MYC-driven aggressive B-cell lymphomas: biology, entity, differential diagnosis and clinical management

Qingqing Cai, L. Jeffrey Medeiros, Xiaolu Xu and Ken H. Young _

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Oncotarget. 2015; 6:38591-38616. https://doi.org/10.18632/oncotarget.5774

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Qingqing Cai1,2, L. Jeffrey Medeiros2, Xiaolu Xu1 and Ken H. Young2,3

1 Department of Medical Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China

2 Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

3 The University of Texas School of Medicine, Graduate School of Biomedical Sciences, Houston, Texas, USA

Correspondence to:

Ken H. Young, email:

Keywords: MYC, Myc protein, translocation, microRNA, lymphoma

Received: May 17, 2015 Accepted: September 04, 2015 Published: September 22, 2015


MYC, a potent oncogene located at chromosome locus 8q24.21, was identified initially by its involvement in Burkitt lymphoma with t(8;14)(q24;q32). MYC encodes a helix-loop-helix transcription factor that accentuates many cellular functions including proliferation, growth and apoptosis. MYC alterations also have been identified in other mature B-cell neoplasms and are associated with aggressive clinical behavior. There are several regulatory factors and dysregulated signaling that lead to MYC up-regulation in B-cell lymphomas. One typical example is the failure of physiological repressors such as Bcl6 or BLIMP1 to suppress MYC over-expression. In addition, MYC alterations are often developed concurrently with other genetic alterations that counteract the proapoptotic function of MYC. In this review, we discuss the physiologic function of MYC and the role that MYC likely plays in the pathogenesis of B-cell lymphomas. We also summarize the role MYC plays in the diagnosis, prognostication and various strategies to detect MYC rearrangement and expression.

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