Epigenomics最新文献_第3页

Epigenetic synthetic lethality as a cancer therapeutic strategy: synergy of experimental and computational approaches. 表观遗传合成致死率作为一种癌症治疗策略：实验和计算方法的协同作用。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-10-01 Epub Date: 2025-08-25 DOI: 10.1080/17501911.2025.2548756

Maria Farina-Morillas, Laia Ollé-Monràs, Silvana Ce Maas, Isabel de Rojas-P, Miguel F Segura, Jose A Seoane

{"title":"Epigenetic synthetic lethality as a cancer therapeutic strategy: synergy of experimental and computational approaches.","authors":"Maria Farina-Morillas, Laia Ollé-Monràs, Silvana Ce Maas, Isabel de Rojas-P, Miguel F Segura, Jose A Seoane","doi":"10.1080/17501911.2025.2548756","DOIUrl":"10.1080/17501911.2025.2548756","url":null,"abstract":"Cancer treatment is an ongoing challenge, as directly targeting oncogenic drivers is often unfeasible in many patients due to the lack of druggable targets. This has led to the exploration of alternative strategies, such as exploiting synthetic lethality (SL) relationships between genes. SL facilitates the indirect targeting of oncogenic drivers, as exemplified by the clinical success of PARP inhibitors against BRCA-mutated tumors. Advances in high-throughput perturbation screens and multi-omics technologies have deepened our understanding of SL relationships, while computational models enhance SL predictions to better reflect biological complexity. However, while numerous experimental and computational methods have been developed to identify SL interactions, difficulties remain in translating these findings into clinical applications.This review combines recent progress on SL relationships in cancer with emerging insights into epigenetic regulation, highlighting how epigenetic drugs (epidrugs) can provide new opportunities for targeted interventions, offering a way to minimize off-target effects and enhance therapeutic precision. To advance SL-based therapies, efforts must focus not only on identifying new SL interactions but also on consolidating existing knowledge and integrating experimental and computational approaches to characterize the vulnerabilities of cancer cells. Strengthening this foundation will be critical for the effective development of SL-based cancer treatments.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1069-1081"},"PeriodicalIF":2.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12520091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144947496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Blood-based DNA methylation markers for autism spectrum disorder identification using machine learning. 使用机器学习识别自闭症谱系障碍的血液DNA甲基化标记。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-10-01 Epub Date: 2025-09-09 DOI: 10.1080/17501911.2025.2557186

Yahui Yang, Zhiyuan Sun, Fengshu Zhu, Aiguo Chen

{"title":"Blood-based DNA methylation markers for autism spectrum disorder identification using machine learning.","authors":"Yahui Yang, Zhiyuan Sun, Fengshu Zhu, Aiguo Chen","doi":"10.1080/17501911.2025.2557186","DOIUrl":"10.1080/17501911.2025.2557186","url":null,"abstract":"Background: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder lacking objective biomarkers for early diagnosis. DNA methylation is a promising epigenetic marker, and machine learning offers a data-driven classification approach. However, few studies have examined whole-blood, genome-wide DNA methylation profiles for ASD diagnosis in school-aged children.Methods: We analyzed genome-wide DNA methylation data from GEO dataset GSE113967, including 52 children with ASD and 48 typically developing (TD) controls. Differentially methylated positions (DMPs) were identified, and feature selection was performed using support vector machine-recursive feature elimination with cross-validation (SVM-RFECV). Classification models were developed using random forest (RF), extreme gradient boosting (XGBoost), and decision tree (DT) classifiers. A nomogram visualized feature contributions.Results: A total of 138 DMPs differentiated ASD from TD children. Eleven CpG sites selected by SVM-RFECV formed the basis for model construction. RF and XGBoost achieved the highest accuracy (75%), with DT reaching 70%. Functional annotation indicated enrichment in cell adhesion and immune-related pathways.Conclusions: This exploratory study demonstrates the feasibility of integrating peripheral blood DNA methylation data with machine learning to distinguish children with ASD. While limited by sample size and moderate accuracy, this study provides methodological insights into the feasibility of integrating epigenetic and computational approaches for ASD-related biomarker exploration.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1029-1042"},"PeriodicalIF":2.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12520114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MDM2 and DNMT1 inhibitors induce neuroblastoma cell death through p53-dependent and independent pathways. MDM2和DNMT1抑制剂通过p53依赖和独立途径诱导神经母细胞瘤细胞死亡。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-10-01 Epub Date: 2025-09-17 DOI: 10.1080/17501911.2025.2558497

