Abstract P3-08-01: Clonal hematopoiesis of indeterminate potential (CHIP) in metastatic triple negative breast cancer

Clonal hematopoiesis (CH) of indeterminate potential (CHIP) is a risk factor for cardiovascular disease. The relationship between CHIP and coronary microvascular dysfunction (CMD) is unknown. The current study examines the association between CHIP and CH with CMD and the potential relationships in risk for adverse cardiovascular outcomes. In this retrospective observational study, targeted next-generation sequencing was performed for 177 participants with no coronary artery disease who presented with chest pain and underwent routine coronary functional angiogram. Patients with somatic mutations in leukemia-associated driver genes in hematopoietic stem and progenitor cells were examined; CHIP was considered at a variant allele fraction ≥2%; CH was considered at a variant allele fraction ≥1%. CMD was defined as coronary flow reserve to intracoronary adenosine of ≤2. Major adverse cardiovascular events considered were myocardial infarction, coronary revascularization, or stroke. A total of 177 participants were examined. Mean follow-up was 12±7 years. A total of 17 patients had CHIP and 28 had CH. Cases with CMD (n=19) were compared with controls with no CMD (n=158). Cases were 56±9 years, were 68% women, and had more CHIP (27%; P=0.028) and CH (42%; P=0.001) than controls. CMD was associated with independent risk for major adverse cardiovascular events (hazard ratio, 3.89 [95% CI, 1.21-12.56]; P=0.023), and 32% of this risk was mediated by CH. The risk mediated by CH was ≈0.5× as large as the direct effect of CMD on major adverse cardiovascular events. In humans, we observe patients with CMD are more likely to have CHIP, and nearly one-third of major adverse cardiovascular events in CMD are mediated by CH.

Clonal hematopoiesis of indeterminate potential (CHIP) is frequent in patients with solid tumors. Prospective data about CHIP prevalence at breast cancer diagnosis and its dynamic evolution under treatment selective pressure are limited. We performed targeted error-corrected sequencing on 614 samples from 380 patients with breast cancer. We investigated the dynamics of CHIP on prospectively collected paired samples from patients with early breast cancer (eBC) receiving chemotherapy (CT) or endocrine therapy (ET). We assessed the correlation of CHIP with survival in patients with metastatic triple-negative breast cancer (mTNBC). We estimated the risk of progression to treatment-related myeloid neoplasms (t-MN) according to the clonal hematopoiesis risk score (CHRS). In exploratory analyses, we considered clonal hematopoiesis (CH) with variant allele fraction (VAF) ≥0.005. CHIP was identified in 15% of patients before treatment. Few CHIP emerged after treatment, and the risk of developing new mutations was similar for patients receiving CT versus ET (odds ratio [OR], 1.16; P = .820). However, CT increased the risk of developing new CH with VAF ≥0.005 (OR, 3.45; P = .002). Five TP53-mutant CH with VAF ≥0.005 emerged among patients receiving CT. Most patients had low risk of t-MN according to the CHRS score. CHIP did not correlate with survival in mTNBC. CHIP is frequent in patients with breast cancer. In this study, CT did not lead to emergence of new CHIP, and most patients had low risk of developing t-MN. This finding is reassuring, given long life expectancy of patients with eBC and the association of CHIP with morbidity and mortality. However, TP53-mutant CH with VAF ≥0.005 emerged with CT, which carries high risk of t-MN. Evolution of these small clones and their clinical significance warrant further investigation.

The Effect of Clonal Hematopoiesis of Indeterminate Potential (CHIP) and Aspirin on Clinical Outcomes in the Healthy Elderly: A Sub-Study of the Aspirin in Reducing Events in the Elderly (ASPREE) Randomized Controlled Trial

Clonal Hematopoiesis of Indeterminate Potential Is Associated with Decreased Inflammatory Toxicity and Increased Late Cytopenia in Patients with Multiple Myeloma and Non-Hodgkin Lymphoma Treated with Chimeric Antigen Receptor T-Cell Therapy

