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:T6d6,Clonal hematopoiesis (CH) refers to the presence of somatic variants in hematopoietic stem and progenitor cells (HSPC) that result in expansion over time. CH of indeterminate potential (CHIP) is operationally defined as pathogenic variants in oncogenic driver genes occurring in HSPCs at variant allele frequencies ≥ 2%. CH is associated with increased risk for progressive cytopenias (also called clonal cytopenia of undetermined significance), hematological (predominantly myeloid but also lymphoid) neoplasms, cytosis (including monocytosis), and nonhematological conditions such as atherosclerotic cardiovascular and cerebrovascular disease. CH is linked to numerous other diseases including venous thromboembolism, type 2 diabetes mellitus, chronic obstructive pulmonary disease, osteoporosis, and gout, with a potential protective impact in Alzheimer's disease (AD). CH detection is becoming increasingly common due to the ubiquitous use of somatic and germline sequencing in clinical practice, particularly, in oncology. The clinical implications of CH are most relevant in therapy-related myeloid neoplasms (t-MN), with antecedent CH clones in genes such as TP53, PPM1D, and/or CHEK2 having a clear selection advantage. Furthermore, genetic predisposition to CH has provided some clarity on the origin and evolution of CH. We are currently defining the role for CH assessment in individuals with persistent (≥ 4 months) unexplained cytopenias, in patients with malignancies prior to adjuvant cytotoxic chemotherapy and/or radiation or radionuclide therapy, screening prior to autologous hematopoietic stem cell transplantation or chimeric antigen receptor T cell (CAR-T) therapy, and to work-up potentially germline mosaic variants.31:Ta3c,ABSTRACT Condition Overview Clonal hematopoiesis (CH) refers to the presence of somatic variants in hematopoietic stem and progenitor cells (HSPC) that result in expansion over time. Diagnosis CH of indeterminate potential (CHIP) is operationally defined as pathogenic variants in oncogenic driver genes occurring in HSPCs at variant allele frequencies ≥ 2%. Clinical Associations CH is associated with increased risk for progressive cytopenias (also called clonal cytopenia of undetermined significance), hematological (predominantly myeloid but also lymphoid) neoplasms, cytosis (including monocytosis), and nonhematological conditions such as atherosclerotic cardiovascular and cerebrovascular disease. CH is linked to numerous other diseases including venous thromboembolism, type 2 diabetes mellitus, chronic obstructive pulmonary disease, osteoporosis, and gout, with a potential protective impact in Alzheimer's disease (AD). Management Recommendations CH detection is becoming increasingly common due to the ubiquitous use of somatic and germline sequencing in clinical practice, particularly, in oncology. The clinical implications of CH are most relevant in therapy‐related myeloid neoplasms (t‐MN), with antecedent CH clones in genes such as TP53, PPM1D, and/or CHEK2 having a clear selection advantage. Furthermore, genetic predisposition to CH has provided some clarity on the origin and evolution of CH. We are currently defining the role for CH assessment in individuals with persistent (≥ 4 months) unexplained cytopenias, in patients with malignancies prior to adjuvant cytotoxic chemotherapy and/or radiation or radionuclide therapy, screening prior to autologous hematopoietic stem cell transplantation or chimeric antigen receptor T cell (CAR‐T) therapy, and to work‐up potentially germline mosaic variants. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Clonal Cytopenia of Undetermined Significance: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Clonal Cytopenia of Undetermined Significance (condition). Clinician-written summaries and actionable practice insights. Updated daily.