Evidence map›Paper›PMID 19796244›Full record

ArticleAnnals of the New York Academy of Sciences2009

Antitumor immunity and cancer stem cells.

Tobias Schatton, Markus H Frank

Open access · greenAbstract read
In one paragraph

Article in Annals of the New York Academy of Sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
4.4field-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

89 citing papers in PubMed, 165 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Targeting CD20 in melanoma patients at high risk of disease recurrence.Molecular therapy : the journal of the American Society of Gene Therapy · 2012
    Trial
  4. Review
  5. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Frontiers in immunology · 2022
    Article
  17. Article
  18. Review
  19. Review
  20. Overcoming biological barriers to improve solid tumor immunotherapy.Drug delivery and translational research · 2021
    Review

29 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

2 authors at 1 institution in 1 country.

Tobias SchattonTransplantation Research Center, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA.
Markus H Frank
Harvard University · US

Funding

Targeting Raf in Melanoma: Mechanisms for Effect & Resistance & Opportunities forP50CA093683 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI GOLUB, TODD R. · 2001 to 2012
$25.8M
Melanoma Stem Cells, Vasculogenesis and Neoplastic ProgressionR01CA138231 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI FRANK, MARKUS H. · 2008 to 2012
$1.7M
ABCB5 P-Glycoprotein in Cancer Multidrug ResistanceR01CA113796 · NCI · BOSTON CHILDREN'S HOSPITAL · PI FRANK, MARKUS H. · 2006 to 2010
$1.5M
NCI NIH HHS 1R01CA113796-01A1NCI NIH HHS 1R01CA138231-01NCI NIH HHS 2P50CA093683-05S2NCI NIH HHS P50 CA093683NCI NIH HHS R01 CA113796NCI NIH HHS R01 CA138231
6 · The paper itself

Abstract

Self-renewing cancer stem cells (CSC) capable of spawning more differentiated tumor cell progeny are required for tumorigenesis and neoplastic progression of leukemias and several solid cancers. The mechanisms by which CSC cause tumor initiation and growth are currently unknown. Recent findings that suggest a negative correlation between degrees of host immunocompetence and rates of cancer development raise the possibility that only a restricted minority of malignant cells, namely CSC, may possess the phenotypic and functional characteristics to evade host antitumor immunity. In human malignant melanoma, a highly immunogenic cancer, we recently identified malignant melanoma initiating cells (MMIC), a novel type of CSC, based on selective expression of the chemoresistance mediator ABCB5. Here we present evidence of a relative immune privilege of ABCB5(+) MMIC, suggesting refractoriness to current immunotherapeutic treatment strategies. We discuss our findings in the context of established immunomodulatory functions of physiologic stem cells and in relation to mechanisms responsible for the downregulation of immune responses against tumors. We propose that the MMIC subset might be responsible for melanoma immune evasion and that immunomodulation might represent one mechanism by which CSC advance tumorigenic growth and resistance to immunotherapy. Accordingly, the possibility of an MMIC-driven tumor escape from immune-mediated rejection has important implications for current melanoma immunotherapy.

Indexed as

Immunologic SurveillanceTumor EscapeAnimalsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily BATP Binding Cassette Transporter, Subfamily B, Member 1Disease Models, AnimalHumansImmunotherapyMelanomaMiceNeoplastic Stem CellsABCB5 protein, humanABCB5 protein, mouseATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily BATP Binding Cassette Transporter, Subfamily B, Member 1

Identifiers

PMID19796244
PMCPMC2893543
OpenAlexW2116170249

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.