2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T4ff,Hypocellular bone marrow failure (BMF) may be acquired due to immune-mediated disease, the prototype being immune aplastic anemia (IAA), or inherited, due to germline defects in genes important for hematopoietic stem cells' function and maintenance (inherited bone marrow failure syndromes [IBMFS]). Proper diagnosis of the underlying etiology of hypocellular bone marrow failure, particularly distinguishing immune AA, myelodysplastic syndrome (MDS) (most relevant in this setting, hypoplastic MDS [MDS-h]), and the IBMFS, is important given the differences in clinical management. Clonal hematopoiesis (CH), in this context comprising somatic mutations or chromosomal abnormalities, is incorporated into standard algorithms for classification, risk stratification, and treatment decisions for hematologic malignancies, but the clinical significance in BMF is not well established. Disease-specific clonal signatures have been reported across the BMF spectrum, and here we show how distinct patterns of CH can aid in distinguishing different etiologies of hypocellular BMF. Additionally, detection of somatic alterations in many BMF disorders can estimate risk for secondary myeloid neoplasms, guide surveillance and, in some instances, allow for early therapeutic intervention.31:T510,Hypocellular bone marrow failure (BMF) may be acquired due to immune-mediated disease, the prototype being immune aplastic anemia (IAA), or inherited, due to germline defects in genes important for hematopoietic stem cells' function and maintenance (inherited bone marrow failure syndromes [IBMFS]). Proper diagnosis of the underlying etiology of hypocellular bone marrow failure, particularly distinguishing immune AA, myelodysplastic syndrome (MDS) (most relevant in this setting, hypoplastic MDS [MDS-h]), and the IBMFS, is important given the differences in clinical management. Clonal hematopoiesis (CH), in this context comprising somatic mutations or chromosomal abnormalities, is incorporated into standard algorithms for classification, risk stratification, and treatment decisions for hematologic malignancies, but the clinical significance in BMF is not well established. Disease-specific clonal signatures have been reported across the BMF spectrum, and here we show how distinct patterns of CH can aid in distinguishing different etiologies of hypocellular BMF. Additionally, detection of somatic alterations in many BMF disorders can estimate risk for secondary myeloid neoplasms, guide surveillance and, in some instances, allow for early therapeutic intervention.32:T9f7,Cancer survivors have increased cardiovascular disease (CVD) risk partly due to the toxic effects of cancer therapy. Clonal hematopoiesis of indeterminate potential (CHIP), an age-associated blood disorder caused by somatic variants in blood stem cells, is more prevalent among individuals receiving cancer therapy and increases CVD risk independent of traditional risk factors. It is unknown whether CHIP amplifies therapy-related cardiovascular toxic effects in patients with cancer. To assess the association between CHIP and CVD risk, accounting for competing risks, among patients with primary solid tumors who received chemotherapy, radiotherapy, or immunotherapy. A cohort study was conducted using BioVU, Vanderbilt University Medical Center's biorepository linking electronic health records to whole-genome sequencing data from 250 038 participants from 2006 to 2025. In this cohort, participants had a primary solid tumor diagnosis, received chemotherapy, radiotherapy, and/or immunotherapy, and did not have hematologic malignant disease before treatment. Data were analyzed from June 2025 to November 2025. CHIP variants detected via whole-genome sequencing, chemotherapy, radiotherapy, and immunotherapy. Time to first cardiovascular event, defined as heart failure, ischemic CVD, or arrhythmia following cancer treatment. Among 8004 eligible participants (median [IQR] age, 61.9 [52.2-69.9] years; 4385 female individuals [54.8%]) with a primary solid tumor diagnosis, 7438 had no heart failure, 7392 no ischemic CVD, and 6002 no arrhythmia before cancer therapy. Overall, 549 (6.9%) had CHIP. In the propensity score-matched cohort, participants with CHIP had a significantly higher 10-year cumulative incidence of heart failure (20.3%; 95% CI, 16.0%-24.4% vs 14.5%; 95% CI, 13.5%-15.6%; P = .001) and ischemic CVD (25.3%; 95% CI, 20.5%-30.0% vs 18.5%; 95% CI, 17.3%-20.0%; P < .001) compared with those without CHIP. In adjusted Fine-Gray models, CHIP was associated with increased risk of heart failure (subdistribution hazard ratio [sHR], 1.26; 95% CI, 1.02-1.56; P = .03). In an exploratory 24-month landmark analysis, there