\",\"url\":\"https://www.reachrx.ai/hub/tag/condition/Clonal%20Cytopenia%20of%20Undetermined%20Significance\",\"breadcrumb\":{\"@type\":\"BreadcrumbList\",\"itemListElement\":[{\"@type\":\"ListItem\",\"position\":1,\"name\":\"Home\",\"item\":\"https://www.reachrx.ai\"},{\"@type\":\"ListItem\",\"position\":2,\"name\":\"Research Hub\",\"item\":\"https://www.reachrx.ai/hub\"},{\"@type\":\"ListItem\",\"position\":3,\"name\":\"Conditions\",\"item\":\"https://www.reachrx.ai/hub/tag/condition\"},{\"@type\":\"ListItem\",\"position\":4,\"name\":\"Clonal Cytopenia of Undetermined Significance\",\"item\":\"https://www.reachrx.ai/hub/tag/condition/Clonal%20Cytopenia%20of%20Undetermined%20Significance\"}]}}"}}]],["$","$L2f",null,{"title":"Clonal Cytopenia of Undetermined Significance: Research & Clinical Takeaways","description":"Discover peer-reviewed research on Clonal Cytopenia of Undetermined Significance with concise clinician summaries and next-step guidance.","papers":[{"doi":"10.1038/s41375-026-03029-7","pmid":"42380663","title":"Spatial remodeling of bone marrow architecture defines tissue-state signatures of disease activity and therapeutic response in myelodysplastic neoplasms","journal_title":"Leukemia","journal_issn":"0887-6924","published_at":"2026-06-30T00:00:00.000Z","url":"https://doi.org/10.1038/s41375-026-03029-7","source_score":11,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-09T13:35:58.474Z","updated_at":"2026-07-09T13:35:58.474Z","tags":[{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"condition","value":"Clonal Cytopenia of Undetermined Significance","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"condition","value":"Myelodysplastic Neoplasms","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"generic","value":"azacitidine","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"generic","value":"decitabine","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"generic","value":"venetoclax","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"modality","value":"BCL-2 Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"modality","value":"Hypomethylating Agent","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"modality","value":"Multiplex Immunofluorescence Imaging","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"sample_size","value":"n=99","value_numeric":99},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"study_design","value":"Longitudinal Cohort Study with Cross-Sectional Diagnostic Component","value_numeric":null},{"paper_doi":"10.1038/s41375-026-03029-7","tag_type":"warning","value":"The study design combines cross-sectional diagnostic and longitudinal samples; the level of evidence reflects the best applicable single-institution observational design without external validation. The 'practice_changing' impact flag is applied cautiously—MDS-MAPS is a research tool not yet validated for routine clinical use. Sample sizes for key subanalyses (e.g., blast progression modeling, n=16) are small, limiting generalizability. The total sample size tag reflects biopsy samples; unique patient count is lower (n=49 MDS/CCUS + 21 controls).","value_numeric":null}],"summaries":{"what_studied":"Whole-slide multiplex immunofluorescence (MxIF) imaging with single-cell spatial phenotyping was applied to bone marrow trephines from MDS patients (n=36 diagnostic, n=29 longitudinal), CCUS precursors (n=13), and normal controls (n=21), totaling >5 million spatially resolved cells, to map microarchitectural remodeling and derive a composite Microarchitectural Perturbation Score (MDS-MAPS) from 82 cellular and spatial features.","key_result":"In leave-one-patient-out cross-validation, MDS-MAPS distinguished remission from active disease with AUC 0.883 vs. AUC 0.660 for blast percentage alone, and separated low-blast MDS from CCUS with AUC 0.815 vs. AUC 0.706–0.706 for VAF-based mutation burden; mixed-effects modeling confirmed MAPS decreased in remission independent of blast burden, with architectural normalization during remission and re-emergence at relapse.","limitations":"- Small longitudinal cohort (14 MDS patients, 29 serial biopsies; blast progression modeling limited to n=16).\n- MDS-MAPS weights were expert-curated, introducing potential subjectivity, and random slopes were not modeled due to limited serial samples per patient.\n- Whole-slide images require institutional data use agreements; external validation in independent cohorts was not performed.","practice_takeaway":"Quantitative bone marrow microarchitecture scoring (MDS-MAPS) outperforms blast counting for detecting remission and distinguishing CCUS from low-blast MDS—consider spatial imaging biomarkers as a complement to standard blast enumeration and molecular testing in MDS assessment. Architectural normalization may serve as an early signal of treatment response even when blast counts remain low."