Evidence map›Paper›PMID 38969020›Full record

ArticleExperimental hematology2024

Differences in the mutational landscape of clonal hematopoiesis of indeterminate potential among races and between male and female patients with cancer.

Kanaka Dhuri, Houda Alachkar

Abstract read
In one paragraph

Article in Experimental hematology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
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  3. 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

2 authors.

Kanaka DhuriDepartment of Clinical Pharmacy, USC Alfred E. Mann School of Pharmacy and Pharmaceutical Sciences, University of Southern California, Los Angeles, CA.
Houda AlachkarDepartment of Clinical Pharmacy, USC Alfred E. Mann School of Pharmacy and Pharmaceutical Sciences, University of Southern California, Los Angeles, CA; USC Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA. Electronic address: alachkar@usc.edu.

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fumito Ito · 1985 to 2026
$181.4M
Leveraging the TCR Repertoire to identify target neoantigens in FLT3-ITD positive Acute Myeloid LeukemiaR01CA248381 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ALACHKAR, HOUDA · 2021 to 2025
$1.8M
Mitochondrial Dysfunction underlies treatment related hepatotoxicity in Hispanics with acute lymphoblastic leukemiaR21CA274416 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ALACHKAR, HOUDA · 2023 to 2023
$442k
NCI NIH HHS P30 CA014089NCI NIH HHS R01 CA248381NCI NIH HHS R21 CA274416
6 · The paper itself

Abstract

Clonal hematopoiesis of indeterminate potential (CHIP) has emerged as a significant precursor to hematological malignancies and is associated with several age-related diseases. We leveraged public data to explore differences in the mutational landscape of CHIP between males (Ms) and females (Fs) and across diverse racial populations. DNA (cytosine-5) methyltransferase 3 alpha (DNMT3A) mutations were substantially more prevalent in Fs than in Ms (38.94% vs. 31.37%, p-value: < 0.001, q-value: < 0.001). Additional sex combs-like 1 (ASXL1) mutations were more frequent in Ms than Fs (5.82% vs. 2.69%, p-value < 0.001, q-value < 0.001). In the racial cohorts with sufficient sample sizes, STAT5B and CSF1R mutations were most frequent in Asian populations (1.40% and 0.84%), followed by Black populations (0.98% and 0.24%) and White populations (0.29% and 0.09%) (p-value: < 0.001 , q-value: 0.023 for both genes). Several other CHIP mutations were enriched in Black: RARA, SMAD2, CDKN1B, CENPA, CTLA4, EIF1AX, ELF3, MSI1, MYC, SOX17, and AURKA. On the other hand, H3C1, H3C4, and MYCL were enriched in the Asian cohort. Our analysis highlights sex and racial differences in CHIP mutations among patients with cancer. As CHIP continues to gain recognition as a critical precursor to malignancies and other diseases, understanding how these differences contribute to CHIP's underlying mechanisms and clinical implications is critical.

Indexed as

Clonal HematopoiesisMutationDNA Methyltransferase 3AFemaleHumansMaleNeoplasmsDNA Methyltransferase 3ADNMT3A protein, human

Identifiers

PMID38969020
PMCPMC12045072

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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.