Ask about this productRelated genes to: Rad21 antibody
- Gene:
- RAD21 NIH gene
- Name:
- RAD21 cohesin complex component
- Previous symbol:
- -
- Synonyms:
- KIAA0078, hHR21, SCC1
- Chromosome:
- 8q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-12
- Date modifiied:
- 2019-04-23
Related products to: Rad21 antibody
Related articles to: Rad21 antibody
- Acute erythroid leukemia (AEL) or AML-M6 predominantly affects older adults and is rare in childhood. Compared with other AML subtypes, AEL remains relatively understudied because of its rarity. We established LS-CHM, a novel AEL cell line derived from the ascitic fluid of a patient with congenital leukemia. Interestingly, leukemic cells persisted in the ascitic fluid even after successful eradication from the bone marrow and extramedullary sites. - Source: PubMed
Publication date: 2026/04/28
Sitaula PrasikshaGadgeel ManishaEdwards HollyPolin LisaKushner JuiwannaDzinic Sijana HWhite KathrynGe YubinTaub Jeffrey WGurdziel KatherineDlugas HunterDyson GregArlene RozzelleCarr DavidMoussa OmarSavaşan Süreyya - Olaparib is registered for use in ovarian, breast, pancreatic and prostate cancers with a BRCA1/2 mutation and/or mutations in other homologous recombination deficiency (HRD) genes. HRD gene mutations are also found in other cancer types, and these cancers may also benefit from olaparib therapy. We aimed to evaluate the efficacy of olaparib in advanced cancers harboring a (likely) pathogenic germline or somatic mutation in a gene involved in homologous recombination (HR). - Source: PubMed
Publication date: 2026/05/08
Joris SDenys HCollignon JRasschaert Mde Roodenbeke D TDuhoux F PCanon J LTejpar SMebis JDecoster LAftimos PDe Grève J - Extrachromosomal circular DNAs (eccDNAs) have been discovered in various species and play a significant role in cancer development. However, our understanding of their chromosomal biogenesis is limited. Here, we identified a correlation between eccDNA generation and the density of transcription regulatory elements, such as enhancers and promoters. We find that the regulators of enhancer-promoter interactions, including RAD21, LDB1 and YY1, may contribute to eccDNA production, with only a modest effect from transcriptional activity itself. The BRD4 inhibitor JQ1 reduces eccDNA production, while the HDAC inhibitor TSA induces an increase of eccDNAs. This TSA-induced effect can be rescued by the TSA antagonist, ITSA. The generation of eccDNA positively correlates with the density of R loops. Furthermore, large eccDNA breakpoints are found to be coordinated with TAD boundaries and inclined to align at enhancers and promoters. Our study suggests that eccDNAs are more frequently detected from regulatory regions in the genome, consistent with their generation being associated with enhancer-promoter dynamics. - Source: PubMed
Publication date: 2026/04/30
Gu YuxiSong YidanWang ShuhuaWang YueZhao ZhiheLiu Jun - Hemophagocytic lymphohistiocytosis (HLH) is a rare but fatal complication of acute myeloid leukemia (AML), and contemporary data on its clinical and genomic correlates remain sparse. We retrospectively identified 19 adults with AML who developed HLH across 3 Mayo Clinic sites (2020-2024) and compared them with 73 patients with AML without HLH. HLH occurred at a median of 34 days from AML diagnosis (range, 0-472) and was associated with fever, multiorgan dysfunction, and rapidly rising biomarkers. Morphologic hemophagocytosis was observed in only 18% of cases, underscoring its poor sensitivity. HLH was associated with markedly inferior overall survival (median, 5.7 vs 14.8 months, = .005), including within adverse risk and -mutated AML subsets. When modeled as a time-dependent covariate, HLH remained strongly associated with inferior survival (hazard ratio [HR], 3.9; < .001). Genomic profiling demonstrated enrichment of (58%), (16%), and (11%) mutations, with tumor suppressor and/or DNA damage repair pathway alterations in 68% vs 34% of controls ( = .009). On multivariable analysis, HLH (HR, 3.1; = .003) and adverse-risk cytogenetics (HR, 2.2; = .040) independently predicted worse survival. Age of ≥65 years was associated with accelerated HLH onset (14 vs 84 days, = .032) and higher mortality (HR, 13.4; = .005). All patients received high-dose corticosteroids; some received tocilizumab or ruxolitinib, and none received etoposide. Despite diverse leukemia-directed therapies, only 3 patients achieved long-term survival. Collectively, these findings indicate that AML-associated HLH arises predominantly in older patients with genomically unstable leukemias, portends poor prognosis, and warrants biomarker-guided surveillance and improved targeted immunomodulatory strategies with antileukemic therapy. - Source: PubMed
Publication date: 2026/03/26
Zarka JabraCsizmar Clifford MMina SyedaHickman AshleyAndres EricaMatin AasiyaGangat NaseemaBadar TalhaMangaonkar Abhishek APatnaik Mrinal MLitzow Mark RHogan William JTorghabeh Mehrdad HefaziForan James MYi Cecilia AranaShah Mithun VBegna Kebede HAl-Kali ArefAlkhateeb Hassan BSaliba Antoine N - Penile squamous cell carcinomas (SCC) develop via a transforming human papillomavirus (HPV) infection or independent of HPV. We assessed the role of copy-number alterations (CNA) affecting chromosome arms, oncogenes and tumor suppressor genes (TSG) in 121 penile SCC (52% HPV-associated and 48% HPV-independent) using shallow whole-genome sequencing. CNA were common and complex, with frequent co-occurrences. Neither etiology had exclusive CNA. Arm-level changes included gains of 3q and 8q (48% each), 1q (36%), 1p (26%), 9q (36%) and 9p (31%) and losses of 19p (48%), 8p (44%), 1q (36%), and 3p (33%) of SCC. Oncogene amplifications included broad 3q alterations affecting TP63, SOX2, PIK3CA (43%) and 8q including MYC, HEY, RAD21 (40%). Homozygous deletions affected WRN, NRG1 (8p;29%), BAP1, FANCD2, VHL (3p) and ARHGEF12, BCL9L, ATM (11q22/23) in 19% each. CNA affecting TP53, CDKN2A/B, CDKN1A/B, and RB1 occurred in similar numbers in HPV-induced (16%) and HPV-independent SCC (24%) quite in contrast to TSG somatic mutations exclusive to HPV-independent SCC associated with lichenoid dermatoses. HPV-induced SCC had more 1p amplifications (adj. p=.003), while HPV-independent SCC carried more 8q full-arm gains (adj. p=.00003), amplifications of oncogenes on 8q (adj. p=.006) including MYC and homozygous deletions of 8p (adj. p=.03). MYC amplifications coincided with an increased fraction of genome altered indicative for genomic instability (p=.00001). EGFR amplifications dominated in HPV-negative wild-type TP53/CDKN2A SCC without dermatoses. Together with mutations in PIK3CA, HRAS and FGFR3 they represent an alternative RTK/Ras/PI3K-mediated carcinogenesis pathway. More than half of advanced SCC irrespective of etiology harbored targetable CNA such as EGFR, MTAP, ATM. - Source: PubMed
Publication date: 2026/04/22
Ermakov Mikhail SRegauer SigridKashofer Karl