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Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE112211 | GEO | 2018/05/29

REPOSITORIES: GEO

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Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response (CAL1 vs PMDC05)

Project description:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare skin-tropic hematological malignancy of uncertain pathogenesis and poor prognosis. We examined 118 BPDCN cases for cytomorphology, MYC locus rearrangement, and MYC expression. Sixty-two (53%) and 41 (35%) showed the classic and immunoblastoid cytomorphology, respectively. Forty-one (38%) MYC+BPDCN (positive for rearrangement and expression) and 59 (54%) MYC-BPDCN (both negative) cases were identified. Immunoblastoid cytomorphology was significantly associated with MYC+BPDCN. All examined MYC+BPDCNs were negative for MYB/MYBL1 rearrangement (0/36). Clinically, MYC+BPDCN showed older onset, poorer outcome, and localized skin tumors more commonly than MYC-BPDCN. MYC was demonstrated by expression profiling as one of the clearest discriminators between CAL-1 (MYC+BPDCN) and PMDC05 (MYC-BPDCN) cell lines, and its shRNA knockdown suppressed CAL-1 viability. Inhibitors for bromodomain and extraterminal protein (BETis) and aurora kinases (AKis) inhibited CAL-1 growth more effectively than PMDC05. We further showed that a BCL2 inhibitor was effective in both CAL-1 and PMDC05, indicating that this inhibitor can be used to treat MYC-BPDCN, to which BETis and AKis are probably less effective. Our data will provide a rationale for the development of new treatment strategies for patients with BPDCN in accordance with precision medicine.

2018-05-29 | GSE112209 | GEO

Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response (CAL-1, JQ1 treatment)

2018-05-29 | GSE112210 | GEO

Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response

Project description:Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response

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Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response (CAL1 vs PMDC05)

Project description:Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response (CAL1 vs PMDC05)

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Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response (CAL-1, JQ1 treatment)

Project description:Recurrent 8q24 rearrangement in BPDCN: association with immunoblastoid cytomorphology, MYC expression, and drug response (CAL-1, JQ1 treatment)

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Chromosome 8q24-Associated Cancers and MYC.

Project description:Genome-wide association studies (GWAS) have successfully identified common polymorphisms that are strongly associated with many traits, including cancer. A gene desert located on chromosome 8q24 is associated with multiple cancer types. One of the closest genes is the MYC proto-oncogene. Investigations are now turning toward a mechanistic understanding of these (and other) risk loci. Recent studies demonstrate that the 8q24 loci are enhancers and that they physically interact with MYC. A still unresolved issue is the absence of a consistent association between genotype status at the risk loci and steady-state MYC expression levels in adult human tissues. Clarifying the function of the 8q24 variants and their link to MYC regulation by further in vivo and in vitro functional studies will allow a deeper understanding of the mechanisms underlying human cancer development.

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Long-range enhancers on 8q24 regulate c-Myc.

Project description:Recent genomewide association studies have found multiple genetic variants on chromosome 8q24 that are significantly associated with an increased susceptibility to prostate, colorectal, and breast cancer. These risk loci are located in a "gene desert," a few hundred kilobases telomeric to the Myc gene. To date, the biological mechanism(s) underlying these associations remain unclear. It has been speculated that these 8q24 genetic variant(s) might affect Myc expression by altering its regulation or amplification status. Here, we show that multiple enhancer elements are present within this region and that they can regulate transcription of Myc. We also demonstrate that one such enhancer element physically interacts with the Myc promoter via transcription factor Tcf-4 binding and acts in an allele specific manner to regulate Myc expression.

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Expression analysis of prostate tissue on locus 8q24

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