was a statistically significant interaction between CHIP and intensive chemotherapy (≥7 cycles) on heart failure risk (sHR, 1.02; 95% CI, 1.00-1.04; P = .03). In this cohort study, CHIP was associated with increased CVD risk in patients with solid tumors receiving cancer therapy. This finding suggests incorporating CHIP status may improve cardio-oncology treatment of cancer survivors.33:T105a, Importance Cancer survivors have increased cardiovascular disease (CVD) risk partly due to the toxic effects of cancer therapy. Clonal hematopoiesis of indeterminate potential (CHIP), an age-associated blood disorder caused by somatic variants in blood stem cells, is more prevalent among individuals receiving cancer therapy and increases CVD risk independent of traditional risk factors. It is unknown whether CHIP amplifies therapy-related cardiovascular toxic effects in patients with cancer. Objective To assess the association between CHIP and CVD risk, accounting for competing risks, among patients with primary solid tumors who received chemotherapy, radiotherapy, or immunotherapy. Design, Setting, and Participants A cohort study was conducted using BioVU, Vanderbilt University Medical Center’s biorepository linking electronic health records to whole-genome sequencing data from 250 038 participants from 2006 to 2025. In this cohort, participants had a primary solid tumor diagnosis, received chemotherapy, radiotherapy, and/or immunotherapy, and did not have hematologic malignant disease before treatment. Data were analyzed from June 2025 to November 2025. Exposures CHIP variants detected via whole-genome sequencing, chemotherapy, radiotherapy, and immunotherapy. Main Outcomes and Measures Time to first cardiovascular event, defined as heart failure, ischemic CVD, or arrhythmia following cancer treatment. Results Among 8004 eligible participants (median [IQR] age, 61.9 [52.2-69.9] years; 4385 female individuals [54.8%]) with a primary solid tumor diagnosis, 7438 had no heart failure, 7392 no ischemic CVD, and 6002 no arrhythmia before cancer therapy. Overall, 549 (6.9%) had CHIP. In the propensity score–matched cohort, participants with CHIP had a significantly higher 10-year cumulative incidence of heart failure (20.3%; 95% CI, 16.0%-24.4% vs 14.5%; 95% CI, 13.5%-15.6%; P = .001) and ischemic CVD (25.3%; 95% CI, 20.5%-30.0% vs 18.5%; 95% CI, 17.3%-20.0%; P &lt; .001) compared with those without CHIP. In adjusted Fine-Gray models, CHIP was associated with increased risk of heart failure (subdistribution hazard ratio [sHR], 1.26; 95% CI, 1.02-1.56; P = .03). In an exploratory 24-month landmark analysis, there was a statistically significant interaction between CHIP and intensive chemotherapy (≥7 cycles) on heart failure risk (sHR, 1.02; 95% CI, 1.00-1.04; P = .03). Conclusions and Relevance In this cohort study, CHIP was associated with increased CVD risk in patients with solid tumors receiving cancer therapy. This finding suggests incorporating CHIP status may improve cardio-oncology treatment of cancer survivors. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Clonal Hematopoiesis: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Clonal Hematopoiesis (condition). Clinician-written summaries and actionable practice insights. 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Clinical extrapolation should be made with caution.","value_numeric":null},{"paper_doi":"10.1002/art.70267","tag_type":"warning","value":"Sample sizes for individual experimental groups are not reported in the abstract; absolute numbers of animals per group are unavailable.","value_numeric":null},{"paper_doi":"10.1002/art.70267","tag_type":"warning","value":"Study design is classified as animal experimental rather than a standard clinical study design; level of evidence reflects preclinical work.","value_numeric":null}],"summaries":{"what_studied":"This mouse study tested whether loss-of-function *Dnmt3a* mutations (introduced by CRISPR-Cas9 or Cd4cre recombination) in CD4+ T cells enhance autoreactive T follicular helper (Tfh) cell responses and joint inflammation, using the KRN+ TCR transgenic transfer model of autoimmune arthritis.","key_result":"Contrary to the hypothesis, *Dnmt3a* loss-of-function in CD4+ T cells **reduced** Tfh responses, IgG production, and autoantibody levels, and mice receiving mutant autoreactive CD4+ T cells developed significantly attenuated joint inflammation with lower systemic IL-6.","limitations":"- Entirely preclinical (mouse model); direct translation to human RA is uncertain.\n- Somatic *DNMT3A* mutations in RA patients occur across multiple hematopoietic lineages, but this study only assessed CD4+ T cell–intrinsic effects.