IF 2.6 4区医学

Epigenomics Pub Date : 2026-05-06 DOI: 10.1080/17501911.2026.2667346

K L Milan, M Anuradha, K M Ramkumar

{"title":"Altered HDAC expression is associated with CYP24A1-mediated vitamin D deficiency in gestational diabetes mellitus.","authors":"K L Milan, M Anuradha, K M Ramkumar","doi":"10.1080/17501911.2026.2667346","DOIUrl":"https://doi.org/10.1080/17501911.2026.2667346","url":null,"abstract":"Background: Low vitamin D levels during pregnancy are associated with an increased risk of Gestational Diabetes Mellitus (GDM), potentially mediated by altered vitamin D metabolism. Cytochrome P450 family 24 subfamily A member 1 (CYP24A1) plays a key role in vitamin D catabolism, but its epigenetic regulation in GDM remains unclear.Research design and methods: This cross-sectional study included 150 pregnant women [normoglycemic (NGDM, n = 50), early GDM (eGDM, n = 50), and GDM (n = 50)] and 40 placental samples (NGDM, n = 20; GDM, n = 20). Gene expression of histone deacetylases (HDACs), sirtuins (SIRTs), and CYP24A1 was analyzed using real-time PCR. In vitro experiments using BeWo cells assessed the effects of high glucose and trichostatin A (TSA).Results: CYP24A1 expression was significantly increased in GDM participants. Distinct alterations in HDAC and SIRT expression were observed, with HDAC3, HDAC4, and HDAC7 negatively correlated and SIRT7 positively correlated with CYP24A1. HDAC modulation using TSA regulated CYP24A1 expression under hyperglycemic conditions.Conclusions: These findings offer insights into the association of multiple HDACs regulating CYP24A1-mediated vitamin D deficiency in the pathophysiology of GDM. However, further mechanistic and longitudinal studies are required to elucidate the precise mechanism.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-14"},"PeriodicalIF":2.6,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetic mechanisms and therapeutic targeting across diverse malignancies. 不同恶性肿瘤的表观遗传机制和治疗靶向。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-05-05 DOI: 10.1080/17501911.2026.2667351

Akshara Harihar, Rithika Venkataramanan, Marina Alice Mathew, Anuraag Dasgupta, Koustav Sarkar

{"title":"Epigenetic mechanisms and therapeutic targeting across diverse malignancies.","authors":"Akshara Harihar, Rithika Venkataramanan, Marina Alice Mathew, Anuraag Dasgupta, Koustav Sarkar","doi":"10.1080/17501911.2026.2667351","DOIUrl":"https://doi.org/10.1080/17501911.2026.2667351","url":null,"abstract":"Genetic abnormalities cause cancer, a heterogeneous disease. These abnormalities comprise unregulated proliferation, invasion, and metastasis. Transcriptional factors are altered by dysregulation, like DNA methylation, histone modifications, and chromatin remodeling, during tumor formation, progression, and resistance to therapy. These can be reversed and transmitted to subsequent generations. Consequently, tumor suppressor genes can be deactivated without altering DNA sequences. Epigenetic markers have been detected in carcinomas, sarcomas, hematological malignancies, and organ-specific tumors, influencing diagnostic accuracy, prognosis assessment, and treatment strategies. Several epigenetic drugs have been developed due to recent advances in epigenetic research. These include DNA methyltransferase inhibitors, histone deacetylase inhibitors and novel modulators focusing on RNA methylation and chromatin regulation. These pharmaceuticals may facilitate normal gene expression restoration, enhance the sensitivity of treatment-resistant malignancies and improve the efficacy of conventional and immunotherapeutic interventions. Significant challenges, such as tumor heterogeneity, limited target specificity, and off-target toxicity, continue to impede widespread clinical application; others are less challenging. The integration of comprehensive epigenetic profiling with precision oncology frameworks presents transformative opportunities to tailor treatment programs, initiate therapy sooner and enhance long-term patient outcomes. Increasing cancer's epigenome knowledge has led to increased interest in developing personalized, mechanism-based treatments addressing cancer's dynamic and adaptive nature.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-19"},"PeriodicalIF":2.6,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Emerging roles of m⁶A modification in endodontic diseases: a systematic review. m6A修饰在牙髓疾病中的新作用：系统综述。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-05-04 DOI: 10.1080/17501911.2026.2667348

