1988
DOI: 10.1182/blood.v71.1.30.30
|View full text |Cite
|
Sign up to set email alerts
|

Alteration and abnormal expression of the c-myc oncogene in human multiple myeloma

Abstract: 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 o… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

0
28
0
11

Year Published

1992
1992
2005
2005

Publication Types

Select...
6

Relationship

0
6

Authors

Journals

citations
Cited by 100 publications
(39 citation statements)
references
References 32 publications
0
28
0
11
Order By: Relevance
“…Given that c-myc may regulate both proliferation and apoptosis, stimulation of cell growth by myc deregulation in the IL-6-dependent B9 hybridoma seems to require the presence of cytokines to prevent apoptosis (Sabourin & Hawley, 1990). Although the myc gene in a majority of human MM, including the U-266-1970/U-266-1984 pair of cell lines, seems to be structurally normal, high levels of myc mRNA and protein in MM cell lines have been reported (Selvanayagam et al, 1988;Greil et al, 1991;Jernberg Wiklund et al, 1992b;Paulin et al, 1996). The requirement of appropriate survival factors, i.e.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Given that c-myc may regulate both proliferation and apoptosis, stimulation of cell growth by myc deregulation in the IL-6-dependent B9 hybridoma seems to require the presence of cytokines to prevent apoptosis (Sabourin & Hawley, 1990). Although the myc gene in a majority of human MM, including the U-266-1970/U-266-1984 pair of cell lines, seems to be structurally normal, high levels of myc mRNA and protein in MM cell lines have been reported (Selvanayagam et al, 1988;Greil et al, 1991;Jernberg Wiklund et al, 1992b;Paulin et al, 1996). The requirement of appropriate survival factors, i.e.…”
Section: Discussionmentioning
confidence: 99%
“…Stimulation of growth by c-myc deregulation may, at least in part, explain the requirement of growth and survival factors or endogenous expression of Bcl-2 to prevent myc-induced apoptosis in these cells (Bissonnette et al, 1992;Harrington et al, 1994). Although c-myc translocations are rare in human MM, high levels of myc mRNA and protein expression have been consistently observed, suggesting an inappropriate transcription of this gene or prolonged turnover of mRNA and/or protein in MM (Selvanayagam et al, 1988;Greil et al, 1991;Jernberg Wiklund et al, 1992b;Paulin et al, 1996). However, the relative role of a deregulated c-myc in the proliferation and survival of MM has not been studied.…”
mentioning
confidence: 99%
“…Our studies suggest that t(11;14) occurs in malignancies of mature B lymphocytes, with morphology and markers (strong SmIg, CD38 +'-) close to those of plasma cells in many cases. In this respect the occurrence of t(11;14) in myeloma and plasma cell leukemia, which represent R cells at late stages of differentiation, may be relevant (Dewald et al, 1985;Selvanayagam et al, 1987;Gould et al, 1988). The translocation t (11;14) does not appear to be associated with poor prognosis, since it is present in both the more aggressive disease types such as B-PLL and plasma cell leukemia and those with a much less aggressive clinical course such as SLVL (Mulligan et al, 1991), although longer follow-up is needed for the group of cases included here.…”
Section: Discussionmentioning
confidence: 99%
“…A third translocation, t(11;14)(q13;q32), has been described in a wider spectrum of diseases and involves a putative oncogene, BCLl, which maps to chromosome band llq13 (Tsujimoto et al, 1984(Tsujimoto et al, , 1986Kluin and Van Krieken, 1991). The translocation has been reported in diffuse small-and large-cell lymphomas, multiple myeloma, and plasma cell leukemias (Dewald et al, 1985;Selvanayagam et al, 1987;Gould et al, 1988Ince et al, 1988Koduru et al, 1989Rodriguez et al, 1989Athan et al, 1991). More recently, there is evidence that this abnormality may delineate particular subtypes of non-Hodgkin lymphoma (NHL), such as intermediate lymphocytic and centrocytic (Medeiros et al, 1990;Rimokh et al, 1990;Wotherspoon et al, 1990;Frizzera et al, 1991;Leroux et al, 1991;Williams et al, 1990), designations that encompass mantle-cell-derived lymphomas (Raffeld and Jaffe, 1991).…”
Section: Introductionmentioning
confidence: 99%
“…If structural abnormalities corresponding to loss of chromosome material, such as partial deletions or isochromosomes, are pooled with monosomies, the frequency of loss of heterozygosity is increased and becomes as high as 34.8% (16/46) for chromosome 13 and 19.6% (9/46) for the short arm of chromosome 17. Rearrangements and amplification of the protooncogene MYC have been reported in MM (Bakkus et al, 1990; Gazdar et al, 1986Selvanayagam et al, 1988 and in PCL (Siimegi et al, 1985), as well as point mutations of the NRAS and KRAS genes (Neri et al, 1989;Paquette et al, 1990). Rearrangements of the IL6 gene were infrequent and those of the IL6 receptor gene were absent in MM (Fielder et al, 1990).…”
Section: Discussionmentioning
confidence: 99%