Evidence map›Paper›PMID 22649190›Full record

ArticleCancer research2012

Molecular identification of GD3 as a suppressor of the innate immune response in ovarian cancer.

Tonya J Webb, Xiangming Li, Robert L Giuntoli, Pablo H H Lopez, Christoph Heuser, Ronald L Schnaar, Moriya Tsuji, Christian Kurts, Mathias Oelke, Jonathan P Schneck

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

59 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Identification of Functional Immune Biomarkers in Breast Cancer Patients.International journal of molecular sciences · 2024
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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

10 authors at 4 institutions in 1 country.

Tonya J WebbDepartment of Pathology and The Kelly Gynecologic Oncology Service, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD 21201, USA. twebb@som.umaryland.edu
Xiangming Li
Robert L Giuntoli
Pablo H H Lopez
Christoph Heuser
Ronald L Schnaar
Moriya Tsuji
Christian Kurts
Mathias Oelke
Jonathan P Schneck
Johns Hopkins University · USRockefeller University · USAaron Diamond AIDS Research Center · USJohns Hopkins Medicine · US

Funding

The influence of TCR spatial organization on the T cell responsesP01AI072677 · NIAID · JOHNS HOPKINS UNIVERSITY · PI DESIDERIO, STEPHEN V · 2008 to 2012
$10.3M
Use of aAPC for Melanoma Adoptive ImmunotherapyR01CA108835 · NCI · JOHNS HOPKINS UNIVERSITY · PI SCHNECK, JONATHAN P · 2004 to 2015
$3.3M
ANTIGEN SPECIFIC MODULATION OF T CELL RESPONSESR01AI044129 · NIAID · JOHNS HOPKINS UNIVERSITY · PI SCHNECK, JONATHAN P · 1999 to 2009
$3.0M
CD1d/NKT-binding glycolipids in enhancing the immunogenicity of a malaria vaccineR01AI070258 · NIAID · AARON DIAMOND AIDS RESEARCH CENTER · PI TSUJI, MORIYA · 2012 to 2016
$2.2M
CD1d/NKT-binding Glycolipids as an Adjuvant for a T cell-based Malaria VaccineR56AI070258 · NIAID · AARON DIAMOND AIDS RESEARCH CENTER · PI TSUJI, MORIYA · 2008 to 2009
$934k
aAPC-Mediated NKT cell Modulation to Enhance Cancer ImmunotherapyK01CA131487 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI WEBB, TONYA J. · 2008 to 2012
$584k
Restoring NKT cell function: a novel immunotherapeutic strategy for Breast CancerR21CA162273 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI WEBB, TONYA J. · 2011 to 2012
$367k
Altered cellular bioenergetics influences NKT cell mediated responses to LymphomaR21CA162277 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI WEBB, TONYA J. · 2011 to 2012
$359k
NCI NIH HHS CA 108835NCI NIH HHS K01 CA131487NCI NIH HHS R01 CA108835NCI NIH HHS R21 CA162273NCI NIH HHS R21 CA162277NIAID NIH HHS AI 44129NIAID NIH HHS AI 70258NIAID NIH HHS P01 AI072677NIAID NIH HHS R01 AI044129NIAID NIH HHS R01 AI070258NIAID NIH HHS R56 AI070258PHS HHS K01 131487
6 · The paper itself

Abstract

Tumors often display mechanisms to avoid or suppress immune recognition. One such mechanism is the shedding of gangliosides into the local tumor microenvironment, and a high concentration of circulating gangliosides is associated with poor prognosis. In this study, we identify ganglioside GD3, which was isolated from the polar lipid fraction of ovarian cancer-associated ascites, as an inhibitory factor that prevents innate immune activation of natural killer T (NKT) cells. Purified GD3 displayed a high affinity for both human and mouse CD1d, a molecule involved in the presentation of lipid antigens to T cells. Purified GD3, as well as substances within the ascites, bound to the CD1d antigenic-binding site and did not require additional processing for its inhibitory effect on NKT cells. Importantly, in vivo administration of GD3 inhibited α-galactosylceramide (α-GalCer)-induced NKT cell activation in a dose-dependent manner. These data therefore indicate that ovarian cancer tumors may use GD3 to inhibit the antitumor NKT cell response as an early mechanism of tumor immune evasion.

Indexed as

AnimalsAntigens, CD1dAscitesCarcinomaCells, CulturedDown-RegulationFemaleGangliosidesHumansImmunity, InnateKiller Cells, NaturalLymphocyte ActivationMiceMice, Inbred C57BLOvarian NeoplasmsTumor EscapeAntigens, CD1dCD1D protein, humanganglioside, GD3Gangliosides

Identifiers

PMID22649190
PMCPMC3438513
OpenAlexW1965739428

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.