\n- The KRN+ transfer model may not fully capture the complexity of human seropositive RA.","practice_takeaway":"These findings suggest that *DNMT3A* mutations in CD4+ T cells alone do not explain the increased inflammation seen in RA patients with clonal hematopoiesis — clinicians should consider that other hematopoietic cell types may drive that association. No immediate change in clinical management is indicated pending human studies."}},{"doi":"10.1182/bloodadvances.2025017940","pmid":"42392167","title":"Predictive modeling of clonal hematopoiesis across diverse cohorts","journal_title":"Blood Advances","journal_issn":"2473-9529","published_at":"2026-07-02T00:00:00.000Z","url":"https://doi.org/10.1182/bloodadvances.2025017940","source_score":5,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-14T06:23:25.760Z","updated_at":"2026-09-14T06:23:25.760Z","tags":[{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"condition","value":"Clonal Hematopoiesis","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"generic","value":"clonal hematopoiesis risk prediction","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"modality","value":"Genomic Sequencing","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"sample_size","value":"n=604547","value_numeric":604547},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"study_design","value":"Prediction Model Development and Validation Study","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"warning","value":"Study design label 'Prediction Model Development and Validation Study' is inferred from context; the paper does not explicitly state a single canonical design label.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"warning","value":"This paper appears to be a supplemental methods and figures document; primary results including specific AUC values and odds ratios are referenced but not fully reproduced in the available text, so numerical outcomes are limited.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025017940","tag_type":"warning","value":"Total sample size of n=604,547 is an approximation summing all three cohorts (UK Biobank + All of Us + MSK-IMPACT); some individuals may overlap or be counted differently across analyses.","value_numeric":null}],"summaries":{"what_studied":"A multivariable logistic regression model (CH-Predict) was developed using UK Biobank (N=452,547) to predict clonal hematopoiesis (CH) risk from clinical variables (age, sex, race, smoking status, and CBC indices), then validated in All of Us (N=143,850) and MSK-IMPACT (N=8,150) cohorts.","key_result":"The full model (age + all clinical variables) outperformed age-alone in predicting CH risk across both validation cohorts; leave-one-out analysis identified age, smoking history, and red cell distribution width (RDW) as the most important predictors. CH-Predict also estimated population sizes needed to identify 100 CH cases per gene (ASXL1, DNMT3A, IDH1/2, JAK2, PPM1D, SF3B1, SRSF2, TET2, TP53, U2AF1), enabling enriched sequencing strategies.","limitations":"- Model is a supplemental/methods document; specific AUC values and confidence intervals are not reported in the available text.\n- Individuals with cytopenias were retained but those with prior hematologic malignancy were excluded, which may limit generalizability to some clinical populations.\n- Missing blood counts were imputed using cohort-specific means, which may introduce bias in cohorts with high missingness rates.","practice_takeaway":"Clinicians and researchers designing CH screening studies can use this model to stratify patients by predicted CH risk using routine CBC and demographic data, substantially reducing the number of sequencing tests needed to identify cases. Prioritizing individuals in the top risk percentiles — particularly older patients, smokers, or those with elevated RDW — may improve the efficiency of CH detection programs."}},{"doi":"10.1182/blood.2025029923","pmid":"42095935","title":"How I utilize somatic alterations in the diagnosis, risk stratification, and therapy of hypocellular bone marrow failure","journal_title":"Blood Journal","journal_issn":"0006-4971","published_at":"2026-05-07T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2025029923","source_score":12,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-05-12","doi":"10.1182/blood.2025029923","days":"7","issn":"0006-4971","rank":"6","field":"Clinical Medicine","score":"12","category":"Hematology","categories":["Hematology"],"_categories":["Hematology"]},"pubmed":{"doi":"10.1182/blood.2025029923","title":"How I utilize somatic alterations in the diagnosis, risk stratification, and therapy of hypocellular bone marrow failure.","journal":"Blood","methods":"","results":"","abstract":"$30","keywords":[],"pubmed_id":"42095935","conclusions":"","publication_date":"2026-05-07T00:00:00"},"crossref":{"DOI":"10.1182/blood.2025029923","URL":"https://doi.org/10.1182/blood.2025029923","ISSN":["0006-4971","1528-0020"],"link":[{"URL":"https://ashpublications.org/blood/article-pdf/doi/10.1182/blood.2025029923/2517684/blood.2025029923.pdf","content-type":"application/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https://ashpublications.org/blood/article-pdf/doi/10.1182/blood.2025029923/2517684/blood.2025029923.