Premium
Novel MLL‐CBP fusion transcript in therapy‐related chronic myelomonocytic leukemia with a t(11;16) (q23;p13) chromosome translocation
Author(s) -
Satake Noriko,
Ishida Yasushi,
Otoh Yoshiko,
Hinohara Shinichi,
Kobayashi Hirofumi,
Sakashita Akiko,
Maseki Nobuo,
Kaneko Yasuhiko
Publication year - 1997
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/(sici)1098-2264(199709)20:1<60::aid-gcc9>3.0.co;2-7
Subject(s) - chromosomal translocation , fusion transcript , acute myelomonocytic leukemia , myeloid leukemia , biology , fusion gene , cancer research , leukemia , gene , fusion protein , chronic myelomonocytic leukemia , microbiology and biotechnology , polymerase chain reaction , immunology , bone marrow , genetics , myelodysplastic syndromes , recombinant dna
CBP , which is located on 16p13 and encodes a transcriptional adaptor/coactivator protein, has been shown to fuse by the t(8;16)(p11;p13) translocation to MOZ on 8p11 in acute myeloid leukemia. We found a t(11;16)(q23;p13) in a child with therapy‐related chronic myelomonocytic leukemia. Subsequent reverse transcriptase‐polymerase chain reaction and direct sequencing analyses revealed the MLL‐CBP fusion transcript in CMML cells. Because 11q23 translocations involving MLL and t(8;16) involving MOZ and CBP have been reported in therapy‐related leukemias, both the MLL and CBP genes may be targets for topoisomerase II inhibitors. Accordingly, we believe that most t(11;16)‐associated leukemias may develop in patients who have been treated with cytotoxic chemotherapy for primary malignant diseases. Genes Chromosom. Cancer 20:60–63, 1997. © 1997 Wiley‐Liss, Inc.