Abstract:
:The t(5;12) translocation identified in patients with chronic myelomonocytic leukemia (CMML) encodes a TEL/platelet-derived growth factor receptor beta (PDGFRbeta) fusion protein. A key hypothesis for how the TEL/PDGFRbeta fusion protein would function as an oncogene is that it represents a constitutively active version of the normal PDGFRbeta. A link between the function of the t(5;12)-encoded TEL/PDGFRbeta fusion protein and Myc expression is suggested by the fact that Myc is induced by PDGF and is essential for entry of cells into the S phase of the cell cycle. We here show that the kinase activity of TEL/PDGFRbeta is necessary for Ba/F3 cells to acquire interleukin-3 (IL-3) independence and that, in contrast to their untransfected counterpart, Ba/F3 cells stably transfected with TEL/PDGFRbeta maintain a high level of Myc expression after removal of IL-3. Using dominant negative mutants of Myc, we show that a threshold of active Myc is essential for TEL/PDGFRbeta to transform Ba/F3 and Rat-1 cells. The findings that the kinase activity of TEL/PDGFRbeta and a threshold of active Myc are involved in TEL/PDGFRbeta transformation may allow for the development of therapeutic strategies in patients with t(5;12)+ CMML using specific inhibitors of the PDGFRbeta kinase as well as compounds designed to interfere specifically with Myc.
journal_name
Bloodjournal_title
Bloodauthors
Bourgeade MF,Défachelles AS,Cayre YEsubject
Has Abstractpub_date
1998-05-01 00:00:00pages
3333-9issue
9eissn
0006-4971issn
1528-0020journal_volume
91pub_type
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