Evidence map›Paper›PMID 38522849›Full record

ArticleBritish journal of haematology2024

Natural history of clonal haematopoiesis seen in real-world haematology settings.

Shyam A Patel, William K Gerber, Rena Zheng, Shrinkhala Khanna, Lloyd Hutchinson, Gregory A Abel, Jan Cerny, Brandon A DaSilva, Tian Y Zhang, Muthalagu Ramanathan and 6 more

Abstract read
In one paragraph

Article in British journal of haematology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. 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

16 authors.

Shyam A PatelDivision of Hematology/Oncology, Department of Medicine, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.ORCID https://orcid.org/0000-0002-8208-1902
William K GerberDivision of Hematology/Oncology, Department of Medicine, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Rena ZhengDivision of Hematology/Oncology, Department of Medicine, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Shrinkhala KhannaDivision of Hematology/Oncology, Department of Medicine, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Lloyd HutchinsonDepartment of Pathology, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Gregory A AbelDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Jan CernyDivision of Hematology/Oncology, Department of Medicine, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.ORCID https://orcid.org/0000-0002-6602-5505
Brandon A DaSilvaDivision of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.
Tian Y ZhangDivision of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.
Muthalagu RamanathanDivision of Hematology/Oncology, Department of Medicine, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Salwa KhedrDepartment of Pathology, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
William SeloveDepartment of Pathology, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Bruce WodaDepartment of Pathology, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Patricia M MironDepartment of Pathology, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Anne W HigginsDepartment of Pathology, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.
Jonathan M GerberDivision of Hematology/Oncology, Department of Medicine, UMass Memorial Medical Center, UMass Chan Medical School, Worcester, Massachusetts, USA.

Funding

University of Massachusetts Center for Clinical Science and Translational SupplementUL1TR001453 · NCATS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LUZURIAGA, KATHERINE F · 2015 to 2024
$39.0M
Dissecting the Mechanism of Acute Myeloid Leukemia Induced Bone Marrow Failure to Identify Therapeutic InterventionsK08CA248940 · NCI · STANFORD UNIVERSITY · PI ZHANG, TIAN YI · 2020 to 2024
$817k
Center for Clinical and Translational Science, University of Massachusetts UL1TR001453NCATS NIH HHS UL1 TR001453NCI NIH HHS K08 CA248940
6 · The paper itself

Abstract

Recursive partitioning of healthy consortia led to the development of the Clonal Hematopoiesis Risk Score (CHRS) for clonal haematopoiesis (CH); however, in the practical setting, most cases of CH are diagnosed after patients present with cytopenias or related symptoms. To address this real-world population, we characterize the clinical trajectories of 94 patients with CH and distinguish CH harbouring canonical DNMT3A/TET2/ASXL1 mutations alone ('sole DTA') versus all other groups ('non-sole DTA'). TET2, rather than DNMT3A, was the most prevalent mutation in the real-world setting. Sole DTA patients did not progress to myeloid neoplasm (MN) in the absence of acquisition of other mutations. Contrastingly, 14 (20.1%) of 67 non-sole DTA patients progressed to MN. CHRS assessment showed a higher frequency of high-risk CH in non-sole DTA (vs. sole DTA) patients and in progressors (vs. non-progressors). RUNX1 mutation conferred the strongest risk for progression to MN (odds ratio [OR] 10.27, 95% CI 2.00-52.69, p = 0.0053). The mean variant allele frequency across all genes was higher in progressors than in non-progressors (36.9% ± 4.62% vs. 24.1% ± 1.67%, p = 0.0064). This analysis in the post-CHRS era underscores the natural history of CH, providing insight into patterns of progression to MN.

Indexed as

Clonal HematopoiesisDioxygenasesDNA-Binding ProteinsMutationAdultAgedAged, 80 and overCore Binding Factor Alpha 2 SubunitDisease ProgressionDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AFemaleHumansMaleMiddle AgedProto-Oncogene ProteinsASXL1 protein, humanCore Binding Factor Alpha 2 SubunitDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanProto-Oncogene ProteinsRepressor ProteinsTET2 protein, humanacute myeloid leukaemiaCHIPclonal haematopoiesisepigeneticsmyelodysplastic syndromemyeloid genomics

Identifiers

PMID38522849
PMCPMC11232927

What OpenQuestion 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 OpenQuestion graph.