Extraosseous IL-6 transgenic mouse plasmacytoma sometimes lacks Myc-activating chromosomal translocation.
Extraosseous IL-6 transgenic mouse plasmacytoma sometimes lacks Myc-activating chromosomal translocation.
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骨外 IL-6 转基因小鼠浆细胞瘤有时缺乏 Myc 激活染色体易位。
DOI：
10.1002/gcc.20172
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Janz,Siegfried
中科院分区：
文献类型：
--
作者：
McNeil,Nicole;Kim,JoongSu;Ried,Thomas;Janz,Siegfried
The cellular oncogeneMYCand plasma cell growth, differentiation, and survival factor IL‐6 play critical roles in the natural history of human plasma cell neoplasms such as multiple myeloma (MM).Mycand IL‐6 also are at the center of neoplastic plasma cell transformation in BALB/c mice that carry a human IL‐6 transgene and, therefore, predictably develop plasmacytomas (PCTs). We showed previously that, much like advanced MM or human myeloma cell lines (HMCLs), in whichMYCis frequently deregulated incisbecause of complex cytogenetic aberrations juxtaposingMYCto immunoglobulin enhancers, IL‐6 transgenic PCTs commonly deregulateMycincisby chromosomal translocation, predominantly T(12;15)(Igh–Myc). In this article, we show that, analogous to primary MM in whichMYCis mostly deregulated intransby signaling pathways converging at theMYCpromoter, IL‐6 transgenic PCTs sometimes develop in the absence ofMyctranslocations, thus activatingMycintrans. We present cytogenetic and molecular evidence on two IL‐6 transgenic PCTs that contained overexpressed Myc protein but lacked T(12;15)(Igh–Myc) and two relatedMyc–‐deregulating translocations that juxtaposeMycto immunoglobulin light‐chain instead of heavy‐chain enhancers: T(6;15)(Igκ–Pvt1) and T(15;16)(Pvt1–Igλ). We conclude thatMyctranslocations are not strictly required for IL‐6‐driven PCT development in mice. IL‐6 transgenic PCTs may provide a valuable model system for elucidating bothtransandcismechanisms ofMycderegulation of great relevance forMYCderegulation in human MM. © 2005 Wiley‐Liss, Inc.
