Evidence map›Paper›PMID 37131653›Full record

ArticlebioRxiv : the preprint server for biology2023

Acute myeloid leukemia stratifies as two clinically relevant sphingolipidomic subtypes.

B Bishal Paudel, Su-Fern Tan, Todd E Fox, Johnson Ung, Jeremy Shaw, Wendy Dunton, Irene Lee, Arati Sharma, Aaron D Viny, Brian M Barth and 9 more

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 8 institutions in 1 country.

B Bishal PaudelDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA.
Su-Fern TanDepartment of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA.
Todd E FoxDepartment of Pharmacology, University of Virginia, Charlottesville, VA.
Johnson UngDepartment of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA.
Jeremy ShawDepartment of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA.
Wendy DuntonDepartment of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA.
Irene LeeDepartment of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA.
Arati SharmaDepartment of Pharmacology, Pennsylvania State University College of Medicine, Hershey, PA.
Aaron D VinyDepartments of Medicine, Division of Hematology & Oncology, and of Genetics & Development, Columbia Stem Cell Initiative, Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY.
Brian M BarthDepartment of Chemistry, Biology, and Health Sciences, South Dakota School of Mines and Technology, Rapid City, SD.
Martin S TallmanNorthwestern University Feinberg School of Medicine Robert H. Lurie Comprehensive Cancer Center Chicago, IL.
Myles CabotDepartment of Biochemistry & Molecular Biology, Brody School of Medicine, and the East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC.
Francine E Garrett-BakelmanDepartment of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA.
Ross L LevineHuman Oncology and Pathogenesis Program and Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY.
Mark KesterDepartment of Pharmacology, University of Virginia, Charlottesville, VA.
David ClaxtonPenn State Cancer Institute, Hershey, PA.
David J FeithDepartment of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA.
Kevin A JanesDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA.
Thomas P LoughranDepartment of Medicine, Division of Hematology & Oncology, University of Virginia, Charlottesville, VA.
University of Virginia · USUniversity of Virginia Cancer CenterPennsylvania State University · USColumbia University · USEast Carolina University · USMemorial Sloan Kettering Cancer Center · USNorthwestern University · USSouth Dakota School of Mines and Technology · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Elisa de Stanchina · 1985 to 2026
$347.4M
Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
Tissue Repository and Animal Models CoreP01CA171983 · NCI · UNIVERSITY OF VIRGINIA · PI HORTON, BETHANY JABLONSKI · 2013 to 2024
$19.9M
Synergistic role of signaling and epigenetics in leukemic transformationR35CA197594 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Ross L Levine · 2017 to 2026
$11.4M
Role of the Cohesin complex in normal and malignant hematopoiesisK08CA215317 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI VINY, AARON D · 2018 to 2022
$1.3M
Combinatorial Decitabine and Liposomal Ceramide for Acute Myeloid LeukemiaR03CA252825 · NCI · UNIVERSITY OF NEW HAMPSHIRE · PI BARTH, BRIAN MICHAEL · 2020 to 2020
$151k
Targeting Acid Ceramidase and Bcl-2 in Acute Myeloid LeukemiaF31CA271809 · NCI · UNIVERSITY OF VIRGINIA · PI UNG, JOHNSON · 2022 to 2023
$46k
NCI NIH HHS F31 CA271809NCI NIH HHS K08 CA215317NCI NIH HHS P01 CA171983NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA044579NCI NIH HHS R03 CA252825NCI NIH HHS R35 CA197594
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is an aggressive disease with complex and heterogeneous biology. Although several genomic classifications have been proposed, there is a growing interest in going beyond genomics to stratify AML. In this study, we profile the sphingolipid family of bioactive molecules in 213 primary AML samples and 30 common human AML cell lines. Using an integrative approach, we identify two distinct sphingolipid subtypes in AML characterized by a reciprocal abundance of hexosylceramide (Hex) and sphingomyelin (SM) species. The two Hex-SM clusters organize diverse samples more robustly than known AML driver mutations and are coupled to latent transcriptional states. Using transcriptomic data, we develop a machine-learning classifier to infer the Hex-SM status of AML cases in TCGA and BeatAML clinical repositories. The analyses show that the sphingolipid subtype with deficient Hex and abundant SM is enriched for leukemic stemness transcriptional programs and comprises an unappreciated high-risk subgroup with poor clinical outcomes. Our sphingolipid-focused examination of AML identifies patients least likely to benefit from standard of care and raises the possibility that sphingolipidomic interventions could switch the subtype of AML patients who otherwise lack targetable alternatives.

Identifiers

PMID37131653
PMCPMC10153188
OpenAlexW4366160654

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.