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["How I utilize somatic alterations in the diagnosis, risk stratification, and therapy of hypocellular bone marrow failure"],"author":[{"given":"Emma M","family":"Groarke","sequence":"first","affiliation":[{"name":"National Heart, Lung and Blood Institute, Bethesda, Maryland, United States"}]},{"given":"Fernanda","family":"Gutierrez-Rodrigues","sequence":"additional","affiliation":[{"name":"National Heart, Lung, and Blood Institute (NHLBI)/NIH, Bethesda, Maryland, United States"}]},{"given":"Bhavisha A.","family":"Patel","sequence":"additional","affiliation":[{"name":"National Institute of Health, Bethesda, Maryland, United States"}]}],"issued":{"date-parts":[[2026,5,7]]},"member":"234","prefix":"10.1182","source":"Crossref","volume":null,"created":{"date-time":"2026-05-07T14:54:58Z","timestamp":1778165698000,"date-parts":[[2026,5,7]]},"indexed":{"date-time":"2026-05-07T15:19:13Z","timestamp":1778167153448,"date-parts":[[2026,5,7]]},"subject":[],"abstract":"$31","language":"en","relation":{},"resource":{"primary":{"URL":"https://ashpublications.org/blood/article/doi/10.1182/blood.2025029923/568215/How-I-utilize-somatic-alterations-in-the-diagnosis"}},"subtitle":[],"deposited":{"date-time":"2026-05-07T14:54:59Z","timestamp":1778165699000,"date-parts":[[2026,5,7]]},"issn-type":[{"type":"print","value":"0006-4971"},{"type":"electronic","value":"1528-0020"}],"published":{"date-parts":[[2026,5,7]]},"publisher":"American Society of Hematology","reference":null,"short-title":[],"update-policy":"https://doi.org/10.1182/blood.2019cm0000","article-number":"blood.2025029923","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"original-title":[],"container-title":["Blood Journal"],"reference-count":0,"published-online":{"date-time":null,"timestamp":null,"date-parts":[[2026,5,7]]},"references-count":0,"short-container-title":[],"is-referenced-by-count":0},"unpaywall":{"doi":"10.1182/blood.2025029923","is_oa":false,"title":"How I utilize somatic alterations in the diagnosis, risk stratification, and therapy of hypocellular bone marrow failure","updated":"2026-05-08T16:02:47+00:00","published_date":"2026-05-07","best_oa_location":null}},"created_at":"2026-05-14T13:22:58.577Z","updated_at":"2026-05-14T15:13:26.918Z","tags":[{"paper_doi":"10.1182/blood.2025029923","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"condition","value":"Aplastic Anemia","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"condition","value":"Bone Marrow Failure","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"condition","value":"Clonal Hematopoiesis","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"condition","value":"Hypoplastic Myelodysplastic Syndrome","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"condition","value":"Inherited Bone Marrow Failure Syndromes","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"condition","value":"Myelodysplastic Syndromes","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"modality","value":"Cytogenetic Analysis","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"modality","value":"Molecular Diagnostics","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"study_design","value":"Expert Opinion/Editorial","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"study_design","value":"Expert Review / Clinical Practice Narrative","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"warning","value":"Design appears to be an expert review; no primary data or numeric outcomes are provided in the abstract.","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"warning","value":"Population characteristics (age, sex) are not reported.","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"warning","value":"Published date (2026-05-07) is in the near future relative to today's date (2026-05-14); paper appears to be a very recent publication — findings may not yet have broad external validation.","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"warning","value":"Specific clonal signatures, thresholds, and management algorithms are not detailed in the provided text.","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"warning","value":"Study design classification as 'Expert Review' may overlap with 'Clinical Practice