Evidence map›Paper›PMID 40909626›Full record

ArticlebioRxiv : the preprint server for biology2025

CCAAT-enhancer binding protein delta functions as a tumor suppressor gene in acute myeloid leukemia.

Subhash C Prajapati, Cem Meydan, Yaseswini Neelamraju, Zhenjia Wang, Hao Fan, Nicholas Dunham, Richard Dillon, Jorge A Gandara, Tak Lee, Caroline Sheridan and 11 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. 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.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors.

Subhash C PrajapatiDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA, USA.
Cem MeydanInstitute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA.
Yaseswini NeelamrajuDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA, USA.
Zhenjia WangDepartment of Genome Sciences, University of Virginia, Charlottesville, VA, USA.
Hao FanDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA, USA.
Nicholas DunhamDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA, USA.
Richard DillonKing's College London, London, United Kingdom.
Jorge A GandaraDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Tak LeeDivision of Hematology and Medical Oncology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Caroline SheridanDivision of Hematology and Medical Oncology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Paul ZumboDepartment of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Michael W BeckerDepartment of Medicine, University of Rochester, Rochester, NY, USA.
Lars BullingerDepartment of Internal Medicine III, University Hospital of Ulm, Ulm, Germany.
Martin P CarrollUniversity of Pennsylvania Perelman School of Medicine, Division of Hematology and Oncology, Pennsylvania, PA, USA.
Richard J D'AndreaCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.
Ross L LevineMolecular Cancer Medicine Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Christopher MasonInstitute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA.ORCID 0000-0002-1850-1642
Ari M MelnickDivision of Hematology and Medical Oncology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Chongzhi ZangDepartment of Genome Sciences, University of Virginia, Charlottesville, VA, USA.
Stefan BekiranovDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA, USA.
Francine E Garrett-BakelmanDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA, USA.

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Dina Gould Halme · 1987 to 2026
$72.1M
Integrative computational models for functional epigenomics and transcriptional regulationR35GM133712 · NIGMS · UNIVERSITY OF VIRGINIA · PI Chongzhi Zang · 2019 to 2026
$3.4M
Genetic and epigenetic basis of relapse in acute myeloid leukemiaK08CA169055 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GARRETT-BAKELMAN, FRANCINE EVALINA · 2012 to 2016
$742k
NCI NIH HHS K08 CA169055NCI NIH HHS P30 CA044579NIGMS NIH HHS R35 GM133712
6 · The paper itself

Abstract

There is a continued need for identification of novel disease drivers of acute myeloid leukemia as many patients experience relapse and have poor clinical outcomes. Analyses from our study and publicly available datasets predicted CEBPD as a novel tumor suppressor gene in acute myeloid leukemia. Consistent with the analyses, CEBPD knockdown experiments showed activation of MAPK signaling with concomitant increase in cell growth rate, while upregulation experiments suggested induction of myeloid differentiation marker CD14 expression in AML cell lines OCI-AML2 and OCI-AML5. Consistent with a previous report, our genomics analyses and azacytidine treatment experiments suggested a role for DNA methylation in downregulation of CEBPD expression during AML pathogenesis. Altogether, our results provide experimental evidence for a tumor suppressor function of CEBPD in AML.

Indexed as

Acute myeloid leukemiaCEBPDCyclin D1MAPKMethylationTNFαTumor suppressor

Identifiers

PMID40909626
PMCPMC12407753

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.