Evidence map›Paper›PMID 33558334›Full record

ArticleCancer research2021

Ubiquitin-Specific Protease 6 Functions as a Tumor Suppressor in Ewing Sarcoma through Immune Activation.

Ian C Henrich, Kanika Jain, Robert Young, Laura Quick, Jarrett M Lindsay, Daniel H Park, Andre M Oliveira, Gerd A Blobel, Margaret M Chou

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Ian C HenrichDepartment Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.
Kanika JainDepartment Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.
Robert YoungDepartment Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.
Laura QuickDepartment Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.
Jarrett M LindsayPerelman School of Medicine at University of Pennsylvania, Philadelphia, Pennsylvania.
Daniel H ParkPerelman School of Medicine at University of Pennsylvania, Philadelphia, Pennsylvania.
Andre M OliveiraDepartment Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota.
Gerd A BlobelPerelman School of Medicine at University of Pennsylvania, Philadelphia, Pennsylvania.
Margaret M ChouDepartment Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania. mmc@pennmedicine.upenn.edu.
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · USMayo Clinic · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Robert H. Vonderheide · 1985 to 2026
$222.3M
Virus & Reservoirs CoreP30AI045008 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI DAVID S METZGER · 1999 to 2026
$78.6M
PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM008076 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BLENDY, JULIE A · 1985 to 2023
$10.8M
Bone and Soft Tissue Tumor Etiology: Role and Function of TRE17/USP6R01CA168452 · NCI · CHILDREN'S HOSP OF PHILADELPHIA · PI CHOU, MARGARET MARY · 2013 to 2017
$1.3M
Pathogenic mechanisms of alveolar rhabdomyosarcomaR21CA178601 · NCI · CHILDREN'S HOSP OF PHILADELPHIA · PI CHOU, MARGARET MARY · 2013 to 2014
$395k
NCI NIH HHS P30 CA016520NCI NIH HHS R01 CA168452NCI NIH HHS R21 CA178601NIAID NIH HHS P30 AI045008NIGMS NIH HHS T32 GM008076
6 · The paper itself

Abstract

Ewing sarcoma is the second most common pediatric bone cancer, with a 5-year survival rate for metastatic disease of only 20%. Recent work indicates that survival is strongly correlated with high levels of tumor-infiltrating lymphocytes (TIL), whose abundance is associated with IFN-inducible chemokines CXCL10 and CCL5. However, the tumor-intrinsic factors that drive chemokine production and TIL recruitment have not been fully elucidated. We previously showed that ubiquitin-specific protease 6 (USP6) directly deubiquitinates and stabilizes Jak1, thereby inducing an IFN signature in Ewing sarcoma cells. Here, we show that this gene set comprises chemokines associated with immunostimulatory, antitumorigenic functions, including CXCL10 and CCL5. USP6 synergistically enhanced chemokine production in response to exogenous IFN by inducing surface upregulation of IFNAR1 and IFNGR1. USP6-expressing Ewing sarcoma cells stimulated migration of primary human monocytes and T lymphocytes and triggered activation of natural killer (NK) cells

Indexed as

Lymphocytes, Tumor-InfiltratingAnimalsBone NeoplasmsCell MovementChemokine CCL5Chemokine CXCL10Dendritic CellsHumansImmunotherapyInterferon gamma ReceptorInterferonsJanus Kinase 1Killer Cells, NaturalMacrophagesMiceMice, NudeCCL5 protein, humanChemokine CCL5Chemokine CXCL10IFNAR1 protein, humanInterferon gamma ReceptorInterferonsJAK1 protein, humanJanus Kinase 1Receptor, Interferon alpha-betaReceptors, InterferonTumor Suppressor ProteinsUbiquitin ThiolesteraseUSP6 protein, human

Identifiers

PMID33558334
PMCPMC8137534
OpenAlexW3128616419

What OpenQuestion holds

Textmetadata
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.