Suping Liao, Jihua Guo, Rong Jia

{"title":"Emerging roles of m6A modification in endodontic diseases: a systematic review.","authors":"Suping Liao, Jihua Guo, Rong Jia","doi":"10.1080/17501911.2026.2667348","DOIUrl":"https://doi.org/10.1080/17501911.2026.2667348","url":null,"abstract":"Aim: This review aims to synthesize and evaluate the evidence on the role of N6-methyladenosine (m6A) modification in pathogenesis, progression, and tissue repair of endodontic diseases, focusing on its regulatory functions in dental stem cells.Methods: Two reviewers independently searched four databases for studies published by May 2025. The protocol was registered with PROSPERO (CRD420251233698). The certainty of findings was assessed using the CERQual approach.Results: Of 680 initial records, 27 studies were included. Findings demonstrated that m6A modification dynamically regulates enamel/root development, osteogenic/odontogenic differentiation of dental stem cells, and inflammatory responses in endodontic diseases. Five key themes were identified: pulpitis pathogenesis and repair, apical periodontitis pathogenesis and repair, and tooth development/pulp regeneration. Mechanistically, in pulpitis, METTL3 exacerbates inflammation via NF-κB/MAPK pathways, whereas FTO aggravates bone destruction in apical periodontitis. M6A regulates stem cell differentiation by modulating osteogenic/odontogenic gene expression and lncRNA/miRNA networks. METTL3 promotes tissue repair by stabilizing target mRNAs, while FTO enhances RUNX2 splicing. M6A regulates tooth morphogenesis through WTAP-SHH and METTL3-NFIC pathways.Conclusions: This review establishes m6A modification as an important epitranscriptomic regulator that modulates inflammation and repair in endodontic diseases. Further clinical studies are needed to validate these mechanisms and their therapeutic potential.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-14"},"PeriodicalIF":2.6,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The signaling upstream of DOT1L-mediated H3K79 methylation. dot1l介导的H3K79甲基化的上游信号。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-05-04 DOI: 10.1080/17501911.2026.2665450

Chu Chen, Di Wu, Canran Lv, Peng Zhu, Zihao Chen, Qi Li, Junming Li, Jian Yang, Jing Zhang

引用次数: 0

DNA methylation microarray analysis of human DNA samples contaminated with mouse DNA. 受小鼠DNA污染的人类DNA样本的DNA甲基化微阵列分析。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-30 DOI: 10.1080/17501911.2026.2667134

Takahiro Ebata, Qichun Wang, Hideyuki Takeshima, Yumi Furuichi, Satoshi Yamashita, Kouya Shiraishi, Shigehiro Yagishita, Akinobu Hamada, Toshikazu Ushijima

{"title":"DNA methylation microarray analysis of human DNA samples contaminated with mouse DNA.","authors":"Takahiro Ebata, Qichun Wang, Hideyuki Takeshima, Yumi Furuichi, Satoshi Yamashita, Kouya Shiraishi, Shigehiro Yagishita, Akinobu Hamada, Toshikazu Ushijima","doi":"10.1080/17501911.2026.2667134","DOIUrl":"https://doi.org/10.1080/17501911.2026.2667134","url":null,"abstract":"Aim: To establish an analytical method for human DNA contamination with mouse DNA using a DNA methylation microarray.Materials and methods: A pure human DNA sample was generated by mixing fully methylated and unmethylated DNA originating from the human cell line HCT116 and fully methylated mouse DNA. The pure human DNA sample, human DNA samples mixed with 30% and 60% mouse DNA, and the pure mouse DNA samples were analyzed using the Infinium MethylationEPIC v2.0 kit. Cell line xenografts (CDX) were prepared from RKO and Pa-Tu-8902 cell lines.Results: We identified 7,446 low-reproducibility probes using pure human DNA samples and 133,377 mouse cross-reacting probes using pure mouse DNA. After excluding these probes, functional probes improved the correlation in methylation levels between pure human DNA samples and those mixed with mouse DNA. Functional probes improved the correlation between DNA methylation levels in human CDX samples and their parental cancer cell lines.Conclusion: Our established method can minimize the effect of mouse DNA contamination in human DNA samples, thereby enabling the analysis of human CDX and patient-derived xenograft (PDX) models.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-8"},"PeriodicalIF":2.6,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reduction in ELOVL2 methylation following curative surgery in lung cancer patients: an observational study. 肺癌患者根治性手术后ELOVL2甲基化降低：一项观察性研究

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-28 DOI: 10.1080/17501911.2026.2665461

Peixian Li, Zhuxing Chen, Xiaowen Zhang, Cheng Zeng, Yihao Chen, Shengli Yang, Yaming Xiong

引用次数: 0

Combining epigenetic therapy and immunotherapeutic avenues for chronic HBV infection. 结合表观遗传疗法和免疫治疗途径治疗慢性HBV感染。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-24 DOI: 10.1080/17501911.2026.2664392

Yin-Han Chou, Markus Cornberg

引用次数: 0

miRNA profiling of a mutation-negative PKD cohort reveals PKD1/PKD2 ADPKD shared signatures and differences. 突变阴性PKD队列的miRNA分析显示PKD1/PKD2 ADPKD共享特征和差异。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-04-02 DOI: 10.1080/17501911.2026.2652277