Shyam Sundar Jaganathan, Umamaheswari Natarajan, Appu Rathinavelu

{"title":"MDM2 and DNMT1 inhibitors induce neuroblastoma cell death through p53-dependent and independent pathways.","authors":"Shyam Sundar Jaganathan, Umamaheswari Natarajan, Appu Rathinavelu","doi":"10.1080/17501911.2025.2558497","DOIUrl":"10.1080/17501911.2025.2558497","url":null,"abstract":"Introduction: Neuroblastoma, a highly aggressive pediatric cancer, presents significant treatment challenges due to its rapid proliferation, and resistance to conventional therapies. Growing evidence emphasizes the critical role of epigenetic modifications in tumor progression.Research design and methods: In this study, we explored the therapeutic potential of the MDM2 inhibitor RG-7388 alongside the DNMT inhibitors CM-272 and SGI-1027 in SK-N-SH and IMR-32 neuroblastoma cells. We hypothesized that RG-7388, CM-272, and SGI-1027 would induce p21 upregulation, leading to cell cycle arrest and activation of cell death pathways.Results: Cells treated with the above listed drug exhibited significant cell death, as determined by cell viability and caspase-3/7 activation assays. qRT-PCR and Western blot analyses revealed increased expression of p21 and pro-apoptotic BAX, along with decreased levels of the anti-apoptotic protein BCL-XL. Notably, RG-7388 treatment induced substantial PARP cleavage, consistent with activation of apoptosis.These findings suggest that MDM2 and DNMT1 inhibition promotes apoptosis through a p21-driven mechanism. Importantly, DNMT1 inhibition could provide a therapeutic alternative for neuroblastomas with p53 mutations, where p53 dependent mechanism is ineffective.Conclusion: Our results suggest that, if validated further, RG-7388, CM-272, and SGI-1027 could become effective therapeutic agents for treating aggressive neuroblastoma that may become resistant to first or second line of treatment.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1057-1068"},"PeriodicalIF":2.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12520073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Beyond the genome: intergenerational inheritance through epigenetics and other pathways. 基因组之外：通过表观遗传学和其他途径的代际遗传。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-10-01 DOI: 10.1080/17501911.2025.2568370

Amy L Non, Chantal J Rabay, Lucia C Rejzek

引用次数: 0

Synergistic epigenetic modulation by 5-aza-2'-deoxycytidine and Wnt3a drives osteogenic trans-differentiation of 3T3-L1 pre-adipocytes through Ywhah and Ywhae. 5-aza-2'-脱氧胞苷和Wnt3a协同表观遗传调控通过Ywhah和Ywhae驱动3T3-L1前脂肪细胞成骨反式分化。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-10-01 Epub Date: 2025-08-12 DOI: 10.1080/17501911.2025.2544513

