Interferon response and epigenetic modulation by SMARCA4 mutations drive ovarian tumor immunogenicity.

doi:10.1126/sciadv.adk4851

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Interferon response and epigenetic modulation by SMARCA4 mutations drive ovarian tumor immunogenicity.

Science advances - 6 Dec 2024

Brodeur Melica Nourmoussavi, Dopeso Higinio, Zhu Yingjie, Longhini Ana Leda F, Gazzo Andrea, Sun Siyu, Koche Richard P, Qu Rui, Rosenberg Laura, Hamard Pierre-Jacques, Bykov Yonina, Green Hunter, Gusain Laxmi, Chiappinelli Katherine B, Ozsoy Melih Arda, Chui M Herman, Basili Thais, Gardner Rui, Walderich Sven, DeStanchina Elisa, Greenbaum Benjamin, Gönen Mithat, Vabret Nicolas, Weigelt Britta, Zamarin Dmitriy

Abstract excerpt

Cell-intrinsic mechanisms of immunogenicity in ovarian cancer (OC) are not well understood. Damaging mutations in the SWI/SNF chromatin remodeling complex, such as SMARCA4 (BRG1), are associated with improved response to immune checkpoint blockade; however, the mechanism by which this occurs is unclear. We found that SMARCA4 loss in OC models resulted in increased cancer cell-intrinsic immunogenicity,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Helicases

Share to Epigenesis, Genetic

Share to Gene Expression Regulation, Neoplastic

Share to Interferons

Share to Nuclear Proteins

Share to Ovarian Neoplasms

Share to Tumor Microenvironment

Source

Open in PubMed Open full text

Identifiers

PMID: 39630912
DOI: 10.1126/sciadv.adk4851
PMCID: PMC11616711

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Interferon response and epigenetic modulation by SMARCA4 mutations drive ovarian tumor immunogenicity.PMID 39630912Read ↗

Chromatin Remodelers Are Regulators of the Tumor Immune MicroenvironmentSemantic proximity Read ↗

Chromatin remodeling (SWI/SNF) complexes, cancer, and response to immunotherapySemantic proximity Read ↗

A Pan-Cancer Analysis of SMARCA4 Alterations in Human Cancers.Semantic proximity Read ↗

Impact of Mutations in Subunit Genes of the Mammalian SWI/SNF Complex on Immunological Tumor Microenvironment.Semantic proximity Read ↗

Mutation of SMARCA4 Induces Cancer Cell-Intrinsic Defects in the Enhancer Landscape and Resistance to Immunotherapy.Semantic proximity Read ↗

Enhancing anti-tumor immune responses through combination therapies: epigenetic drugs and immune checkpoint inhibitorsSemantic proximity Read ↗

Loss of SMARCA4 Leads to Intron Retention and Generation of Tumor-Associated Antigens in Small Cell Carcinoma of the Ovary, Hypercalcemic Type.Semantic proximity Read ↗

PTEN and BRCA1 tumor suppressor loss associated tumor immune microenvironment exhibits differential response to therapeutic STING pathway activation in a murine model of ovarian cancerSemantic proximity Read ↗

FOXA1 overexpression suppresses interferon signaling and immune response in cancerSemantic proximity Read ↗

BRD4-Associated Chromatin Remodeling Signature Links Epigenetic Regulation to Immune Landscape in Ovarian CancerSemantic proximity Read ↗

Clonally Expanded T Cells Reveal Immunogenicity of Rhabdoid Tumors.Semantic proximity Read ↗

Cancer cell genotype associated tumor immune microenvironment exhibits differential response to therapeutic STING pathway activation in high-grade serous ovarian cancer.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.