Ask about this productRelated genes to: DNMT3a antibody
- Gene:
- DNMT3A NIH gene
- Name:
- DNA methyltransferase 3 alpha
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-15
- Date modifiied:
- 2019-04-23
Related products to: DNMT3a antibody
Related articles to: DNMT3a antibody
- Clonal hematopoiesis (CH) - the expansion of genetic variants in blood - is a prime example of somatic evolution. Although it often precedes malignant transformation, many aspects of this process remain unknown. We show that a model of polyclonal competition, in which selectively-advantaged clones continually appear and compete, explains observed CH dynamics throughout human life. We quantify the fitness distribution and occurrence rate of clonal expansions using either variant trajectories or HSC genetic heterogeneity. Inferences on both data converge. Approximately three fit clones enter the HSC pool per year, yet rarely more than five achieve >1.5% frequency throughout life. The fittest clones emerge predominantly later in life in accordance with a multistep evolutionary process. DNMT3A-variants were enriched for single-hit clones, whereas TET2, ASXL1, JAK2, SF3B1, and SRSF2 showed enrichment for multi-hit evolution. These findings suggest precursors of hematological malignancies are identifiable prior to transformation and may facilitate early intervention strategies. - Source: PubMed
Publication date: 2026/05/05
Mon Père Nathaniel VTerenzi FrancescoWerner Benjamin - Large vessel vasculitides (LVV), including giant cell arteritis (GCA) and Takayasu arteritis (TAK), share common features such as inflammation of large sized arteries but differ in several key aspects, including age of onset and pathogenic mechanism. This narrative review gives an update of recent insights into pathogenesis of GCA and TAK, and discusses emerging targeted therapies based on these insights. It highlights omics-based signatures, ULK3 and SLAMF7 in GCA, EGR1 in TAK, alongside genetic and somatic risk factors such as clonal haematopoiesis (DNMT3A/TET2) linked to relapse and ischaemic vision loss in GCA, and the IL6R-p.Asp358Ala variant as a predictor of reduced interleukin (IL)-6 receptor blockade response. Common mechanisms include CD4⁺ T-cell, monocyte/macrophage, and B-cell infiltration with activation of IL-6, JAK/STAT/interferon, and IL-17 pathways. Giant cell arteritis is characterised by GM-CSF-driven macrophages and disrupted programmed cell death (PD)-1/PD-L1 checkpoint regulation, while TAK shows dominance of CD8⁺ T cells and tumour necrosis factor (TNF)-α signalling. Interleukin-6 receptor inhibitors (e.g., tocilizumab) show robust efficacy in GCA but with notable non-responders; the JAK inhibitor upadacitinib demonstrated efficacy in a Phase III study, whereas IL-17 blockade (secukinumab) yielded inconsistent results. In TAK, TNF inhibitors and tocilizumab are comparably effective; early data suggest Janus kinases (JAK) inhibitors promote remission, imaging improvement, and glucocorticoid sparing. Mavrilimumab (GM-CSF receptor blockade) is promising in GCA. Recent studies have increasingly focused on short-term glucocorticoid therapy in combination with biologic agents. Advances in biomarker research, including investigation of the IL-6 receptor and IL-17A gene polymorphisms, may enable more targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/05/04
Reisch MyriamThiel JensBosch Philipp - Peripheral T-cell lymphoma (PTCL) remains a formidable challenge in clinical management. Histone deacetylase inhibitor chidamide has demonstrated its anti-tumor effects in real-world studies in relapsed or refractory PTCL. To evaluate the efficacy of real-world utilization of chidamide combined with chemotherapy for untreated PTCL and explore relative prognostic factors, a cohort of 151 PTCL patients treated with chidamide combined with chemotherapy as front-line treatment in our center were enrolled. The overall response rate (ORR) and complete remission rate (CRR) at the end of treatment were 81.5% and 67.5%. The 7-year overall survival (OS) rate and progression-free survival (PFS) rate were 67.6% and 49.7%, with a median follow-up period of 21 months, showing its satisfactory efficacy and survival advantage. Most of adverse events were transient and reversible. Furthermore, several baseline characteristics of patients were relevant to prognosis. The study identified gene mutations in TET2 (30.9%), STAT (22.7%), RHOA (17.5%), TP53 (14.4%), DNMT3A (12.4%), with TP53 and DNMT3A mutations correlating with worse clinical outcomes. The identification of gene mutations contributed to personalizing treatment strategies and predicting patient outcomes. This study raised the preliminary hypothesis that chidamide-containing front-line therapy might be promising for PTCL patients, which warranted further investigation. - Source: PubMed
He JiajieXia FanYu LingziZou RuiZhu QianZhang XiaoLi JunhongKong DanqingWu DepeiJin ZhengmingPing NanaQu Changju - Acute myeloid leukemia (AML) blasts often have high CD135 (FLT3 receptor) expression, but its clinical impact is unclear. We analyzed CD135 expression, and the clinical characteristics and outcomes of 214 patients with de novo AML diagnosed between October 2022 and May 2024. Subsequently, we collected data on additional 78 patients, diagnosed with AML at four medical centers from June to December 2024, for external validation. The high-CD135-expression group had significantly lower CD34 surface expression (p = 0.003) and higher CD33 expression (p = 0.014) on AML blasts. The high-CD135-expression group also showed a higher frequency of NPM1 (p < 0.001) and DNMT3A (p = 0.032) mutations, but was not significantly associated with CD135 expression (p = 0.229). The patients in the high-CD135-expression group had lower initial induction therapy response rates than those in the low-CD135-expression group (p < 0.001). High CD135 expression was independently associated with poorer OS and PFS. In the subgroup of patients with high CD135 expression and FLT3-ITD mutations, those who received TKI combined with chemotherapy had significantly better OS (p = 0.007). Then we developed a prognostic nomogram incorporating CD135 expression. This model performed well both in the development cohort (area under the curve [AUC] = 0.817) and multicenter validation cohort (AUC = 0.722). CD135 expression on AML blasts is a pivotal marker that integrates molecular pathogenesis with clinical outcomes, highlighting its dual role as a prognostic indicator and therapeutic target in precision clinical approaches for AM. - Source: PubMed
Publication date: 2026/05/02
Nie JinhongGao LuShao YingchunYang LiCao JunjieXu JingeWang YuhangZhang YuqiCui TongZhou ShiyuanZhu WenjuanZhu MingqingMa XiaoWu DepeiWu Xiaojin - Ionizing radiation (IR) is known to induce vascular injury and alter immune cell function, yet the molecular mechanisms driving these changes remain incompletely defined. In particular, the role of clonal hematopoiesis-associated proteins expression and stress-responsive signaling pathways in monocyte subsets has not been fully elucidated. - Source: PubMed
Publication date: 2026/04/15
Imanishi MasakiSamanthapudi Venkata S KLe Nhat-TuRivera Luis AntonioKim Jung HyunLee JonghaeMejia Gilbert FHoang OanhDeswal AnitaSchadler Keri LHildebrandt Michelle A TYusuf Syed WamiqueWang GuangyuBurks Jared KNurieva Roza IPalaskas Nicolas LNead Kevin TAmir El-Ad DavidKoutroumpakis EfstratiosLin Steven HAbe Jun-IchiKotla Sivareddy