Seung Gwa Park, Ki-Tae Kim, Woo-Jin Kim, Sungtae Kim, Young-Dan Cho

{"title":"Synergistic epigenetic modulation by 5-aza-2'-deoxycytidine and Wnt3a drives osteogenic trans-differentiation of 3T3-L1 pre-adipocytes through Ywhah and Ywhae.","authors":"Seung Gwa Park, Ki-Tae Kim, Woo-Jin Kim, Sungtae Kim, Young-Dan Cho","doi":"10.1080/17501911.2025.2544513","DOIUrl":"10.1080/17501911.2025.2544513","url":null,"abstract":"Background: In elderly patients, bone regeneration is impeded by age-related shifts in mesenchymal stem cell differentiation propensity toward adipogenesis over osteogenesis. We investigated whether DNA demethylation by 5‑aza‑2'‑deoxycytidine (5azaC) synergizes with Wnt Family Member 3A (Wnt3a) signaling to induce osteogenic potential in 3T3‑L1 pre-adipocytes, generating osteoblast-like cells.Methods: 3T3‑L1 pre-adipocytes were treated with 5azaC and/or Wnt3a. Osteogenic differentiation was assessed via ALP activity, mineralization assays, and marker expression. Transcriptomic and epigenomic profiling were performed and compared with MC3T3-E1 cells. Functional relevance of candidate genes was examined using siRNA knockdown.Results: Transcriptomic and epigenomic profiling revealed that 5azaC and Wnt3a co-treatment induced broader gene expression and methylation changes than either treatment alone, closely resembling the osteogenic profile of MC3T3-E1 pre-osteoblasts. Among the overlapping differentially methylated and steadily expressed genes, Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein Eta (Ywhah) and Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein Epsilon (Ywhae) emerged as key regulators, whose knockdown notably enhanced Alpl expression even without 5azaC.Conclusions: Combining 5azaC-induced demethylation with Wnt3a is a potent strategy to redirect pre-adipocytes toward osteogenesis. Identification of key targets like Ywhah and Ywhae provides mechanistic insight into trans-differentiation and suggests therapeutic potential for bone regeneration, particularly in elderly periodontal patients.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"923-933"},"PeriodicalIF":2.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12490366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dissecting epigenetic age acceleration in amyotrophic lateral sclerosis. 肌萎缩性侧索硬化症的解剖表观遗传年龄加速。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-09-30 DOI: 10.1080/17501911.2025.2563502

Polina Merbaum, Ramona Zwamborn, Paul Hop, Project MinE Als Sequencing Consortium, Wouter van Rheenen, Jan Veldink

{"title":"Dissecting epigenetic age acceleration in amyotrophic lateral sclerosis.","authors":"Polina Merbaum, Ramona Zwamborn, Paul Hop, Project MinE Als Sequencing Consortium, Wouter van Rheenen, Jan Veldink","doi":"10.1080/17501911.2025.2563502","DOIUrl":"https://doi.org/10.1080/17501911.2025.2563502","url":null,"abstract":"Aim: We compared signatures of epigenetic aging in amyotrophic lateral sclerosis (ALS) patients and healthy controls to investigate the role of potential confounders and genetic subgroups.Methods: We used whole-blood methylome profiles for 5,146 ALS patients and 2,156 controls available for Project MinE. We predicted biological age with three generations of epigenetic clocks and estimated age acceleration by regressing our model on control individuals to evaluate case/control differences. To investigate the contribution of C9orf72 expansions, we regressed the model on C9orf72-negative ALS patients. The predicted DunedinPACE pace of aging and telomere length additionally characterized aging dynamics.Results: We found that white blood cell type proportions confound the previously observed increase in the pace of biological aging in ALS. When correcting for cell counts, there is no evidence for accelerated epigenetic aging compared to controls, except for ALS patients with the C9orf72 repeat expansion. None of the epigenetic age acceleration scores contributed to survival.Conclusion: Our study revealed no significant difference in the pace of biological agingbetween ALS patients and controls, except for ALS patients carrying the C9orf72 mutation. We emphasize the importance of altered white blood cell proportions in general ALS pathophysiology as opposed to accelerated aging per se.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-9"},"PeriodicalIF":2.6,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198798","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