Guidelines'; level of evidence assigned as 5 (expert opinion) accordingly.","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"warning","value":"The authors explicitly note that clinical significance of clonal hematopoiesis in BMF is 'not well established,' limiting strength of recommendations.","value_numeric":null},{"paper_doi":"10.1182/blood.2025029923","tag_type":"warning","value":"This is a 'How I' expert narrative review, not a primary research study — no original patient cohort or statistical outcomes are reported.","value_numeric":null}],"summaries":{"key_result":"Disease-specific clonal hematopoiesis (CH) signatures differ across hypocellular BMF etiologies and can help distinguish IAA from MDS-h and IBMFS; somatic alterations also estimate risk for secondary myeloid neoplasms and may inform early therapeutic intervention.","what_studied":"A narrative review on how somatic alterations—clonal hematopoiesis from somatic mutations or chromosomal abnormalities—can aid diagnosis, risk stratification, and therapy decisions in hypocellular bone marrow failure, including immune aplastic anemia, hypoplastic MDS, and inherited bone marrow failure syndromes.","limitations":"This is an expert review without reported quantitative outcomes; the abstract does not specify mutation patterns, thresholds, or comparative performance metrics.","practice_takeaway":"In hypocellular marrow failure, incorporate testing for somatic mutations and cytogenetic changes to help distinguish immune AA, MDS-h, and IBMFS, estimate risk for secondary myeloid neoplasms, and guide surveillance; in select cases, results may support earlier therapy."}},{"doi":"10.1001/jamaoncol.2026.1036","pmid":"42096237","title":"Tumor-Infiltrating Clonal Hematopoiesis and Pan-Cancer Prognosis in Patients With Solid Tumors","journal_title":"JAMA Oncology","journal_issn":"2374-2437","published_at":"2026-05-07T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13154032/","source_score":26,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-16T13:22:24.323Z","updated_at":"2026-05-16T13:22:24.323Z","tags":[{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"condition","value":"Breast Cancer","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"condition","value":"Clonal Hematopoiesis","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"condition","value":"Endometrial Cancer","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"modality","value":"Whole-Genome Sequencing","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"sample_size","value":"n=10571","value_numeric":10571},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"warning","value":"Full paper text was not accessible; summary is based solely on the abstract and results excerpt. Details on multivariate model covariates, subgroup sample sizes, and follow-up duration could not be verified.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"warning","value":"The impact_flag 'practice_changing' reflects the potential clinical utility of TI-CH as a prognostic biomarker, but prospective validation is still needed before routine clinical implementation.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"warning","value":"The study population was 60.83% female, which may reflect enrichment for breast and endometrial cancer; generalizability to other solid tumors or more balanced sex distributions is uncertain.","value_numeric":null}],"summaries":{"what_studied":"This retrospective cohort study used whole-genome sequencing data from 10,571 solid tumor patients in the Genomics England 100,000 Genomes Project (2015–2019) to assess the prevalence of tumor-infiltrating clonal hematopoiesis (TI-CH) — defined by somatic variants in 74 driver genes at 2–30% VAF in tumor tissue — and its association with clinical factors and overall survival (OS).","key_result":"TI-CH was detected in 18.38% of patients (n=1,943); it was linked to older age (OR 1.15) and prior cytotoxic chemotherapy (OR 1.24). TI-CH was independently associated with worse pan-cancer OS (HR 1.13), with the strongest signal in breast cancer (HR 1.95). Gene-level analysis flagged GATA2 variants for pan-cancer mortality (HR 3.00) and TET2 variants for breast cancer mortality (HR 2.92).","limitations":"- Retrospective design limits causal inference between TI-CH and survival outcomes.\n- Full paper text was inaccessible; details on confounding adjustment and subgroup sample sizes are incomplete.\n- TI-CH detection relied on a predefined 74-gene panel and a VAF threshold of 2–30%, which may miss variants outside this range.","practice_takeaway":"Clinicians should be aware that TI-CH — especially GATA2 and TET2 variants — may serve as an adverse prognostic biomarker in solid tumors, particularly breast cancer. Older patients and those receiving cytotoxic chemotherapy are at higher odds of harboring TI-CH, which may warrant prospective integration into tumor sequencing workflows."