Evidence map›Paper›PMID 41499760›Full record

ArticleBlood advances2026

Spectrum, prevalence, and clinical correlates of PPM1D mutations in patients with clonal hematopoiesis and clonal cytopenias.

Talha Badar, Ludovica Marando, Eric Latorre, Terra Lasho, Francyess Denis Olivia, Chenyu Lin, Benjamin J McCormick, Mobachir El Kettani, Kashish J Shah, Yael Kusne and 20 more

Abstract read
In one paragraph

Article in Blood advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

30 authors.

Talha BadarDivision of Hematology-Oncology and Bone Marrow Transplant Program, Mayo Clinic, Jacksonville, FL.ORCID 0000-0003-1548-918X
Ludovica MarandoDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.
Eric LatorreCentre de Recerca Matemàtica, Barcelona, Spain.ORCID 0000-0002-2645-4292
Terra LashoDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.
Francyess Denis OliviaDivision of Hematologic Malignancies and Cellular Therapy, Duke University School of Medicine, Durham, NC.
Chenyu LinDivision of Hematologic Malignancies and Cellular Therapy, Duke University School of Medicine, Durham, NC.ORCID 0000-0002-4542-4232
Benjamin J McCormickDivision of Hematology-Oncology and Bone Marrow Transplant Program, Mayo Clinic, Jacksonville, FL.
Mobachir El KettaniDivision of Hematology-Oncology and Bone Marrow Transplant Program, Mayo Clinic, Jacksonville, FL.ORCID 0009-0005-6354-072X
Kashish J ShahDivision of Hematology-Oncology and Bone Marrow Transplant Program, Mayo Clinic, Jacksonville, FL.
Yael KusneDepartment of Hematology Oncology, Mayo Clinic, Phoenix, AZ.ORCID 0000-0002-7325-8454
Omer JamyDivision of Hematology and Oncology, The University of Alabama at Birmingham, Birmingham, AL.ORCID 0000-0003-2411-4742
Kendall DieboldDivision of Hematology and Oncology, The University of Alabama at Birmingham, Birmingham, AL.
Alexander ColtoffDivision of Hematology and Oncology, Medical University of South Carolina, Charleston, SC.
Christy FinkeDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.
James ForanDivision of Hematology-Oncology and Bone Marrow Transplant Program, Mayo Clinic, Jacksonville, FL.
Mohamed Kharfan-DabajaDivision of Hematology-Oncology and Bone Marrow Transplant Program, Mayo Clinic, Jacksonville, FL.ORCID 0000-0001-7394-5185
Yao-Shan FanDivision of Hematology-Oncology and Bone Marrow Transplant Program, Mayo Clinic, Jacksonville, FL.
Liuyan JiangDivision of Hematology-Oncology and Bone Marrow Transplant Program, Mayo Clinic, Jacksonville, FL.
Rong HeDivision of Hematopathology, Mayo Clinic, Rochester, MN.ORCID 0000-0001-6116-8163
Miles ThomasDivision of Hematology and Oncology, University of Chicago, Chicago, IL.
Anand PatelDivision of Hematology and Oncology, University of Chicago, Chicago, IL.ORCID 0000-0002-0296-8686
David ViswanathaDivision of Hematopathology, Mayo Clinic, Rochester, MN.
Mithun Vinod ShahDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.ORCID 0000-0002-5359-336X
Antoine SalibaDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.ORCID 0000-0001-5134-7336
Abhishek MangaonkarDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.
Kristina KirschnerDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.ORCID 0000-0001-7607-8670
Aref Al-KaliDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.ORCID 0000-0002-0824-3715
Naseema GangatDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.ORCID 0000-0002-9104-6172
Mark LitzowDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.ORCID 0000-0002-9816-6302
Mrinal M PatnaikDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN.ORCID 0000-0001-6998-662X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractTP53 and PPM1D are key regulators of DNA damage response and repair, and somatic mutations in these genes often co-occur in hematopoietic cells, expanding under genotoxic stress. Unlike TP53 mutations, where mechanisms of progression are defined, pathways underlying clonal fitness and transformation in PPM1D mutant cells remain unclear. In collaboration with 5 academic institutions, we analyzed the clinical and molecular landscape of 337 patients with clonal hematopoiesis (CH) and clonal cytopenia of undetermined significance (CCUS) across 4 genotypes: PPM1Dmt/TP53wt (n = 170 [50%]), PPM1Dmt/TP53mt (n = 25 [7%]), TP53mt/PPM1Dwt (n = 17 [5%]), and TP53wt/PPM1Dwt (n = 125 [38%]). All PPM1D variants were truncating, located in exon 6 of the gene, with a median variant allele frequency (VAF) of 6% (range, 0.3%-64%). The PPM1Dmt/TP53mt genotype was most frequently encountered in therapy-related CH/CCUS (t-CH/t-CCUS; 80%, 66.5%, 76.5%, and 19%; P ≤ .001) and had a shorter time interval to detection from last genotoxic exposure (6.2, 5.9, 11.25, and 24.5 months; P ≤ .001) compared with PPM1Dmt/TP53wt, TP53mt/PPM1Dwt, and TP53wt/PPM1Dwt genotypes, respectively. Acknowledging the short follow-up duration, rates of malignant transformation were lower in the PPM1Dmt/TP53wt (2%) and PPM1Dmt/TP53mt (4%) groups compared with PPM1Dwt/TP53wt (12%) and PPM1Dwt/TP53mt (17%) groups (P ≤ .001), respectively. In summary, PPM1D mutations are frequently observed in t-CH/t-CCUS, with low median VAFs, and are associated with low rates of progression, even when comutated with TP53.

Indexed as

Clonal HematopoiesisCytopeniaMutationProtein Phosphatase 2CFemaleGenotypeHumansMalePrevalenceTumor Suppressor Protein p53PPM1D protein, humanProtein Phosphatase 2CTumor Suppressor Protein p53

Identifiers

PMID41499760
PMCPMC12969418

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.