Evidence map›Paper›PMID 34469729›Full record

ArticleCell reports2021

High-grade serous ovarian tumor cells modulate NK cell function to create an immune-tolerant microenvironment.

Veronica D Gonzalez, Ying-Wen Huang, Antonio Delgado-Gonzalez, Shih-Yu Chen, Kenyi Donoso, Karen Sachs, Andrew J Gentles, Grace M Allard, Kevin S Kolahi, Brooke E Howitt and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  4. Trogocytosis in cancer immunity and cellular immunotherapy: mechanisms, therapeutic challenges, and translational opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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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 at 1 institution in 1 country.

Veronica D GonzalezBaxter Laboratory for Stem Cell Biology, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Ying-Wen HuangDepartment of Urology Stanford University School of Medicine, Stanford, CA 94305, USA.
Antonio Delgado-GonzalezDepartment of Urology Stanford University School of Medicine, Stanford, CA 94305, USA.
Shih-Yu ChenBaxter Laboratory for Stem Cell Biology, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Kenyi DonosoDepartment of Urology Stanford University School of Medicine, Stanford, CA 94305, USA.
Karen SachsNext Generation Analytics, Palo Alto, CA 94301, USA.
Andrew J GentlesDepartment of Medicine (Quantitative Sciences Unit, Biomedical Informatics) Biomedical Data Science, Stanford University School of Medicine, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Grace M AllardDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Kevin S KolahiDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Brooke E HowittStanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Ermelinda PorpigliaBaxter Laboratory for Stem Cell Biology, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Wendy J FantlDepartment of Urology Stanford University School of Medicine, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: wjfantl@stanford.edu.
Stanford University · US

Funding

Using a tonsil organoid system to probe conditions for the induction of protective antibody and T cell responses to influenza.U19AI057229 · NIAID · STANFORD UNIVERSITY · PI Mark Morris Davis · 2003 to 2026
$88.5M
The Cellular Response to Elafin in PAHP01HL108797 · NHLBI · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2011 to 2021
$19.7M
Role of the microenvironment in ovarian cancer metastasisR01CA234553 · NCI · WASHINGTON UNIVERSITY · PI FUH, KATHERINE CYNTHIA · 2019 to 2023
$2.1M
(PQD2)New Biomarkers and Pathways to Enhance Cure in Ovarian CancersR01CA184968 · NCI · STANFORD UNIVERSITY · PI FANTL, WENDY JANE, SIKIC, BRANIMIR I · 2014 to 2017
$2.0M
(PQ8) Biomarker identification by mass cytometry in peripheral blood of patients with renal cell carcinoma undergoing immune checkpoint therapyR21CA231280 · NCI · STANFORD UNIVERSITY · PI FANTL, WENDY JANE, LEPPERT, JOHN THOMAS · 2019 to 2020
$377k
NCI NIH HHS R01 CA184968NCI NIH HHS R01 CA234553NCI NIH HHS R21 CA231280NHLBI NIH HHS P01 HL108797NIAID NIH HHS U19 AI057229
6 · The paper itself

Abstract

Tubo-ovarian high-grade serous carcinoma (HGSC) is unresponsive to immune checkpoint blockade despite significant frequencies of exhausted T cells. Here we apply mass cytometry and uncover decidual-like natural killer (dl-NK) cell subpopulations (CD56+CD9+CXCR3+KIR+CD3-CD16-) in newly diagnosed HGSC samples that correlate with both tumor and transitioning epithelial-mesenchymal cell abundance. We show different combinatorial expression patterns of ligands for activating and inhibitory NK receptors within three HGSC tumor compartments: epithelial (E), transitioning epithelial-mesenchymal (EV), and mesenchymal (vimentin expressing [V]), with a more inhibitory ligand phenotype in V cells. In cocultures, NK-92 natural killer cells acquire CD9 from HGSC tumor cells by trogocytosis, resulting in reduced anti-tumor cytokine production and cytotoxicity. Cytotoxicity in these cocultures is restored with a CD9-blocking antibody or CD9 CRISPR knockout, thereby identifying mechanisms of immune suppression in HGSC. CD9 is widely expressed in HGSC tumors and so represents an important new therapeutic target with immediate relevance for NK immunotherapy.

Indexed as

Immune ToleranceTumor EscapeAntineoplastic AgentsCarboplatinCell Line, TumorCoculture TechniquesCytokinesCytotoxicity, ImmunologicFemaleHumansKiller Cells, NaturalLymphocytes, Tumor-InfiltratingNeoplasms, Cystic, Mucinous, and SerousOvarian NeoplasmsPhenotypeReceptors, Natural Killer CellAntineoplastic AgentsCarboplatinCD9 protein, humanCytokinesReceptors, Natural Killer CellTetraspanin 29CD9cytokine productioncytotoxicitydecidual-likeepithelial-mesenchymalepithelial tumorHGSChigh-grade serous carcinomaimmune infiltrateimmune toleranceNK cellsNK immunotherapyT cellstrogocytosistubo-ovarian tumor

Identifiers

PMID34469729
PMCPMC8546503
OpenAlexW3198036444

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.