Alteration and abnormal expression of the c-myc oncogene in human multiple
myeloma
P Selvanayagam, M Blick, F Narni, P van Tuinen, DH Ledbetter, R Alexanian, GF Saunders and B Barlogie
Department of Hematology, University of Texas System Cancer Center, M. D.
Anderson Hospital and Tumor Institute, Houston 77030.
Structural alterations of the c-myc oncogene in human Burkitt's lymphoma
and mouse plasmacytoma suggest that this oncogene is involved in several B
cell neoplasms. The possibility of c-myc alterations in human myeloma has
not been explored, probably because the low proliferative activity
characteristic of this tumor impairs the propagation of representative cell
lines for the performance of adequate cytogenetic studies. This report
describes alterations in the c-myc locus with concomitant elevated
expression of mRNA in the tumor cells of two of 37 patients with multiple
myeloma. In one case, somatic cell hybrid studies revealed that the cloned
rearranged DNA was entirely derived from chromosome 8, thus indicating a
novel mechanism of c-myc activation different from that in Burkitt's
lymphoma. Seven other patients exhibited five- to 12-fold overexpression of
c-myc RNA when compared with normal marrow cells. Elevated mRNA expression
in about one fourth of our patients suggests that the c-myc oncogene has a
pathogenetic role in the evolution of multiple myeloma.
Volume 71,
Issue 1,
pp. 30-35,
01/01/1988
Copyright © 1988 by The American Society of Hematology
