephenson,
Ellen Solomon
Publication year - 1983
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.80.16.5007
Subject(s) - chromosomal translocation , biology , acute promyelocytic leukemia , genetics , chromosome , chromosome 15 , marker chromosome , chromosome 21 , karyotype , somatic cell , breakpoint , chromosome 19 , microbiology and biotechnology , gene , retinoic acid
Somatic cell hybrids have been constructed between a thymidine kinase-deficient mouse cell line and blood leukocytes from a patient with acute promyelocytic leukemia showing the 15q+;17q- chromosome translocation frequently associated with this disease. One hybrid contains the 15q+ translocation chromosome and very little other human material. We have shown that the c-fes oncogene, which has been mapped to chromosome 15, is not present in this hybrid and, therefore, probably is translocated to the 17q- chromosome. Analysis of the genetic markers present in this hybrid has enabled a more precise localization of the translocation breakpoints on chromosomes 15 and 17. Our experiments also have enabled an ordering and more precise mapping of several genetic markers on chromosomes 15 and 17.