Clonal hematopoiesis (CH) of indeterminate potential (CHIP), driven by somatic mutations in leukemia-associated genes, confers increased risk of hematologic malignancies, cardiovascular disease, and all-cause mortality. In blood of healthy individuals, small CH clones can expand over time to reach 2% variant allele frequency (VAF), the current threshold for CHIP. Nevertheless, reliable detection of low-VAF CHIP mutations is challenging, often relying on deep targeted sequencing. Here, we present UNISOM, a streamlined workflow for enhancing CHIP detection from whole-genome and whole-exome sequencing data that are underpowered, especially for low VAFs. UNISOM utilizes a meta-caller for variant detection, in couple with machine learning models which classify variants into CHIP, germline, and artifact. In whole-exome sequencing data, UNISOM recovered nearly 80% of the CHIP mutations identified via deep targeted sequencing in the same cohort. Applied to whole-genome sequencing data from Mayo Clinic Biobank, it recapitulated the patterns previously established in much larger cohorts, including the most frequently mutated CHIP genes and predominant mutation types and signatures, as well as strong associations of CHIP with age and smoking status. Notably, 30% of the identified CHIP mutations had < 5% VAFs, demonstrating its high sensitivity toward small mutant clones. This workflow is applicable to CHIP screening in population genomic studies. The UNISOM pipeline is freely available at https://github.com/shulanmayo/UNISOM and https://ngdc.cncb.ac.cn/biocode/tool/7816.

Clonal hematopoiesis of indeterminate potential (CHIP) has been associated with increased risk of cardiovascular disease (CVD) events and mortality. However, there are no approved therapies for preventing or treating CHIP. To investigate whether low-dose aspirin might benefit older adults with CHIP for the primary prevention of CVD. This was a prespecified substudy of the Aspirin in Reducing Events in the Elderly (ASPREE) double-blind, randomized clinical trial of daily low-dose aspirin vs placebo evaluating disability-free survival, which took place at primary and community care facilities in the US and Australia. Enrollment was from March 2010 to December 2014, and the randomized trial ended in June 2017. Community-dwelling Australian adults aged 70 years and older without a diagnosed cardiovascular event, atrial fibrillation, a serious intercurrent illness likely to cause death within the next 5 years, anemia, or a current or recurrent condition with a high risk of bleeding were included in the original study. Of 19 114 in the original trial, 11 402 were included in the substudy, and 9434 were included in the analysis. Follow-up for this substudy went through June 2022, with data analysis in February 2025. In-trial median (IQR) follow-up time was 4.6 (3.5-5.6) years, and posttrial observational follow-up was 8.7 (7.5-10.1) years from randomization. Participants were randomized to aspirin, 100 mg, daily or placebo. CHIP was measured in blood specimens collected at trial entry. Major adverse cardiovascular events (MACEs), including fatal and nonfatal ischemic stroke, nonfatal myocardial infarction and coronary heart disease death, and clinically significant bleeding were adjudicated by independent expert committees blinded to trial-group assignments. A total of 9434 participants (median [IQR] age, 73.7 [71.6-77.1] years; 5067 [54%] female) provided a sample at baseline for analysis, 2124 of whom (23%) had CHIP at variant allele fraction (VAF) ≥2%, with 532 (5.6%) at ≥10% VAF. CHIP was not associated with increased risk of MACEs at 2% to 10% VAF (adjusted hazard ratio [aHR], 0.84, 95% CI, 0.68-1.03; P = .09) or ≥10% VAF (aHR, 0.80, 95% CI, 0.57-1.12; P = .19). However, CHIP was associated with increased risk of clinically significant bleeding (2%-10% VAF: aHR, 1.24; 95% CI 1.02-1.51; P = .03; ≥10% VAF: aHR, 1.21; 95% CI, 0.85-1.73; P = .28). There was no evidence of a differential effect of aspirin according to presence of CHIP on MACEs (without CHIP: HR, 0.91; 95% CI, 0.72-1.16; 2%-10% VAF: HR, 1.40; 95% CI, 0.77-2.53; ≥10% VAF: HR, 1.33; 95% CI, 0.52-3.37; heterogeneity P = .35) or clinically significant bleeding (without CHIP: HR, 1.64; 95% CI, 1.22-2.30; 2%-10% VAF: HR, 1.45; 95% CI, 0.82-2.57; ≥10% VAF: HR, 1.41; 95% CI, 0.49-4.07; heterogeneity P = .91). In this secondary analysis of a randomized clinical trial of daily low-dose aspirin in healthy adults 70 years and older, CHIP was not associated with higher CVD risk. However, participants with CHIP had a greater risk of clinically significant bleeding. There was no evidence that participants with CHIP were more likely than those without CHIP to benefit or experience more harm from aspirin when used for primary prevention of CVD events. ClinicalTrials.gov Identifier: NCT01038583.