Relationship stress and epigenetic age acceleration among older U.S. adults in the Midlife in the United States study. 美国中年人的关系压力和表观遗传年龄加速研究。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-09-30 DOI: 10.1080/17501911.2025.2568301

Mariana Rodrigues, Jemar R Bather, Adolfo G Cuevas

{"title":"Relationship stress and epigenetic age acceleration among older U.S. adults in the Midlife in the United States study.","authors":"Mariana Rodrigues, Jemar R Bather, Adolfo G Cuevas","doi":"10.1080/17501911.2025.2568301","DOIUrl":"https://doi.org/10.1080/17501911.2025.2568301","url":null,"abstract":"Background: Chronic interpersonal stress has been linked to accelerated biological aging, but questions remain about which relationship stress domains may be most consequential during midlife.Research design and methods: Linear regression models quantified the cross-sectional associations between domain-specific relationship stressors (marital risk, partner strain, family strain, friendship strain) and next-generation epigenetic clocks (DunedinPACE and GrimAge2) in 1,310 midlife adults from the Midlife in the United States study (mean age = 51, SD = 13).Results: Controlling for sociodemographic and health behaviors, we found that friendship strain was uniquely associated with accelerated aging (GrimAge2: 0.03 SD increase, 95% CI: 0.01, 0.05, p = 0.003; DunedinPACE: 0.05 SD increase, 95% CI: 0.01, 0.09, p = 0.030). No statistically significant associations were observed for the other stressors with GrimAge2 or DunedinPACE in fully adjusted models.Conclusions: These findings identify friendship strain as a potential specific risk factor for accelerated biological aging in midlife. Future research should investigate behavioral and physiological mechanisms linking friendship quality to cellular aging.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-9"},"PeriodicalIF":2.6,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191479","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

Pharmacoepigenomic effects of anti-hypertensive drugs on DNA methylation and its implication to drug response and side effects. 抗高血压药物对DNA甲基化的药物-表观基因组效应及其对药物反应和副作用的影响。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-09-29 DOI: 10.1080/17501911.2025.2567232

Samyukta Bhass, Moinak Banerjee

{"title":"Pharmacoepigenomic effects of anti-hypertensive drugs on DNA methylation and its implication to drug response and side effects.","authors":"Samyukta Bhass, Moinak Banerjee","doi":"10.1080/17501911.2025.2567232","DOIUrl":"https://doi.org/10.1080/17501911.2025.2567232","url":null,"abstract":"Background: Antihypertensives are often prescribed in a 'trial and error' mode in management of hypertension. Significant drug response variability for these antihypertensives affects the therapeutic efficacy and increases the chance of developing adverse reactions. The study aims to investigate the influence of antihypertensives on the DNA methylation and its possible role in drug response variability and adverse events.Methods: The study evaluated the expression level of epigenetic genes, global DNA methylation, hydroxy-methylation level, and gene level differential methylation in in-vitro system post antihypertensive treatment.Results: The epigenetic gene expression pattern upon amlodipine, enalapril, telmisartan, and metoprolol treatment indicated a drug, dosage, and duration-dependent expression of DNMTs and TETs. Global methylation and hydroxy-methylation patterns overlap with the gene expression patterns of DNMTs and TETs for amlodipine and telmisartan, but variability was observed with metoprolol and enalapril. Gene-specific methylation pattern revealed several drug and duration-specific differential methylated genes, which can potentially impact therapeutic outcomes and adverse events as evidenced by their HPO terms.Conclusions: The study signifies that antihypertensives influence the methylation pattern and drug-induced differential methylation of certain genes which can potentially contribute to adverse effects while that in other genes may have therapeutic utility for other diseases.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-16"},"PeriodicalIF":2.6,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184867","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

Novel approaches to the use of hypomethylating agents in myeloid malignancies. 在髓系恶性肿瘤中使用低甲基化药物的新方法。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-09-25 DOI: 10.1080/17501911.2025.2557179

