Evidence map›Paper›PMID 38299605›Full record

ArticleHaematologica2024

Patterns of lower risk myelodysplastic syndrome progression: factors predicting progression to high-risk myelodysplastic syndrome and acute myeloid leukemia.

Akriti G Jain, Somedeb Ball, Luis Aguirre, Najla Al Ali, David Kaldas, Sara Tinsley-Vance, Andrew Kuykendall, Onyee Chan, Kendra Sweet, Jeffrey E Lancet and 3 more

Abstract read
In one paragraph

Article in Haematologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

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  18. Treatment of Anemia in Lower-Risk Myelodysplastic Syndrome.Current treatment options in oncology · 2024
    Review
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

13 authors.

Akriti G JainAssociate Staff, Leukemia Division, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH. Jaina9@ccf.org.
Somedeb BallAssistant Professor of Medicine, Vanderbilt-Ingram Cancer Center, Nashville, TN.
Luis AguirreLeukemia Fellow, Dana-Farber Cancer Institute, Boston, MA.
Najla Al AliDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
David KaldasInternal Medicine Resident, University of South Florida, Tampa, FL.
Sara Tinsley-VanceDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Andrew KuykendallDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Onyee ChanDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Kendra SweetDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Jeffrey E LancetDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Eric PadronDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
David A SallmanDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Rami KomrokjiDepartment of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL. Rami.Komrokji@moffitt.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The patterns of low-risk myelodysplastic syndrome (MDS) progression and the clinical and molecular features of those patterns have not been well described. We divided our low-risk (LR) MDS patients (N=1,914) into 4 cohorts: 1) patients who remained LR-MDS (LR-LR; N=1,300; 68%), 2) patients who progressed from LR to high-risk (HR) MDS (LR-HR) without transformation into acute myeloid leukemia (AML) (N=317; 16.5%), 3) patients who progressed from LR to HR MDS and then AML (LR-HR-AML; N=124; 6.5%), and 4) patients who progressed from LR MDS directly to AML (LR-AML; N=173; 9%). Risk factors for progression included: male gender, low absolute neutrophil count (ANC), low platelet count, high bone marrow (BM) blasts, ferritin >1000 mcg/L, albumin <3.5 g/dL, multi-lineage dysplasia (MLD), and lack of ring sideroblasts. Among patients with marked BM fibrosis (N=49), 18% progressed directly to AML. Somatic mutations (SM) associated with an increased risk of direct or indirect AML progression included SRSF2 and NRAS. SM in IDH1, IDH2 and NPM1 were more common in patients with direct AML transformation. SM associated with progression to higher risk disease only, without AML transformation, were ASXL1, TP53, RUNX1, and CBL. SF3B1 mutation was associated with less progression. About 171 patients (13.1% of all LR-LR patients) died within two years of diagnosis of LR-MDS without disease progression. Among the 61 cases with documented cause of death, 18 patients (29.5%) died from cytopenia and MDS-related complications. Identifying patterns of disease progression of LR MDS patients and their predictive factors will be crucial to be able to tailor therapy accordingly.

Indexed as

Disease ProgressionLeukemia, Myeloid, AcuteMyelodysplastic SyndromesNucleophosminAdolescentAdultAgedAged, 80 and overFemaleHumansMaleMiddle AgedMutationPrognosisRisk FactorsYoung AdultNPM1 protein, humanNucleophosmin

Identifiers

PMID38299605
PMCPMC11215361

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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.