INTRO: Clonal hematopoiesis (CH) of indeterminate potential (CHIP) is associated with poor outcomes in those with non-hematologic cancers. CH mutated macrophages and neutrophils have increased capacity to home to peripheral tissues, driving local inflammation; they are also implicated in immunotherapy related toxicity. The relationship between CH and the microbiome in those treated with immunotherapy is not well understood. RESULTS: 35 patients with stage IV melanoma treated with upfront immunotherapy; treatment and cohort characteristics are below (Table 1). We performed error corrected duplex sequencing on peripheral blood mononuclear cells using a panel previously validated for CH mutations. With a cutoff of 0.5% variant allele frequency (VAF), among 10 CHIP positive patients, we found mutations in TET2 (8/10), DNMT3A (7/10), PPM1D (2/10), and JAK2 (1/10). There was no difference in either survival or response based on CHIP status (Log-Rank Chi-Square p=0.44); however, CHIP positivity was associated with greater microbiome richness as measured by alpha diversity (p=0.0012 Shannon diversity) and distinct structural/compositional diversity vs CHIP negative patients as measured by beta diversity (p=0.032, R Squared= 0.045). We inferred KEGG pathway activity from whole genome sequencing and identified that CHIP positive patients were enriched for exopolysaccharide biosynthesis while CHIP negative patients had higher expression of nucleotide sugars biosynthesis and amino acid metabolism pathways. DISCUSSION: In patients treated with immunotherapy for melanoma, microbiome diversity signatures correlate with presence of CHIP. The analysis suggests that there are distinct taxonomic and functional features defining CHIP positivity. The effect of these cells in the tumor microenvironment and their role in immunotherapy response requires further exploration. Citation Format: Eleanor A. Fallon, Samuel Urrutia, Reed Ayabe, Manoj Chelvanambi, Ashish Damania, Sarah Johnson, Tomoyuki Tanaka, Zongrui Li, Yongwoo David Seo, Samuel Cass, Matthew C. Wong, Nadim Ajami, Jennifer Wargo, Koichi Takahashi. Identifying gut microbial determinants of clonal hematopoiesis of indeterminate potential (CHIP) in immunotherapy treated melanoma patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 2801.

Pre-existing clonal hematopoiesis in CAR-T recipients is not associated with increased immunotoxicity and inflammatory serum signatures