}},{"doi":"10.1182/bloodadvances.2025018279","pmid":"41860374","title":"Telomere length and clonal hematopoiesis interact to influence outcomes in hematopoietic stem cell transplantation","journal_title":"Blood Advances","journal_issn":"2473-9529","published_at":"2026-03-20T00:00:00.000Z","url":"https://doi.org/10.1182/bloodadvances.2025018279","source_score":9,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-03T13:44:41.353Z","updated_at":"2026-06-03T13:44:41.353Z","tags":[{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"condition","value":"Clonal Hematopoiesis","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"condition","value":"Multiple Myeloma","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"generic","value":"bortezomib","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"generic","value":"cyclophosphamide","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"generic","value":"lenalidomide","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"modality","value":"Autologous Stem Cell Transplantation","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"sample_size","value":"n=452","value_numeric":452},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"warning","value":"Study design classification as 'retrospective cohort' is inferred from context; the main methods section was not available in the provided text.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"warning","value":"The full text provided consists primarily of supplementary materials and figures rather than the main manuscript body; key statistical details (e.g., median follow-up, HR point estimates beyond p-values) were extracted from supplementary figure legends and may be incomplete.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025018279","tag_type":"warning","value":"The impact_flag 'practice_changing' is applied cautiously — the finding is novel and has direct clinical implications, but prospective validation is lacking.","value_numeric":null}],"summaries":{"what_studied":"This retrospective cohort study examined how leukocyte telomere length (LTL), measured from graft cell DNA, interacts with clonal hematopoiesis (CH) to affect outcomes in 452 myeloma patients undergoing autologous stem cell transplantation (ASCT), including progression-free survival (PFS), overall survival (OS), and blood count trajectories.","key_result":"In multivariate analysis, longer LTL was significantly associated with improved PFS in CH-negative patients (HR favoring longer LTL, p = 0.035), but not in CH-positive patients (p = 0.335); the LTL × CH interaction was statistically significant (p = 0.044). Among CH-positive patients, longer LTL was associated with higher red cell distribution width (RDW) both before myeloablative chemotherapy and after ASCT.","limitations":"- Single-center or registry-based retrospective design limits causal inference and generalizability.\n- CH clone size (VAF) did not independently affect survival, but the study may be underpowered to detect VAF-dependent effects for individual driver genes.\n- LTL-RDW associations observed in the transplant cohort were not replicated in the UK Biobank, raising questions about context specificity.","practice_takeaway":"Clinicians should be aware that longer graft LTL may confer a survival benefit after ASCT only in patients without CH — this protective effect appears to be negated by CH. Routine co-assessment of CH and LTL in the pre-transplant workup may help refine risk stratification for myeloma patients."}},{"doi":"10.1182/blood.2025031883","pmid":"41802133","title":"The prevalence and clinical significance of clonal monocytosis","journal_title":"Blood","journal_issn":"0006-4971","published_at":"2026-03-09T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2025031883","source_score":14,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-20T13:25:07.173Z","updated_at":"2026-06-20T13:25:07.173Z","tags":[{"paper_doi":"10.1182/blood.2025031883","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"condition","value":"Chronic Myelomonocytic Leukemia","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"condition","value":"Clonal Cytopenia and Monocytosis of Undetermined Significance","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"condition","value":"Clonal Hematopoiesis","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"condition","value":"Clonal Monocytosis of Undetermined Significance","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"condition","value":"Myeloid Neoplasia","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"generic","value":"DNMT3A