Evidence map›Paper›PMID 40462988›Full record

ArticlebioRxiv : the preprint server for biology2025

Serine auxotrophy is a targetable vulnerability driven by PSAT1 suppression in AML.

Ilias Sinanidis, Panagiotis Tsakiroglou, Benjamin Dubner, Rebecca Foertsch, Julia Gondek, InYoung Choi, Bogdan Paun, Liang Zhao, Gabriel Ghiaur, W Brian Dalton

Abstract readPreprint
PubMed Full text at PMC Publisher
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

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

10 authors.

Ilias SinanidisDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0009-0006-1112-3761
Panagiotis TsakiroglouDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-8823-9507
Benjamin DubnerDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Rebecca FoertschDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Julia GondekDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
InYoung ChoiDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Bogdan PaunDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Liang ZhaoComplete Omics, Baltimore, MD, USA.
Gabriel GhiaurDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-3955-7944
W Brian DaltonDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-1314-0534

Funding

Biologic and Therapeutic Consequences of Distinct Hotspot SF3B1 Mutations in MDSR01HL159306 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI DALTON, WILLIAM BRIAN, DEZERN, AMY E · 2022 to 2025
$1.6M
NHLBI NIH HHS R01 HL159306
6 · The paper itself

Abstract

Serine metabolism is of growing biologic and therapeutic interest in cancer. Upregulation of the serine synthesis pathway (SSP) can fuel tumor growth, and cancers with this phenotype are often sensitive to SSP inhibitors. In parallel, dietary restriction of serine and glycine (SG) can suppress some cancers, but the determinants of sensitivity to this approach are poorly understood. This is especially true in acute myeloid leukemia (AML), where serine metabolism has been less explored. We report that a subset of human AML cell lines and primary samples are completely dependent on external serine, known as serine auxotrophy. These leukemias consistently suppressed the SSP enzyme PSAT1, failed to synthesize serine, responded to SG restriction

Identifiers

PMID40462988
PMCPMC12132333

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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.