Clonal hematopoiesis of indeterminate potential after (neo)adjuvant chemotherapy versus endocrine therapy for early breast cancer: the CIRCE-eBC prospective cohort study Background: Clonal hematopoiesis of indeterminate potential (CHIP) is an age-related condition associated with higher risk of hematologic malignancies, cardiovascular disease, and all-cause mortality. Patients (pts) with early breast cancer (eBC) receiving chemotherapy (CT) have increased risk of treatment-related myeloid neoplasms (tMN); the benefit of CT in eBC pts is often limited. Little is known about the prevalence and dynamics of CHIP in eBC pts. Methods: We prospectively identified two cohorts of pts with eBC: cohort A – pts receiving (neo)adjuvant CT with or without adjuvant endocrine therapy (ET); cohort B – pts receiving ET only. Blood was collected prior to initiation of treatment (T1) and after either (neo)adjuvant CT or 6-18 months of adjuvant ET (T2). We performed targeted sequencing of cryopreserved peripheral blood mononuclear cell (PBMC)-derived genomic DNA and defined CHIP as the presence of ≥1 pathogenic somatic mutation at variant allele fraction (VAF) ≥0.02. In additional analyses we used VAF≥0.005. Results: We enrolled 118 and 116 pts in cohorts A and B, respectively. Pts in cohort A were younger (median age 51 vs 57, p&amp;lt; 0.001), less frequently Caucasian (83.9 vs 96.6%; p=0.005) and former/current smokers (28.0 vs 43.1%, p=0.038). All pts in cohort B had hormone receptor-positive (HR+) eBC; in cohort A 50% of pts had HR+/HER2-, 16% had HR+/HER2+, 8.5% had HR-/HER2+ and 25.4% had HR-/HER2- eBC (p&amp;lt; 0.001). Pts in cohort A had higher stage (stage II-III 68.7 vs 27.6%; p&amp;lt; 0.001) and grade (grade 3 65.3 vs 15.5%; p&amp;lt; 0.001) tumors. Genetic testing was more frequently performed in pts receiving CT (88.1 vs 68.1%, p&amp;lt; 0.001), though the rate of germline pathogenic variants was similar (13.5 vs 17.7%, p=0.079). In cohort A, 38% received anthracyclines, 7% platinum and 57% anthracycline/platinum-sparing CT. Median time between T1 and T2 was 189.5 (150,406) and 280 (147, 425) days in cohort A and B (p&amp;lt; 0.001). The prevalence of CHIP, defined by mutations at VAF ≥ 0.02, was similar at T1 in cohort A (14.4%) vs B (18.1%) (p=0.556). Number of pts with new CHIP variants at T2 was also similar (A 3.4% vs B 6.0%) (p=0.373). After adjusting for age and stage, odds ratio (OR) of developing new CHIP variants in cohort B vs A was 1.28 (95% CI 0.32 – 5.68, p=0.733). Age correlated with baseline prevalence of CHIP (p&amp;lt; 0.001). Most frequent new CHIP variants at T2 in cohort A were DNMT3A (3), PPM1D (1), NF1 (1). To investigate whether pts receiving CT were more likely to have emergence of small hematopoietic clones, we assessed pathogenic variants present at VAF ≥0.005. These were detected at T1 in 55 (46.6%) and 61 (52.6%) pts in cohort A and B, respectively. Few pts without pathogenic variants at T1 developed them at T2 (3 pts in cohort A and 4 in cohort B). 21 pts (27 variants) in cohort A and 11 pts (12 variants) in cohort B had new variants at T2. Pts with new variants vs not (32 vs 202 pts) had similar characteristics, excepting age (median 60.5 vs 54.0, p=0.011). After correcting for age and stage, OR of developing new pathogenic variants given ET vs CT was 0.25 (95% CI 0.10-0.62, p=0.003). Most frequent newly detected variants were in DNMT3A (14), PPM1D (5), TET2 (4) and TP53 (2) in cohort A; DNMT3A (3), TET2 (3) and ZNF318 (2) in cohort B. Conclusions: In the CIRCE-eBC study, CT administration did not lead to emergence of CHIP over a 6-9 month period vs ET alone. This finding is reassuring in the setting of long life-expectancy for eBC pts and the association of CHIP with significant morbidity and mortality. However, consistent with known risk of development of MN, CT was associated with emergence of low frequency pathogenic variants in PPM1D and TP53, which have been associated with elevated risk of tMN. The evolution and prognostic role of these small clones is unclear and warrants additional investigation. Citation Format: Stefania Morganti, Qingchun Jin, Katheryn Santos, Christopher Gibson, Ashka Patel, Alex Wilson, Margaret Merrill, Julie Vincuilla, Samantha Stokes, Marla Lipsyc-Sharf, Tonia Parker, Tari King, Elizabeth A. Mittendorf, Giuseppe Curigliano, Melissa E. Hughes, Nabihah Tayob, Nancy U. Lin, Peter Miller, Sara Tolaney, Judy Garber, Heather A. Parsons. Clonal hematopoiesis of indeterminate potential after (neo)adjuvant chemotherapy versus endocrine therapy for early breast cancer: the CIRCE-eBC prospective cohort study [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P5-14-03.