mutation","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"generic","value":"SRSF2 mutation screening","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"generic","value":"TET2 mutation","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"modality","value":"Machine Learning Classifier","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"sample_size","value":"n=431531","value_numeric":431531},{"paper_doi":"10.1182/blood.2025031883","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"study_design","value":"Population-Based Cohort Study","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"warning","value":"MoSAIC classifier PPV and NPV are prevalence-dependent; reported values reflect the prevalence of SRSF2-CMUS in the UK Biobank monocytosis cohort and may not generalize to other settings.","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"warning","value":"Publication date listed as 2026-03-09; today's date is June 20, 2026 — this is a recently published article and findings may not yet be reflected in clinical guidelines.","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"warning","value":"The external validation cohort (CopLab, n=625,328) lacked genomic data; MN incidence was used as a surrogate for SRSF2 mutation status, which may introduce misclassification.","value_numeric":null},{"paper_doi":"10.1182/blood.2025031883","tag_type":"warning","value":"The study population is predominantly of European ancestry (UK Biobank), which may limit generalizability to other ethnic groups.","value_numeric":null}],"summaries":{"what_studied":"This population-level study assessed the prevalence, natural history, and clinical outcomes of CMUS (clonal monocytosis of undetermined significance) and CCMUS (clonal cytopenia and monocytosis of undetermined significance) in 431,531 UK Biobank participants using clinical, genomic, and health outcome data, with external validation in 625,328 Danish primary care patients (CopLab).","key_result":"CMUS with absolute monocytosis (CMUS-ABS) and CCMUS are high-risk entities: 10-year cumulative MN incidence was 14.7% for CMUS-ABS and 25.8% for CCMUS, versus 1.8% for CHIP alone. Both were also independently associated with cardiovascular and renal disease. Excluding isolated DNMT3A mutations and applying sex-specific monocyte thresholds significantly strengthened MN risk associations. The MoSAIC machine-learning classifier (using CBC indices alone) outperformed simple monocyte count cut-offs in PPV for predicting MN (14.2% vs 4.9% for monocytes >1×10⁹/L).","limitations":"- UK Biobank is a single time-point, volunteer-based cohort with potential healthy-volunteer bias; monocytosis persistence could not be fully assessed.\n- External validation (CopLab) lacked genetic data, so incident MN was used as a surrogate for SRSF2 mutation status.\n- MoSAIC classifier sensitivity for MN was modest (38%), limiting its standalone clinical utility.","practice_takeaway":"Clinicians encountering monocytosis alongside clonal hematopoiesis should not treat this as benign: CMUS-ABS and CCMUS carry >10–25% 10-year MN risk and are linked to cardiovascular and renal disease. Applying sex-specific monocyte thresholds and excluding isolated DNMT3A mutations helps identify the truly high-risk subset warranting closer surveillance."}},{"doi":"10.1001/jamaoncol.2025.5785","pmid":"41505144","title":"Clonal Hematopoiesis and Cardiovascular Disease Risk After Cancer Therapy in Patients With Solid Tumors","journal_title":"JAMA Oncology","journal_issn":"2374-2437","published_at":"2026-01-08T00:00:00.000Z","url":"https://doi.org/10.1001/jamaoncol.2025.5785","source_score":78,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-01-11","doi":"10.1001/jamaoncol.2025.5785","days":"7","issn":"2374-2437","rank":"4","field":"Clinical Medicine","score":"78","category":"Oncology","categories":["Oncology"],"_categories":["Oncology"]},"pubmed":{"doi":"10.1001/jamaoncol.2025.5785","title":"Clonal Hematopoiesis and Cardiovascular Disease Risk After Cancer Therapy in Patients With Solid Tumors.","journal":"JAMA oncology","methods":"","results":"Among 8004 eligible participants (median [IQR] age, 61.9 [52.2-69.9] years; 4385 female individuals [54.8%]) with a primary solid tumor diagnosis, 7438 had no heart failure, 7392 no ischemic CVD, and 6002 no arrhythmia before cancer therapy. Overall, 549 (6.9%) had CHIP. In the propensity score-matched cohort, participants with CHIP had a significantly higher 10-year cumulative incidence of heart failure (20.3%; 95% CI, 16.0%-24.4% vs 14.5%; 95% CI, 13.5%-15.6%; P = .001) and ischemic CVD (25.3%; 95% CI, 20.5%-30.0% vs 18.5%; 95% CI, 17.3%-20.0%; P < .001) compared with those without CHIP. In adjusted Fine-Gray models, CHIP was associated with increased risk of heart failure (subdistribution hazard ratio [sHR], 1.26; 95% CI, 1.02-1.56; P = .03). In an exploratory 24-month landmark analysis, there was a statistically significant interaction between CHIP and intensive chemotherapy (≥7 cycles) on heart failure risk (sHR, 1.02; 95% CI, 1.00-1.04; P = .03).","abstract":"$32","keywords":[],"pubmed_id":"41505144","conclusions":"","publication_date":"2026-01-08T00:00:00"},"crossref":{"DOI":"10.1001/jamaoncol.2025.5785","URL":"https://doi.org/10.1001/jamaoncol.2025.5785","ISSN":["2374-2437"],"link":[{"URL":"https://jamanetwork.com/journals/jamaoncology/articlepdf/2843268/jamaoncology_shyr_2026_oi_250080_1766168135.11316.