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A synovial sarcoma with a complex t(X; 18;5;4) and a break in the ornithine aminotransferase (OAT)LI cluster on Xp11.2
Author(s) -
Olde Weghuis D.,
De Leeuw B.,
Suijkerbuijk R. F.,
Van Kessel A. Geurts,
Stoepker M. E. J.,
Van Den Berg E.,
De Jong B.,
Molenaar W. M.
Publication year - 1994
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.2870090409
Subject(s) - synovial sarcoma , biology , fluorescence in situ hybridization , chromosome , microbiology and biotechnology , breakpoint , chromosomal translocation , genetics , gene , ornithine aminotransferase , plasmid , ornithine , sarcoma , pathology , medicine , amino acid , arginine
The initial cytogenetic analysis of a biphasic synovial sarcoma revealed complex anomalies involving six different chromosomes: 46,Y,t(X185;4)(p11;q11;p13;q12),t(2;5)(q35;q11). After fluorescence in situ hybridization (FISH) analysis, using chromosome X‐specific plasmid library and YAC probes, the situation appeared to be even more complex, with an insertion of part of the X chromosome short arm into the der(5)t(5;18). In spite of these complex chromosomal rearrangements, the Xp11 breakpoint could be mapped to within the ornithine aminotransferase ( OAT )LI cluster, very similar to that reported previously for the standard t(X 18)(p11;q11) in synovial sarcomas. These findings suggest common pathogenetic pathways in these cytogenetically different but morphologically similar tumors. Genes Chrom Cancer 9:288‐291 (1994). © 1994 Wiley‐Liss, Inc.
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