Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hilton LK, Tang J, Ben-Neriah S, et al. The double-hit signature identifies double-hit diffuse large B-cell lymphoma with genetic events cryptic to FISH. Blood. 2019;134(18):1528-1532.

ABSTRACT:

SUBMITTER:

PROVIDER: S-EPMC7844883 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Hilton LK, Tang J, Ben-Neriah S, et al. The double-hit signature identifies double-hit diffuse large B-cell lymphoma with genetic events cryptic to FISH. Blood. 2019;134(18):1528-1532.

Blood 20200401 17

PMID: 32324871

Similar Datasets

The double-hit signature identifies double-hit diffuse large B-cell lymphoma with genetic events cryptic to FISH.

Project description:High-grade B-cell lymphomas with MYC and BCL2 and/or BCL6 rearrangements (HGBL-DH/THs) include a group of diffuse large B-cell lymphomas (DLBCLs) with inferior outcomes after standard chemoimmunotherapy. We recently described a gene expression signature that identifies 27% of germinal center B-cell DLBCLs (GCB-DLBCLs) as having a double-hit-like expression pattern (DHITsig) and inferior outcomes; however, only half of these cases have both MYC and BCL2 translocations identifiable using standard breakapart fluorescence in situ hybridization (FISH). Here, 20 DHITsig+ GCB-DLBCLs apparently lacking MYC and/or BCL2 rearrangements underwent whole-genome sequencing. This revealed 6 tumors with MYC or BCL2 rearrangements that were cryptic to breakapart FISH. Copy-number analysis identified 3 tumors with MYC and 6 tumors with MIR17HG gains or amplifications, both of which may contribute to dysregulation of MYC and its downstream pathways. Focal deletions of the PVT1 promoter were observed exclusively among DHITsig+ tumors lacking MYC translocations; this may also contribute to MYC overexpression. These results highlight that FISH fails to identify all HGBL-DH/THs, while revealing a range of other genetic mechanisms potentially underlying MYC dysregulation in DHITsig+ DLBCL, suggesting that gene expression profiling is more sensitive for identifying the biology underlying poor outcomes in GCB-DLBCL.

| S-EPMC6839951 | biostudies-literature

Reply to Soman et al, Alffenaar et al, Metcalfe et al, and Raoult.