Evidence map›Paper›PMID 42429323›Full record

ArticleMolecular oncology2026

Interferon beta drives therapy resistance in a patient-derived model of high-grade serous ovarian cancer.

Ashlyn Conant, Tise Suzuki, Kiera McGivney, V S S Abhinav Ayyadevara, Sharon Asariah, Jay Deng, Ethan Nyein, Jacqueline Coats, Gary Yu, Yevgeniya J Ioffe and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Ashlyn ConantDivision of Biochemistry, Department of Basic Sciences, Loma Linda University, California, USA.
Tise SuzukiDivision of Biochemistry, Department of Basic Sciences, Loma Linda University, California, USA.
Kiera McGivneyDivision of Biochemistry, Department of Basic Sciences, Loma Linda University, California, USA.
V S S Abhinav AyyadevaraDivision of Cancer Sciences, Department of Basic Sciences, Loma Linda University, California, USA.ORCID https://orcid.org/0000-0003-2085-2588
Sharon AsariahDivision of Biochemistry, Department of Basic Sciences, Loma Linda University, California, USA.
Jay DengDivision of Biochemistry, Department of Basic Sciences, Loma Linda University, California, USA.
Ethan NyeinDepartment of Gynecology and Obstetrics, Loma Linda University, California, USA.
Jacqueline CoatsDivision of Biochemistry, Department of Basic Sciences, Loma Linda University, California, USA.
Gary YuDivision of Biochemistry, Department of Basic Sciences, Loma Linda University, California, USA.
Yevgeniya J IoffeDivision of Gynecologic Oncology, Department of Gynecology and Obstetrics, Loma Linda University, California, USA.
Christian HurtzDivision of Cancer Sciences, Department of Basic Sciences, Loma Linda University, California, USA.
Juli J UnternaehrerDivision of Biochemistry, Department of Basic Sciences, Loma Linda University, California, USA.ORCID https://orcid.org/0000-0001-5864-4704

Funding

Targeting Kinase Inhibitor Induced Signaling Plasticity in Patients with Ph-Like ALLK22CA251649 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI HURTZ, CHRISTIAN · 2022 to 2024
$579k
Loma Linda University 2230289NCI NIH HHS K22CA251649
6 · The paper itself

Abstract

Type 1 interferon (IFN-1) production and signaling are frequently activated in response to DNA damage and have been associated with the development of therapy resistance in cancer. However, the cell-autonomous role of IFN-1 in driving resistance in high-grade serous ovarian cancer (HGSOC) remains unclear. Specifically, whether IFN-1 functions in HGSOC as solely a response to genotoxic stress due to genotoxic therapy as frontline treatment, or can independently act in driving resistance phenotypes, has not been studied. Utilizing a patient-derived model of cisplatin-sensitive (SE) and -resistant (CR) HGSOC, we demonstrate that chronic cisplatin exposure is associated with enrichment of IFN-1 signaling and an interferon-related DNA damage resistance signature. Acute cisplatin treatment elicited dynamic IFN-1 signaling in both SE and CR cells, indicating a conserved stress response. However, chronic, low-level exposure to exogenous IFNβ, without a DNA-damaging agent, phenocopied several features of chronic cisplatin-driven resistance, including reduced therapeutic sensitivity and decreased proliferation. Together, these findings identify IFNβ as a driver of resistance-associated phenotypes and highlight cell-autonomous IFN-1 signaling as a potential biomarker for resistance and therapeutic target in platinum-resistant disease.

Indexed as

cisplatin resistanceDNA‐damageinterferon‐betaJAK/STAT signalingovarian cancer

Identifiers

PMID42429323
PMCPMC13398636

What Socratic holds

Textmetadata
LicenceCC BY
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.