FUSION OF PDGF RECEPTOR-BETA TO A NOVEL ETS-LIKE GENE, TEL, IN CHRONIC MYELOMONOCYTIC LEUKEMIA WITH T(512) CHROMOSOMAL TRANSLOCATION

被引:1019
作者
GOLUB, TR
BARKER, GF
LOVETT, M
GILLILAND, DG
机构
[1] HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL & ONCOL,BOSTON,MA 02115
[2] HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115
[3] UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235
[4] UNIV TEXAS,SW MED CTR,MCDERMOTT CTR,DALLAS,TX 75235
关键词
D O I
10.1016/0092-8674(94)90322-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chronic myelomonocytic leukemia (CMML) is a myelodysplastic syndrome characterized by abnormal clonal myeloid proliferation and by progression to acute myelogenous leukemia (AML). CMML thus offers an opportunity to study early genetic events in the transition to AML. A recently recognized subgroup of CMML has a t(5;12)(q33;p13) balanced translocation. We report that the consequence of the t(5;12) translocation is expression of a fusion transcript in which the tyrosine kinase domain of the platelet-derived growth factor receptor beta (PDGFR beta) on chromosome 5 is coupled to a novel ets-like gene, tel, on chromosome 12. The tel-PDGFR beta fusion demonstrates the oncogenic potential of PDGFR beta and may provide a paradigm for early events in the pathogenesis of AML.
引用
收藏
页码:307 / 316
页数:10
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