Bruna De Felice, Ersilia Nigro, Maria Amicone, Antonio Pisani, Aurora Daniele, Federica Farinella

{"title":"miRNA profiling of a mutation-negative PKD cohort reveals PKD1/PKD2 ADPKD shared signatures and differences.","authors":"Bruna De Felice, Ersilia Nigro, Maria Amicone, Antonio Pisani, Aurora Daniele, Federica Farinella","doi":"10.1080/17501911.2026.2652277","DOIUrl":"10.1080/17501911.2026.2652277","url":null,"abstract":"Background: Autosomal dominant polycystic kidney disease (ADPKD) is mainly caused by mutations in PKD1 or PKD2 genes, but a subgroup of patients has no detectable mutation and remains understudied. We profiled microRNAs (miRNAs) in this mutation-negative group and compared them with PKD1, PKD2, and healthy controls.Methods: Targeted miRNA profiling was used to measure miRNAs expression. We tested five prespecified contrasts using Welch's two-sided t-test (p < 0.05). For interpretation, experimentally supported miRNA-mRNA interactions were assembled and visualized into networks.Results: miR-92a was found upregulated across all patient-control groups. Interestingly, the mutation-negative cohort showed the broadest deregulation, pointing toward higher expression together with enhanced extracellular-matrix remodeling. PKD1 vs controls displayed a more restricted number of deregulated miRNAs; when PKD1 was compared directly with the mutation-negative group, we observed selective reductions, most notably miR-134-5p. PKD2 vs controls showed fewer changes overall but overlapped with the core signature observed in other groups and no miRNAs met the threshold in PKD2 vs mutation-negative.Discussion: The results indicate that miRNA dysregulation is present in the absence of identifiable PKD1/PKD2 mutations, supporting the idea of common pathways and highlighting the translational potential of miRNAs as biomarkers or therapeutic targets.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"371-383"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

S-adenosylmethionine as an epigenetic treatment of depression in adults with childhood trauma. s -腺苷蛋氨酸对儿童期创伤成人抑郁症的表观遗传治疗作用。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-04-24 DOI: 10.1080/17501911.2026.2645001

Anne Alkema, Winni Schalkwijk, Evelien Bohte, Luc Draisma, Astrid Hoppe, Charlotte Koch, Veerle Refuge, Birgit Romberg, Jurjen J Luykx, Judith J M Jans, Wiepke Cahn, Eline Regeer, Marco P M Boks

{"title":"S-adenosylmethionine as an epigenetic treatment of depression in adults with childhood trauma.","authors":"Anne Alkema, Winni Schalkwijk, Evelien Bohte, Luc Draisma, Astrid Hoppe, Charlotte Koch, Veerle Refuge, Birgit Romberg, Jurjen J Luykx, Judith J M Jans, Wiepke Cahn, Eline Regeer, Marco P M Boks","doi":"10.1080/17501911.2026.2645001","DOIUrl":"10.1080/17501911.2026.2645001","url":null,"abstract":"Background: Childhood trauma is associated with increased risk of depression and epigenetic alterations in stress-related pathways. Preclinical studies suggest that methyl donors may facilitate DNA methylation changes. This first-in-human trial of epigenetic treatment investigated methyl donor S-adenosylmethionine (SAMe) as add-on to trauma-focused therapy for depression.Methods: In this randomized, double-blind, placebo-controlled trial with 6-month follow-up, 31 adults with trauma-related depression were enrolled. Participants received 1200 mg SAMe or placebo alongside 12-weeks trauma-focused therapy. Depression symptoms were assessed using the Hamilton Rating Scale of Depression (HAM-D). Plasma SAMe levels and genome-wide DNA methylation were measured pre- and post-treatment, including epigenome-wide association analyses, differentially methylated region analyses, and epigenetic clock measures.Results: Twenty-eight participants completed the study. Depression symptoms decreased significantly during treatment and remained improved at follow-up, reflecting the effect of psychotherapy, without clinical benefit of SAMe. SAMe supplementation did not alter plasma SAMe levels. However, SAMe treatment was associated with differential methylation across 66 regions. Epigenetic clock analyses showed no consistent treatment-related changes.Conclusions: This first-in-human epigenetic intervention study in psychiatry demonstrates the feasibility of combining trauma-focused psychotherapy with targeted epigenetic analyses. While SAMe showed no additive clinical effects, the results provide important leads for future trials.Clinical trial identifier (eudract): 2017-002097-38.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"437-449"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Timing matters in population epigenomics. 时间在种群表观基因组学中很重要。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-04-06 DOI: 10.1080/17501911.2026.2652837

Charlotte A M Cecil, Janine F Felix, Alexander Neumann

引用次数: 0

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