Lessons from Using Genetically Engineered Mouse Models of MYC-Induced Lymphoma

被引:3
|
作者
Winkler, Rene [1 ,2 ]
Piskor, Eva-Maria [1 ]
Kosan, Christian [1 ]
机构
[1] Friedrich Schiller Univ Jena, Ctr Mol Biomed CMB, Dept Biochem, D-07745 Jena, Germany
[2] Josep Carreras Leukaemia Res Inst IJC, Campus ICO Germans Trias & Pujol, Badalona 08916, Spain
关键词
MYC; B-cells; lymphoma; E mu-Myc transgene; genetically engineered mouse models; B-CELL LYMPHOMAGENESIS; C-MYC; TUMOR-SUPPRESSOR; DRIVEN LYMPHOMAGENESIS; GERMINAL CENTER; IN-VIVO; TRANSCRIPTIONAL REGULATION; HAPLO-INSUFFICIENT; PROTEIN-SYNTHESIS; INDUCED APOPTOSIS;
D O I
10.3390/cells12010037
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oncogenic overexpression of MYC leads to the fatal deregulation of signaling pathways, cellular metabolism, and cell growth. MYC rearrangements are found frequently among non-Hodgkin B-cell lymphomas enforcing MYC overexpression. Genetically engineered mouse models (GEMMs) were developed to understand MYC-induced B-cell lymphomagenesis. Here, we highlight the advantages of using E mu-Myc transgenic mice. We thoroughly compiled the available literature to discuss common challenges when using such mouse models. Furthermore, we give an overview of pathways affected by MYC based on knowledge gained from the use of GEMMs. We identified top regulators of MYC-induced lymphomagenesis, including some candidates that are not pharmacologically targeted yet.
引用
收藏
页数:28
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