Blood: Genomics and Epigenetic Analysis of The Subtypes of Cell Lymphoma

Set cellslymphoma(MCL) are mature B-cell tumors, initially driven by CCND1 rearrangement, with two molecular subtypes, conventional (cMCL) and non-lymph node leukemia (nnMCL), which have different clinical biological behaviorsin order to determine the genetic/epigenetic changes that determine this diversity, the researchers analyzed 82 MCL samples (74% cMCL, 26% nnMCL) using genome-wide sequencing (61 cases) and exosome sequencing (21 cases) combined with transcription groups and DNA methylation spectraanalysis found that open and active chromatin at the gene base of the main translocation cluster may promote t (11; 14) (q13; 32), thus modifying the 3D structure of the area involvedThis translocation is obtained mainly in rag-mediated precursor B cells in two MCL subtypes, while 8% of the cases occur in AID-mediated mature B cellsThe researchers identified new recurrent MCL-driven genes, including CDKN1B, SAMHD1, BCOR, SYNE1, HNRNPH1, SMARCB1, and DAZAP1compound structure changes appear as the associated early carcinogenic mechanism of MCL targeting key driving genesFracture fusion bridge cycle and translocation activate cancer genes (BMI1, MIR17HG, TERT, MYC and MYCN) to produce gene amplification and refactoring regulatory regionsCMCL carries significantly more structural variation, copy number variation and driving gene change than nnMCL, but cMCL does not occur at-M mutation, and TP53 and TERT variation are enriched in nnMCLSeveral driven genes have an effect on the prognosis, but only TP53 and MYC distortion can increase prognosticsignificanity independently of genetic complexityin general, patients with different clinical advances can be distinguished by increased genomic complexity and changes in fracture fusion bridge circulation and DNA methylation