Cell
Volume 47, Issue 1, 10 October 1986, Pages 11-18
ArticleThe c-myc oncogene perturbs B lymphocyte development in Eμ-myc transgenic mice
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MicroRNA dysregulation and multi-targeted therapy for cancer treatment
2020, Advances in Biological RegulationPIM activity in tumours: A key node of therapy resistance
2018, Advances in Biological RegulationCitation Excerpt :PIM kinases are often considered ‘weak’ oncogenes and seem to be mostly effective in modulating the activity of ‘stronger’ oncogenes, such as MYC. For example, the EμMYC model of lymphoma gives rise to rapidly progressing, lethal lymphoid malignancy (Harris et al., 1988; Langdon et al., 1986) but EμPIM mice have comparably longer disease latency (Breuer et al., 1989; van Lohuizen et al., 1989). As reported for PIM1 in EμMYC lymphoma (Breuer et al., 1991), PIM2 also cooperates with MYC to accelerate lymphomagenesis and lethal disease (Allen et al., 1997).
Deletion of the transcriptional regulator TFAP4 accelerates c-MYC-driven lymphomagenesis
2023, Cell Death and Differentiation
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