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MLL amplification in myeloid leukemias: A study of 14 cases with multiple copies of 11q23
Author(s) -
Michaux Lucienne,
Wlodarska Iwona,
Stul Michel,
Dierlamm Judith,
Mugneret Francine,
Herens Christian,
Beverloo Berna,
Verhest Alain,
VerellenDumoulin Christine,
Verhoef Gregor,
Selleslag Dominik,
Madoe Vincent,
Lecomte Marianne,
Deprijck Bernard,
Ferrant Augustin,
Delannoy André,
Marichal Sabine,
Duhem Caroline,
Dicato Mario,
Hagemeijer Anne
Publication year - 2000
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 - 10.1002/1098-2264(2000)9999:9999<::aid-gcc1003>3.0.co;2-u
Subject(s) - biology , fluorescence in situ hybridization , southern blot , gene duplication , comparative genomic hybridization , chromosome , myeloid , breakpoint , malignancy , cancer research , gene , karyotype , cytogenetics , microbiology and biotechnology , in situ hybridization , genetics , gene expression
We here report the clinical, cytogenetic, fluorescence in situ hybridization (FISH), and Southern blot data on 14 patients with a myeloid malignancy and structural aberration of chromosome band 11q23 associated with overrepresentation or amplification of the MLL gene. The number of copies of MLL varied from three (two cases) to a cluster consisting of multiple hybridization spots. Together with previous reports, available data indicate that amplification of 11q23/ MLL is a recurrent genetic change in myeloid malignancy. It affects mainly elderly patients and is often associated with dysplastic bone marrow changes or with complex karyotypic aberrations, suggestive of genotoxic exposure. It is associated with a poor prognosis. In addition, FISH analysis of nine cases with additional 11q probes showed that the overrepresented chromosomal region is generally not restricted to MLL , and Southern blot analysis indicated that amplification does not involve a rearranged copy of this gene. The significance of MLL amplification and the mechanisms by which it could play a role in leukemogenesis and/or disease progression remain to be elucidated. Genes Chromosomes Cancer 29:40–47, 2000. © 2000 Wiley‐Liss, Inc.