Expression of DHX32 in lymphoid tissues

Liang

et al. 2009

J Exp Clin Cancer Res

Section: Discussionmentioning

confidence: 99%

Up-regulation and clinical relevance of novel helicase homologue DHX32 in colorectal cancer

Liang

et al. 2009

J Exp Clin Cancer Res

“…DHX32 is an RNA helicase that is reported to associate with the acute lymphoblastic leukemia [53,54]. Notably, its dysregulation is believed to contribute to carcinogenesis [55]. RAD51B (rs2025009) encodes one of the RAD51 paralogs that participate in DNA repair, and the polymorphisms in the gene and the gene inactivation through chromosome translocation have been demonstrated to be linked to AML, breast cancer, head and neck cancer [56][57][58][59].…”

Section: Discussionmentioning

confidence: 99%

Iterative feature selection method to discover predictive variables and interactions for high-dimensional transplant genomic data

Vierra-Green²,

Spellman³

et al. 2019

Preprint

After allogeneic hematopoietic stem cell transplantation (allo-HCT), donor-derived immune cells can trigger devastating graft-versus-host disease (GVHD). The clinical effects of GVHD are well established; however, genetic mechanisms that contribute to the condition remain unclear.Candidate gene studies and genome-wide association studies have shown promising results, but they are limited to a few functionally derived genes and those with strong main effects. Transplantrelated genomic studies examine two individuals simultaneously as a single case, which adds additional analytical challenges. In this study, we propose a hybrid feature selection algorithm, iterative Relief-based algorithm followed by a random forest (iRBA-RF), to reduce the SNPs from the original donor-recipient paired genotype data and select the most predictive SNP sets in association with the phenotypic outcome in question. The proposed method does not assume any main effect of the SNPs; instead, it takes into account the SNP interactions. We applied the iRBA-RF to a cohort (n=331) of acute myeloid leukemia (AML) patients and their fully 10 of 10 (HLA-A, -B, -C, -DRB1, and -DQB1) HLA-matched healthy unrelated donors and assessed two casecontrol scenarios: AML patients vs healthy donor as case vs control and acute GVHD group vs non-GVHD group as case vs control, respectively. The results show that iRBA-RF can efficiently reduce the size of SNPs set down to less than 0.05%. Moreover, the literature review showed that the selected SNPs appear functionally involved in the pathologic pathways of the phenotypic diseases in question, which may potentially explain the underlying mechanisms. This proposed method can effectively and efficiently analyze ultra-high dimensional genomic data and could help provide new insights into the development of transplant-related complications from a genomic perspective.

J Cellular Molecular Medi

“…12 The multiplication and self-renewal of primary human CD34+ cells can also be highly accelerated by NUP98-DDX10. 13 Dysregulation of DDX32 expression has been demonstrated in lymphoid neoplasms, 14,15 suggesting that this gene may contribute to carcinogenesis. These limited studies reveal that some members of the human RNA helicase family may play diverse biological roles in haematologic malignancies.…”

mentioning

confidence: 99%

ETS1 and SP1 drive DHX15 expression in acute lymphoblastic leukaemia

Chen

Cai

et al. 2018

DHX15 plays a role in leukaemogenesis and leukaemia relapse. However, the mechanism underlying the transcriptional regulation of DHX15 in ALL has not been elucidated. Our present study aimed to explore the functional promoter region of DHX15 and to investigate the transcription factors controlling the transcription of this gene. A luciferase assay performed with several truncated constructs identified a 501‐bp region as the core promoter region of DHX15. Site‐directed mutagenesis, electrophoretic mobility shift and chromatin immunoprecipitation assays showed that ETS1 and SP1 occupied the DHX15 promoter. Furthermore, knockdown of ETS1 and SP1 resulted in suppression of DHX15, whereas the overexpression of these genes led to up‐regulation of DHX15. Interestingly, in samples obtained from patients with ALL at diagnosis, both ETS1 and SP1 correlated positively with DHX15 expression. Additionally, differences in methylation of the DHX15 core promoter region were not observed between the patients and controls. In conclusion, we identified the core promoter region of DHX15 and demonstrated that ETS1 and SP1 regulated DHX15 expression in ALL.