Justin Cheng, Casey O'Connell

{"title":"Novel approaches to the use of hypomethylating agents in myeloid malignancies.","authors":"Justin Cheng, Casey O'Connell","doi":"10.1080/17501911.2025.2557179","DOIUrl":"https://doi.org/10.1080/17501911.2025.2557179","url":null,"abstract":"Epigenetic dysregulation has been increasingly understood to be a key factor in the development of myeloid malignancies, often acting alongside genetic alterations to disrupt normal hematopoiesis. The inherent reversibility of epigenetic changes has provided an excellent opportunity for therapeutic intervention. Hypomethylating agents (HMA) preferentially alter gene expression in heavily methylated malignant myeloid cells by inhibiting DNA methyltransferases thereby altering gene expression. They have since become foundation therapies in myelodysplastic syndrome (MDS) and in older patients with acute myeloid leukemia (AML). However, complete responses to HMA monotherapy are limited and usually non-durable. In recent years, novel approaches have been sought to overcome resistance and expand the role of epigenetic therapies in MDS and AML as well as in less well-studied myeloid malignancies such as myeloproliferative neoplasms (MPNs) and MDS/MPN overlap syndromes. Combination regimens that synergistically pair HMAs or other epigenetically active therapeutics with agents targeting apoptosis, cellular metabolism, and immune evasion have also shown early promise in improving patient outcomes. Oral formulations of HMAs have made maintenance strategies more convenient and tolerable for patients, with demonstrated benefits in AML and ongoing investigations in MDS and post-transplant settings. This review will explore these novel therapeutic strategies in the treatment of myeloid malignancies.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-12"},"PeriodicalIF":2.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136994","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 paradigm of DNA methylation for understanding the pathophysiology, diagnostics, and therapeutics in sarcomas. DNA甲基化的表观遗传学范式，用于理解肉瘤的病理生理、诊断和治疗。

IF 2.6 4区医学

Epigenomics Pub Date : 2025-09-19 DOI: 10.1080/17501911.2025.2563500

Sujata Bhattacharya, Harshita Makkar, Jagdish Prasad Meena, Aditya Kumar Gupta, Rachna Seth

{"title":"Epigenetic paradigm of DNA methylation for understanding the pathophysiology, diagnostics, and therapeutics in sarcomas.","authors":"Sujata Bhattacharya, Harshita Makkar, Jagdish Prasad Meena, Aditya Kumar Gupta, Rachna Seth","doi":"10.1080/17501911.2025.2563500","DOIUrl":"https://doi.org/10.1080/17501911.2025.2563500","url":null,"abstract":"Sarcomas are heterogeneous malignant tumors originating from mesenchymal tissues, presenting substantial diagnostic and therapeutic challenges. The diverse genetic and epigenetic landscape provides significant heterogeneity and complexity to the disease, ultimately leading to poor outcomes for affected individuals, especially in metastatic diseases. As research in this field evolves, incorporating methylation profiling into routine clinical practice could significantly enhance the early diagnosis, risk stratification, and personalized treatment strategies for sarcoma patients. Moreover, the integration of advanced genetic techniques and ongoing upgradation in treatment strategies, predominantly those targeting methylation modifications, may lead to improved survival outcomes in sarcomas. We conducted a structured literature review using PubMed, Scopus, Embase, Google Scholar, and Web of Science, encompassing publications up to 30 November 2024. The search focused on DNA methylation in sarcoma pathogenesis, diagnostics, and therapeutics. Relevant articles were screened, and key findings were synthesized thematically. In this review, we provide a comprehensive insight into the role of DNA methylation in promoting sarcomas. We emphasize subtype-associated methylation patterns in sarcomas and their value as prognostic and diagnostic biomarkers, revealing their synergistic effects with the existing treatment regimens. Despite having preclinical outcomes, the translation of these therapies into clinical practice remains a challenge.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-12"},"PeriodicalIF":2.6,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091482","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