Evidence map›Paper›PMID 22585577›Full record

Trial reportThe Journal of clinical investigation2012

Ganglioside GD2 identifies breast cancer stem cells and promotes tumorigenesis.

Venkata Lokesh Battula, Yuexi Shi, Kurt W Evans, Rui-Yu Wang, Erika L Spaeth, Rodrigo O Jacamo, Rudy Guerra, Aysegul A Sahin, Frank C Marini, Gabriel Hortobagyi and 2 more

Abstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed
9.0field-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

187 citing papers in PubMed, 291 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Review
  5. Article
  6. Review
  7. Immunotherapeutic Strategies Targeting GD2-Expressing Malignancies.Advances in experimental medicine and biology · 2026
    Review
  8. Review
  9. Article
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  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
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  17. Article
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127 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

12 authors at 4 institutions in 2 countries.

Venkata Lokesh BattulaSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Yuexi Shi
Kurt W Evans
Rui-Yu Wang
Erika L Spaeth
Rodrigo O Jacamo
Rudy Guerra
Aysegul A Sahin
Frank C Marini
Gabriel Hortobagyi
Sendurai A Mani
Michael Andreeff
The University of Texas MD Anderson Cancer Center · USLeukemia Research Foundation · USCenter for Translational Molecular Medicine · NLRice University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
THE THERAPY OF AMLP01CA055164 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMAS, MATTIE J · 1992 to 2011
$25.3M
UTMDACC SPORE in Breast CancerP50CA116199 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BERRY, DONALD A · 2005 to 2009
$11.9M
NCI NIH HHS CA116199NCI NIH HHS CA-16672NCI NIH HHS CA-55164NCI NIH HHS P01 CA055164NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA116199
6 · The paper itself

Abstract

Cancer stem cells (CSCs) are a small subpopulation of cancer cells that have increased resistance to conventional therapies and are capable of establishing metastasis. However, only a few biomarkers of CSCs have been identified. Here, we report that ganglioside GD2 (a glycosphingolipid) identifies a small fraction of cells in human breast cancer cell lines and patient samples that are capable of forming mammospheres and initiating tumors with as few as 10 GD2+ cells. In addition, the majority of GD2+ cells are also CD44hiCD24lo, the previously established CSC-associated cell surface phenotype. Gene expression analysis revealed that GD3 synthase (GD3S) is highly expressed in GD2+ as well as in CD44hiCD24lo cells and that interference with GD3S expression, either by shRNA or using a pharmacological inhibitor, reduced the CSC population and CSC-associated properties. GD3S knockdown completely abrogated tumor formation in vivo. Also, induction of epithelial-mesenchymal transition (EMT) in transformed human mammary epithelial cells (HMLER cells) dramatically increased GD2 as well as GD3S expression in these cells, suggesting a role of EMT in the origin of GD2+ breast CSCs. In summary, we identified GD2 as a new CSC-specific cell surface marker and GD3S as a potential therapeutic target for CSCs, with the possibility of improving survival and cure rates in patients with breast cancer.

Indexed as

AnimalsBiomarkers, TumorBreast NeoplasmsCD24 AntigenCell Line, TransformedCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGangliosidesGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansHyaluronan ReceptorsMiceMice, Inbred NODalpha-N-acetylneuraminate alpha-2,8-sialyltransferaseBiomarkers, TumorCD24 AntigenCD24 protein, humanganglioside, GD2GangliosidesHyaluronan ReceptorsNeoplasm ProteinsSialyltransferases

Identifiers

PMID22585577
PMCPMC3591166
OpenAlexW2142210663

What OpenQuestion holds

Textmetadata
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.