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Extrachromosomal gene amplification in acute myeloid leukemia; Characterization by metaphase analysis, comparative genomic hybridization, and semi‐quantitative PCR
Author(s) -
Mohamed A. N.,
Macoska J. A.,
Kallioniemi A.,
Kallioniemi O.P.,
Waldman F.,
Ratanatharathorn V.,
Wolman S. R.
Publication year - 1993
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.2870080308
Subject(s) - extrachromosomal dna , myeloid leukemia , biology , oncogene , metaphase , gene duplication , comparative genomic hybridization , myeloid , cancer research , gene , microbiology and biotechnology , in situ hybridization , chromosome , leukemia , polymerase chain reaction , genetics , genome , gene expression , cell cycle
A case of acute myeloid leukemia (M‐3) with complex karyotypic aberrations and double minute (dmin) chromosomes is presented. The patient had no history of prior exposure to mutagenic or carcinogenic agents or of other malignancies. She died from CNS involvement six weeks after the initial diagnosis. We used comparative genomic hybridization to identify the amplified sequences presumed to represent the dmin of the leukemic cells; the tumor/normal ratios indicated increased signal intensity at 8q24. This localization prompted investigation by semi‐quantitative PCR that revealed amplification of the MYC oncogene. The extent of chromosome aberrations and the oncogene amplification, both linked with poor prognosis, may relate to the rapid course of this patient's disease. © 1993 Wiley‐Liss, Inc.