Evidence map›Paper›PMID 41979920›Full record

ArticleCell reports2026

SCD1 and SCD5 modulate PARP-dependent DNA repair via fatty acid desaturation in glioblastoma.

Hayk Mnatsakanyan, Alessandro Sammarco, Abigail Hewett, Rami Awwad, Elie Roumieh, Caline Pechdimaljian, Cagri Cakici, Caroline M Spangler, Yana Azar, Richa Pradhan and 4 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
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  3. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Hayk MnatsakanyanDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA; Neuroscience Program, Harvard Medical School, Boston, MA, USA. Electronic address: hmnatsakanyanmovsesyan@mgh.harvard.edu.
Alessandro SammarcoDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA.
Abigail HewettDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Rami AwwadDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Elie RoumiehDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Caline PechdimaljianDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Cagri CakiciDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA; Neuroscience Program, Harvard Medical School, Boston, MA, USA.
Caroline M SpanglerDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Yana AzarDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Richa PradhanDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Baolong SuUCLA Lipidomics Laboratory, University of California, Los Angeles, Los Angeles, CA, USA; Department of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Kevin J WilliamsUCLA Lipidomics Laboratory, University of California, Los Angeles, Los Angeles, CA, USA; Department of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Steven J BensingerDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA; UCLA Lipidomics Laboratory, University of California, Los Angeles, Los Angeles, CA, USA.
Christian E BadrDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA; Neuroscience Program, Harvard Medical School, Boston, MA, USA. Electronic address: badr.christian@mgh.harvard.edu.

Funding

Role of ER Stress and Fatty Acid Metabolism in Glioma Stem CellsR01NS113822 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI BADR, CHRISTIAN ELIAS · 2020 to 2024
$2.0M
NINDS NIH HHS R01 NS113822
6 · The paper itself

Abstract

Glioblastoma (GBM) relies on fatty acid metabolism for aggressive growth. This study identifies stearoyl-CoA desaturase-5 (SCD5), a brain-enriched isoform, as a critical driver of glioblastoma stem cell (GSC) maintenance and genomic stability. While SCD1's role in GBM is well-established, our research reveals that SCD5 plays a non-redundant role by preferentially desaturating C18:0 and uniquely remodeling sphingolipids. Genetic silencing of SCD5 disrupts the cell cycle, impairs DNA repair, and triggers parthanatos-a form of cell death caused by PARP1 hyperactivation. Mechanistically, loss of SCD activity or saturated fatty acid accumulation triggers PARP1 hyperactivation and subsequent degradation, depleting RAD51 to compromise homologous recombination and induce parthanatos. These findings uncover a lipid-mediated vulnerability in GBM, linking fatty acid desaturation to PARP1-dependent genome integrity. Targeting SCD5 may offer a therapeutic strategy to eliminate therapy-resistant GSCs and enhance the efficacy of genotoxic or immunotherapeutic interventions.

Indexed as

cerebral organoidsCP: cancerCP: metabolismDNA repairfatty acid desaturationglioma stem cellslipid metabolismPARP1parthanatosstearoyl-CoA desaturase

Identifiers

PMID41979920
PMCPMC13181748

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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.