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Blood, Vol. 95 No. 8 (April 15), 2000:
pp. 2691-2698
Concurrent activation of a novel putative transforming gene,
myeov, and cyclin D1 in a subset of multiple
myeloma cell lines with t(11;14)(q13;q32)
Johannes W. G. Janssen,
Jan-Willem Vaandrager,
Tanja Heuser,
Anna Jauch,
Philip M. Kluin,
Erik Geelen,
P. Leif Bergsagel,
W. Michael Kuehl,
Hans G. Drexler,
Takemi Otsuki,
Claus
R. Bartram, and
Ed Schuuring
From the Institute of Human Genetics, University of Heidelberg,
Heidelberg, Germany; the Department of Pathology, Leiden University
Medical Center, Leiden, The Netherlands; the Division of Hematology and
Oncology, Department of Medicine, Weill Medical College of Cornell
University, New York, NY; the Genetics Department, Medicine Branch,
National Cancer Institute, Bethesda, MD; the DSMZ-German Collection of
Microorganisms and Cell Cultures, Department of Human and Animal Cell
Cultures, Braunschweig, Germany; and the Department of
Hygiene, Kawasaki Medical School, Kurashiki, Okayama, Japan.
Through the application of the NIH/3T3 tumorigenicity assay to DNA
from a gastric carcinoma, we have identified a novel transforming gene,
designated myeov (myeloma overexpressed gene in a subset of
t[11;14]-positive multiple myelomas). Sequence analyses did not
reveal any homology with sequences present in the GenBank, except the
deduced protein structure predicts a transmembrane localization.
Myeov was mapped to chromosome 11q13 and localized by DNA fiber
fluorescence in situ hybridization (FISH) 360-kilobase (kb) centromeric
of cyclin D1. In 3 of 7 multiple myeloma (MM) cell lines
with a t(11;14)(q13;q32) and cyclin-D1 overexpression, Northern
blot analysis revealed overexpression of myeov as well. In all
7 cell lines, the translocation breakpoint was mapped within the 360-kb
region between myeov and cyclin D1. DNA fiber FISH with
a contig of probes covering the constant region of the immunoglobulin heavy chain (IgH) revealed that exclusively in the 3 myeov-overexpressing cell lines (KMS-12, KMS-21, and XG-5),
either the 5' Eµ enhancer or the most telomeric 3' E
enhancer was juxtaposed to myeov. Although cyclin D1
overexpression represents a characteristic feature of all MM cell lines
with t(11;14), our results demonstrate aberrant expression of a second
putative oncogene in a subset of these cases, due to juxtaposition to
IgH enhancers. The clinical relevance of this dual activation remains
to be elucidated.
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