Evidence map›Paper›PMID 35082152›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Senescence induction dictates response to chemo- and immunotherapy in preclinical models of ovarian cancer.

Stella V Paffenholz, Camilla Salvagno, Yu-Jui Ho, Matthew Limjoco, Timour Baslan, Sha Tian, Amanda Kulick, Elisa de Stanchina, John E Wilkinson, Francisco M Barriga and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
8.6field-weighted citation impact, top 1% of its field
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

61 citing papers in PubMed, 83 citations in OpenAlex.

  1. Trial
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  3. BCLXSignal transduction and targeted therapy · 2026
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  17. Talazoparib and radiation enhance the senolytic efficacy of venetoclax in therapy-induced senescent triple-negative breast cancer cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025
    Article
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1 more citing papers are in PubMed but not listed here.

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

14 authors at 3 institutions in 2 countries.

Stella V PaffenholzCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Camilla SalvagnoDepartment of Obstetrics and Gynecology, Weill Cornell Medicine, New York, NY 10065.
Yu-Jui HoCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Matthew LimjocoCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Timour BaslanCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Sha TianCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Amanda KulickDepartment of Molecular Pharmacology, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Elisa de StanchinaDepartment of Molecular Pharmacology, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
John E WilkinsonDepartment of Pathology, University of Michigan School of Medicine, Ann Arbor, MI 48109.
Francisco M BarrigaCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Dmitriy ZamarinDepartment of Medicine, Gynecologic Medical Oncology Service, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Juan R Cubillos-RuizDepartment of Obstetrics and Gynecology, Weill Cornell Medicine, New York, NY 10065.
Josef LeiboldCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065; lowes@mskcc.org Josef.Leibold@med.uni-tuebingen.de.
Scott W LoweCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065; lowes@mskcc.org Josef.Leibold@med.uni-tuebingen.de.ORCID 0000-0002-5284-9650
Memorial Sloan Kettering Cancer Center · USCornell University · USUniversity of Michigan · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Rapid and flexible precision oncology mouse models of epithelial malignancies epithelial malignanciesR01CA233944 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LOWE, SCOTT W. · 2020 to 2024
$2.4M
Endoplasmic Reticulum Stress Responses in PainR01NS114653 · NINDS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BOADA, MARIO DANILO, ROMERO-SANDOVAL, E. ALFONSO · 2020 to 2024
$2.0M
IRE1a-XBP1 Signaling as a Driver of Chemotherapy-Induced Peripheral NeuropathyR21CA248106 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CUBILLOS-RUIZ, JUAN R, ROMERO-SANDOVAL, E. ALFONSO · 2020 to 2021
$420k
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA233944NCI NIH HHS R21 CA248106NINDS NIH HHS R01 NS114653
6 · The paper itself

Abstract

High-grade serous ovarian carcinoma (HGSOC) is a cancer with dismal prognosis due to the limited effectiveness of existing chemo- and immunotherapies. To elucidate mechanisms mediating sensitivity or resistance to these therapies, we developed a fast and flexible autochthonous mouse model based on somatic introduction of HGSOC-associated genetic alterations into the ovary of immunocompetent mice using tissue electroporation. Tumors arising in these mice recapitulate the metastatic patterns and histological, molecular, and treatment response features of the human disease. By leveraging these models, we show that the ability to undergo senescence underlies the clinically observed increase in sensitivity of homologous recombination (HR)-deficient HGSOC tumors to platinum-based chemotherapy. Further, cGas/STING-mediated activation of a restricted senescence-associated secretory phenotype (SASP) was sufficient to induce immune infiltration and sensitize HR-deficient tumors to immune checkpoint blockade. In sum, our study identifies senescence propensity as a predictor of therapy response and defines a limited SASP profile that appears sufficient to confer added vulnerability to concurrent immunotherapy and, more broadly, provides a blueprint for the implementation of electroporation-based mouse models to reveal mechanisms of oncogenesis and therapy response in HGSOC.

Indexed as

AnimalsAntineoplastic AgentsCarcinoma, Ovarian EpithelialCell Line, TumorDisease Models, AnimalFemaleHumansImmune Checkpoint InhibitorsImmunotherapyMiceMice, Inbred C57BLOvarian NeoplasmsAntineoplastic AgentsImmune Checkpoint Inhibitorscancer immunotherapymouse modelsovarian cancersenescence

Identifiers

PMID35082152
PMCPMC8812522
OpenAlexW4210615291

What OpenQuestion 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 OpenQuestion graph.