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CD3G is within 200 kb of the leukemic t(4;II) translocation breakpoint
Author(s) -
Das Soma,
Cotter Finbarr E.,
Gibbons Barbara,
Dhut Susheela,
Young Bryan D.
Publication year - 1991
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.2870030108
Subject(s) - breakpoint , chromosomal translocation , biology , genetics , microbiology and biotechnology , gene , chromosome , restriction enzyme
The t(4; II )(q21;q23) has been associated with acute lymphocytic leukemia (ALL) especially in infants. The t(4; II) breakpoint on chromosome II is cytogenetically indistinguishable from breakpoints for other leukemia‐associated translations affecting 11q23. The molecular basis of the t(4;lI) is unknown although a number of genes have been mapped to IIq23. The CD3D, G , and E genes have been positioned proximal to the IIq23 breakpoint of the 4; II translocation while the THY I and ETSI genes have been mapped distal to this breakpoint. We report evidence that CD3G is within 200 kb of the 4; II breakpoint as observed by pulsed field gel analysis. A rearrangement of the CD3G gene has been observed in a cell line derived from a patient with the t(4;II) translocation and in a hybrid cell line containing the derivative IIq chromosome derived from this cell line, using the restriction enzymes Sacll and Clal . Similar rearrangements using Sacll were observed in 2 further patients with ALL and the t(4; II) translocation. No rearrangements in the same DNA were observed using ETSI, THY I , and Dl IS29 and a range of rare cutter restriction enzymes. CD3G thus provides a tool for the cloning and analysis of the 4; II trasnslocation, and poses a question of its possible involvement at long range with this translocation.