Background:Clonal hematopoiesis of indeterminate potential (CHIP) is the age-related presence of expanded somatic clones secondary to leukemogenic driver mutations and is associated with cardiovascular (CV) disease and mortality. We sought to evaluate relationships between CHIP with cardiometabolic diseases and incident outcomes in high-risk individuals.Methods:CHIP genotyping was performed in 8469 individuals referred for cardiac catheterization at Duke University (CATHGEN study) to identify variants present at a variant allele fraction (VAF) ≥2%. Associations were tested among any CHIP variant, large CHIP clones (VAF ≥10%) and individual CHIP genes with prevalent cardiometabolic traits. Cox proportional hazard models tested CHIP associations with time-to-overall mortality and Fine-Gray analyses tested CHIP associations with incident cardiovascular outcomes.Results:We identified 463 CHIP variants in 427 individuals (5.0%) of which 268 (3.2%) harbored large CHIP clones. CHIP and large CHIP were associated with lower odds of obesity (OR 0.79 [95% CI 0.65–0.98], p=0.03; OR 0.76 [95% CI 0.57–0.99], p=0.04, respectively). CHIP was associated with prevalent HF (OR 1.25 [95% CI 1.01 – 1.55], p=0.04; especially for non-DNMT3A CHIP (OR 1.38 [95% CI 1.04–1.82], p=0.02). CHIP was also associated with incident events: Non-DNMT3A CHIP was associated with increased risk of time-to-HF hospitalization (HR 1.29 [95% CI 1.02–1.63], p=0.03).Conclusions:In high-risk individuals referred for cardiac catheterization, large CHIP and non-DNTM3A CHIP were associated with obesity, prevalent HF, incident CV events. These findings strengthen the importance of CHIP as a biomarker for CV disease and highlight the contributing risk of large CHIP clones and non-DNMT3A CHIP variants.

Clonal Hematopoiesis of Indeterminate Potential (CHIP) is characterized by expanded blood cell clones containing somatic mutations in leukemia-associated genes in patients without hematologic malignancies. CHIP incidence increases with age, and it is primarily associated with an increased risk of transformation to myeloid neoplasms and cardiovascular disease. Growing evidence indicates that CHIP is associated with aberrant inflammatory signaling, and retrospective analyses have revealed increased risk or poor outcomes in a wide range of diseases. We hypothesized that CHIP alters the immune response to solid tumors by dysregulating tumor-infiltrating leukocytes, resulting in increased tumor growth. Indeed, CHIP mutations have been identified in tumor-infiltrating leukocytes in patients, and some observational studies have reported an association between CHIP and decreased overall survival among patients with solid tumors. Using multiple solid tumor models, we investigated the impact of CHIP on tumor progression and the functional effects of CHIP mutations on tumor-infiltrating leukocytes. We used bone marrow transplantation to develop chimeric mouse models of CHIP containing mixtures of wild type and CHIP-mutant hematopoietic cells representing the two most common CHIP genotypes observed in patients (Dnmt3a and Tet2). Once transplants were engrafted, CHIP mice were injected with syngeneic melanoma or triple negative breast cancer cells at their orthotopic site. We observed genotype-specific effects on tumor growth, with Tet2-CHIP displaying increased tumor growth and aberrant inflammatory signaling compared to control mice. Immunophenotyping of tumor-infiltrating leukocytes uncovered altered immune infiltrate between control, Dnmt3a-CHIP, and Tet2-CHIP. We further observed a trend towards greater metastatic outgrowth in mice with CHIP, which was similarly observed in a retrospective clinical cohort of patients with breast cancer. These results suggest that while CHIP may mediate differential outcomes in solid tumors via altered immune cell function, the effects of common CHIP genotypes must each be considered independently. They further support the need for additional mechanistic and translational studies into the relationship between CHIP and solid tumors. Citation Format: Sarah C. Reed, Chad Potts, P. Brent Ferrell, Ben H. Park. Modeling clonal hematopoiesis of indeterminate potential (CHIP) in solid tumors: genotype-specific effects on tumor growth and immune microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 1210.

Recipients of Myelotoxic Chemotherapy Have Increased Prevalence of Clonal Hematopoiesis of Indeterminate Potential (CHIP) with a Typical Distribution of Chip-Associated Mutations