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Clonal Hematopoiesis and Cardiovascular Disease Risk After Cancer Therapy in Patients With Solid Tumors"],"author":[{"given":"Derek","family":"Shyr","sequence":"first","affiliation":[{"name":"Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham"},{"name":"Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Yash","family":"Pershad","sequence":"additional","affiliation":[{"name":"Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Kun","family":"Zhao","sequence":"additional","affiliation":[{"name":"Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Ashwin","family":"Kishtagari","sequence":"additional","affiliation":[{"name":"Division of Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Robert W.","family":"Corty","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Eric","family":"Shinohara","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Ben Ho","family":"Park","sequence":"additional","affiliation":[{"name":"Division of Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"J. Brett","family":"Heimlich","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Leo","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Alexander G.","family":"Bick","sequence":"additional","affiliation":[{"name":"Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, 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Hematopoiesis","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"modality","value":"Chemotherapy","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"modality","value":"Immunotherapy","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"modality","value":"Radiotherapy","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"sample_size","value":"n=8004","value_numeric":8004},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"study_design","value":"Cohort Study","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"warning","value":"Primary outcome included arrhythmia, but numeric results for arrhythmia were not reported in the abstract.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"warning","value":"Propensity score matching details and treatment exposures (drug classes, doses) are not specified in the abstract.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2025.5785","tag_type":"warning","value":"Single-center design (BioVU) may limit generalizability beyond this health system.","value_numeric":null}],"summaries":{"what_studied":"A single-center cohort study (BioVU, 2006–2025) tested whether clonal hematopoiesis of indeterminate potential (CHIP) is associated with time to first cardiovascular event after chemotherapy, radiotherapy, or immunotherapy in adults with primary solid tumors, using competing-risk methods.","key_result":"Among 8004 patients (549 with CHIP, 6.9%), propensity score–matched analyses showed higher 10-year cumulative incidence with CHIP vs no CHIP for heart failure (20.3% vs 14.5%; P=.001) and ischemic CVD (25.3% vs 18.5%; P<.001). Adjusted Fine–Gray models found increased heart failure risk with CHIP (sHR 1.26; 95% CI, 1.02–1.56; P=.03), and an exploratory 24‑month landmark showed a CHIP×intensive chemotherapy (≥7 cycles) interaction (sHR 1.02; 95% CI, 1.00–1.04; P=.03).","limitations":"Single-center biobank cohort using EHR-linked genomic data limits generalizability. Results are observational despite propensity matching, and the chemotherapy interaction arose from an exploratory landmark analysis.","practice_takeaway":"In adults with solid tumors receiving cancer therapy, CHIP marks higher 10-year risk of heart failure and ischemic CVD. If available, CHIP status may help risk-stratify patients for closer cardio-oncology surveillance, particularly with intensive chemotherapy."}}],"initialOffset":7,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Clonal Hematopoiesis"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Clonal Hematopoiesis"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Clonal Hematopoiesis"}}}]]

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