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Jumping translocations, a novel finding in chronic lymphocytic leukaemia
Author(s) -
Miller Cecelia R.,
Stephens Deborah,
Ruppert Amy S.,
Racke Frederick,
McFaddin Andrew,
Breidenbach Heather,
Lin HueyJen,
Waller Kathy,
Bannerman Tammy,
Jones Jeffrey A.,
Woyach Jennifer A.,
Andritsos Leslie A.,
Maddocks Kami,
Zhao Weiqiang,
Lozanski Gerard,
Flynn Joseph M.,
Grever Michael,
Byrd John C.,
Heerema Nyla A.
Publication year - 2015
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.13422
Subject(s) - chromosomal translocation , karyotype , chronic lymphocytic leukemia , breakpoint , malignancy , cytogenetics , chromosome , biology , medicine , pathology , immunology , oncology , genetics , leukemia , gene
Summary A jumping translocation ( JT ) is a rare cytogenetic aberration that can occur in haematological malignancy. It involves the translocation of the same fragment of donor chromosome onto two or more recipient chromosomes, typically in different cells. In this study, we describe the first series of chronic lymphocytic leukaemia ( CLL ) patients with JT s reported to date. Following a review of 878 CLL patient karyotypes, we identified 26 patients (3%) with 97 JT s. The most commonly occurring breakpoint in these translocations was 17p11.2. Loss of TP53 was identified prior to or at the same time as JT in 23 of 26 patients (88%). All patients eventually developed a complex karyotype. All but one patient has required treatment for CLL , with estimated median time to treatment of 11·5 months. This study establishes JT s as a recurrent abnormality found in CLL patients with aggressive disease. JT s contribute to complex karyotypes and, in many cases, are involved in chromosomal rearrangements that result in loss of the tumour suppressor gene TP53 .