Clonal hematopoiesis of indeterminate potential (CHIP) is an emerging risk factor for cardiovascular diseases. Genetic IL (interleukin)-6 signaling deficiency reduced cardiovascular disease risk in CHIP carriers. However, the association between CHIP and incident abdominal aortic aneurysm (AAA) and whether IL-6 signaling inhibition attenuates AAA risk among individuals with CHIP remained unclear. Participants without prevalent AAA from the UK Biobank were included. The associations of any CHIP (variant allele fraction, ≥2%), large CHIP (variant allele fraction, ≥10%), and gene-specific CHIP subtypes with incident AAA were investigated. The protection role of IL6R p.Asp358Ala, a genetic proxy for IL-6 deficiency, was tested after stratification by CHIP status. Furthermore, the interaction and joint effects of CHIP and genetic susceptibility on AAA risk were tested. This study included 425 211 participants. Any CHIP and large CHIP was identified in 13 768 (3.2%) and 8576 (2.0%) participants, respectively. CHIP was associated with an increased risk of incident AAA (hazard ratio [HR], 1.21 [95% CI, 1.01-1.44]; P=0.034), with large CHIP clones exhibiting greater effect size (HR, 1.35 [95% CI, 1.10-1.66]; P=0.0045). Driver gene-specific analyses revealed that ASXL1-mediated CHIP exerted the strongest effect size on AAA risk (HR, 2.10 [95% CI, 1.54-2.88]; P<0.001). The presence of 2 IL6R p.Asp358Ala alleles attenuated the risk of AAA in large CHIP carriers (HR, 0.48 [95% CI, 0.23-0.99]; P=0.046). In the joint analysis, participants with CHIP and high genetic risk had a higher risk of developing AAA than those without CHIP and with low genetic risk (HR, 2.15 [95% CI, 1.63-2.85]; P<0.001). CHIP is associated with an increased risk of AAA. Genetic IL-6 signaling deficiency attenuates the risk of AAA in large CHIP carriers. CHIP may serve as an attractive target for the prevention and treatment of AAA.

e24108 Background: Clonal hematopoiesis of Indeterminate Potential (CHIP) is associated with adverse clinical outcomes including increased risk of hematologic malignancies and heart disease. Limited data suggest an increased prevalence of CHIP in patients treated for solid tumors, particularly after exposure to radiation and chemotherapy. CHIP testing may inform risk-reduction strategies for cancer survivors. Little is known about patient knowledge, attitudes, and preferences regarding CHIP testing. Methods: We surveyed survivors without history of recurrence participating in an ongoing prospective cohort study of young women with breast cancer (BC). The survey was sent by email and included an introduction to CHIP including risk factors and clinical associations. Respondents then reviewed a vignette and were asked about CHIP testing preferences (definitely/probably test vs. definitely/probably not test) considering sequentially: 1) population-based 10-year risk of BC recurrence, hematological malignancy and heart disease; 2) estimated increase in these risks with CHIP; 3) current CHIP management; 4) a dedicated CHIP clinic; and 5) a theoretical CHIP treatment. Changes in preferences from the prior scenario were evaluated with the McNemar's test using a type I error rate of 5%. Results: 528/642 (82.2%) eligible women responded to the survey, at a median age of 46 (range: 31-54) years (median time from diagnosis: 108 months (range: 60-168)), and 88% were white. Most had stage 1/2 BC (78.8%) and had received chemotherapy (73.1%) and/or radiation (61.9%). 93.6% had never heard of CHIP prior to survey. After initial patient vignette presentation, most women (87.1%,) recommended CHIP testing if offered. Preferences for testing decreased (p&lt;0.05) when considering population-based risks, with 11.1% shifting their preference from CHIP testing to not testing. After considering increased risks associated with CHIP, interest in testing increased (p&lt;0.05), with 10.1% shifting their preference to testing. Interest significantly (p&lt;0.05) increased with the possibility of managing CHIP through a clinic or a hypothetical CHIP treatment, with 7.2% and 14.1% switching their preferences towards testing, respectively. Finally, 75.8% responded that they themselves, after learning about CHIP and reviewing the vignette, would want to have CHIP testing; 28.2% reported that learning about CHIP and the associated risks caused them at least moderate anxiety. Conclusion: Few young BC survivors were aware of CHIP yet most indicated an interest in testing after learning about it. Testing preferences were influenced by risks presented and potential management strategies. Findings highlight the importance of effective risk communication and the need for adequate psychosocial support when considering testing for CHIP and other potential clinical biomarkers predictive of cancer and other medical risks in cancer survivors.

Clonal Compositions Involving Epigenetic Regulator Gene Mutations in Clonal Hematopoiesis, Clonal Cytopenias of Undetermined Significance and Chronic Myelomonocytic Leukemia