}},{"doi":"10.1182/bloodadvances.2025019262","pmid":"41734386","title":"Exposure to Agent Orange and association with myelodysplastic syndromes","journal_title":"Blood Advances","journal_issn":"2473-9529","published_at":"2026-02-24T00:00:00.000Z","url":"https://doi.org/10.1182/bloodadvances.2025019262","source_score":61,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-05-06","doi":"10.1182/bloodadvances.2025019262","days":"14","issn":"2473-9529","rank":"3","field":"Clinical Medicine","score":"61","category":"Hematology","categories":["Hematology"],"_categories":["Hematology"]},"pubmed":{"doi":"10.1182/bloodadvances.2025019262","title":"Exposure to Agent Orange and association with myelodysplastic syndromes.","journal":"Blood advances","methods":"","results":"","abstract":"","keywords":[],"pubmed_id":"41734386","conclusions":"","publication_date":"2026-02-24T00:00:00"},"crossref":{"DOI":"10.1182/bloodadvances.2025019262","URL":"https://doi.org/10.1182/bloodadvances.2025019262","ISSN":["2473-9529","2473-9537"],"link":[{"URL":"https://ashpublications.org/bloodadvances/article-pdf/10/9/3054/2515905/blooda_adv-2025-019262-main.pdf","content-type":"application/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https://ashpublications.org/bloodadvances/article-pdf/10/9/3054/2515905/blooda_adv-2025-019262-main.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"3054-3058","type":"journal-article","issue":"9","score":1,"title":["Exposure to Agent Orange and association with myelodysplastic syndromes"],"author":[{"given":"Mikkael A.","family":"Sekeres","sequence":"first","affiliation":[{"name":"1Division of Hematology, Sylvester Cancer Center, University of Miami, Miami, FL"}]},{"given":"Amy E.","family":"DeZern","sequence":"additional","affiliation":[{"name":"2Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD"}]},{"given":"Michael","family":"Otterstatter","sequence":"additional","affiliation":[{"name":"3The Emmes Company, Rockville, MD"}]},{"given":"Eric","family":"Padron","sequence":"additional","affiliation":[{"name":"4Department of Malignant Hematology, H. 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dose and duration data are absent.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019262","tag_type":"warning","value":"Only 6.1% of the cohort reported AO exposure (n=130), limiting statistical power for subgroup analyses.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019262","tag_type":"warning","value":"Study design is labeled prospective cohort (enrollment), but the Agent Orange exposure analysis is retrospective/observational — causal inference is limited.","value_numeric":null},{"paper_doi":"10.1182/bloodadvances.2025019262","tag_type":"warning","value":"The cohort was enriched for patients referred for bone marrow biopsy (all had cytopenias), which may overestimate AO–MDS association relative to the general veteran population.","value_numeric":null}],"summaries":{"what_studied":"This retrospective cohort study used data from the National MDS Natural History Study (n=2,115 patients with ≥1 cytopenia enrolled at 161 US sites, 2016–2024) to assess whether Agent Orange (AO) exposure is associated with MDS diagnosis, molecular features, cytogenetics, and clinical outcomes, comparing 130 AO-exposed vs. 1,985 non-exposed patients.","key_result":"AO-exposed patients were significantly more likely to be diagnosed with MDS or CCUS (54% vs. 37%, P=.022). On multivariable analysis, AO exposure was associated with more molecular mutations (OR 1.10; 95% CI 1.0–1.2; P=.047), poor/very poor cytogenetics (OR 2.39; 95% CI 1.04–5.14; P=.03), younger age at MDS diagnosis (OR 0.96/year; P=.008), TET2 mutations (26% vs. 17%; P=.008), RNA splicing pathway alterations (35% vs. 23%; P=.004), and a higher 2-year risk of disease progression (HR 1.8; 95% CI 1.2–2.8; P=.004); overall survival did not differ (HR 1.1; P=.72).","limitations":"- No data on AO exposure dose or duration, limiting dose-response analysis.\n- Unable to control for subsequent occupational exposures linked to MDS.\n- AO exposure was self-reported, introducing potential recall or ascertainment bias.","practice_takeaway":"Clinicians evaluating unexplained cytopenias in Vietnam-era veterans should inquire about AO exposure, as it is independently linked to MDS diagnosis and faster disease progression within 2 years. 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