Evidence map›Paper›PMID 34380633›Full record

ArticleCancer research2021

Oncostatin M Receptor-Targeted Antibodies Suppress STAT3 Signaling and Inhibit Ovarian Cancer Growth.

Anjali Geethadevi, Ajay Nair, Deepak Parashar, Zhiqiang Ku, Wei Xiong, Hui Deng, Yongsheng Li, Jasmine George, Donna M McAllister, Yunguang Sun and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

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  6. The role of cytokines in ovarian cancer drug resistance.International journal of cancer · 2026
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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

21 authors at 4 institutions in 2 countries.

Anjali Geethadevi *Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0001-5486-7919
Ajay Nair *Department of Medicine, Columbia University, New York, New York.ORCID 0000-0003-4521-5614
Deepak Parashar *Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0002-5062-8950
Zhiqiang Ku *Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas.
Wei XiongTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas.
Hui DengTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas.
Yongsheng LiKey Laboratory of Tropical Translational Medicine of Ministry of Education, College of Biomedical Information and Engineering, Hainan Medical University, Haikou, China.ORCID 0000-0003-1914-0727
Jasmine GeorgeDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Donna M McAllisterDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0001-7332-1292
Yunguang SunDepartment of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0003-4004-9514
Ishaque P KadamberiDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Prachi GuptaDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Michael B DwinellDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin.
William H BradleyDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Janet S RaderDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0001-7031-3385
Hallgeir RuiDepartment of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Robert F SchwabeDepartment of Medicine, Columbia University, New York, New York.
Ningyan ZhangTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas.ORCID 0000-0002-4348-2180
Sunila PradeepDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0003-2441-7727
Zhiqiang AnTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center, Houston, Texas. pchaluvally@mcw.edu Zhiqiang.An@uth.tmc.edu.
Pradeep Chaluvally-RaghavanDepartment of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin. pchaluvally@mcw.edu Zhiqiang.An@uth.tmc.edu.ORCID 0000-0002-8268-3460
Medical College of Wisconsin · USBrown Foundation · USColumbia University · USHainan Medical University · CN

Funding

Biased chemokine receptor signaling in cancer progressionR01CA226279 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI DWINELL, MICHAEL B · 2019 to 2023
$1.9M
Role of RNA activation in Tumor Progression and MetastasisR01CA229907 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI CHALUVALLY-RAGHAVAN, PRADEEP · 2019 to 2023
$1.7M
Defining HPV integration sites of unknown significance in invasive cervical cancerR21CA241013 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI RADER, JANET S. · 2020 to 2020
$401k
NCI NIH HHS R01 CA226279NCI NIH HHS R01 CA229907NCI NIH HHS R21 CA241013
6 · The paper itself

Abstract

Although patients with advanced ovarian cancer may respond initially to treatment, disease relapse is common, and nearly 50% of patients do not survive beyond five years, indicating an urgent need for improved therapies. To identify new therapeutic targets, we performed single-cell and nuclear RNA-seq data set analyses on 17 human ovarian cancer specimens, revealing the oncostatin M receptor (OSMR) as highly expressed in ovarian cancer cells. Conversely, oncostatin M (OSM), the ligand of OSMR, was highly expressed by tumor-associated macrophages and promoted proliferation and metastasis in cancer cells. Ovarian cancer cell lines and additional patient samples also exhibited elevated levels of OSMR when compared with other cell types in the tumor microenvironment or to normal ovarian tissue samples. OSMR was found to be important for ovarian cancer cell proliferation and migration. Binding of OSM to OSMR caused OSMR-IL6ST dimerization, which is required to produce oncogenic signaling cues for prolonged STAT3 activation. Human monoclonal antibody clones B14 and B21 directed to the extracellular domain of OSMR abrogated OSM-induced OSMR-IL6ST heterodimerization, promoted the internalization and degradation of OSMR, and effectively blocked OSMR-mediated signaling

Indexed as

Tumor MicroenvironmentAnimalsAntibodies, MonoclonalApoptosisBiomarkers, TumorCancer-Associated FibroblastsCell ProliferationCytokine Receptor gp130FemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeNeoplasm MetastasisOncostatin MOncostatin M Receptor beta SubunitAntibodies, MonoclonalBiomarkers, TumorCytokine Receptor gp130IL6ST protein, humanOncostatin MOncostatin M Receptor beta SubunitOSM protein, humanOSMR protein, humanSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID34380633
PMCPMC8530981
OpenAlexW3190526992

What OpenQuestion holds

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LicenceTDM
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.