Evidence map›Paper›PMID 21118964›Full record

ArticleCancer research2010

Targeting STAT3 in adoptively transferred T cells promotes their in vivo expansion and antitumor effects.

Maciej Kujawski, Chunyan Zhang, Andreas Herrmann, Karen Reckamp, Anna Scuto, Michael Jensen, Jiehui Deng, Stephen Forman, Robert Figlin, Hua Yu

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
5.0field-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

79 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Exploring the molecular mechanism of cancer radiosensitization: the impact of physical stimulation therapy.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2025
    Review
  6. Orchestration of Tumor-Associated Macrophages in the Tumor Cell-Macrophage-CD8International journal of biological sciences · 2025
    Review
  7. Review
  8. Article
  9. Unraveling the complexity of STAT3 in cancer: molecular understanding and drug discovery.Journal of experimental & clinical cancer research : CR · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. STAT3 Role in T-Cell Memory Formation.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

19 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

10 authors at 2 institutions in 1 country.

Maciej KujawskiDepartment of Cancer Immunotherapeutics & Tumor Immunology, Beckman Research Institute at City of Hope, Duarte, California, USA.
Chunyan Zhang
Andreas Herrmann
Karen Reckamp
Anna Scuto
Michael Jensen
Jiehui Deng
Stephen Forman
Robert Figlin
Hua Yu
City of Hope · USBeckman Research Institute

Funding

Role of Stat3 in Tumor Immune Evasion and Immune SuppressionR01CA122976 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI YU, HUA E · 2006 to 2015
$2.9M
Targeting Stat3 to Improve ImmunotherapyR01CA140692 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI YU, HUA E · 2009 to 2013
$1.7M
NCI NIH HHS R01 CA122976NCI NIH HHS R01CA122976NCI NIH HHS R01 CA140692NCI NIH HHS R01CA146092
6 · The paper itself

Abstract

Adoptive cell therapy with engineered T cells to improve natural immune response and antitumor functions has shown promise for treating cancer. However, the requirement for extensive ex vivo manipulation of T cells and the immunosuppressive effects of the tumor microenvironment limit this therapeutic modality. In the present study, we investigated the possibility to circumvent these limitations by engineering Stat3 -deficient CD8(+) T cells or by targeting Stat3 in the tumor microenvironment. We show that ablating Stat3in CD8(+) T cells prior to their transfer allows their efficient tumor infiltration and robust proliferation, resulting in increased tumor antigen-specific T-cell activity and tumor growth inhibition. For potential clinical translation, we combined adoptive T-cell therapy with a Food and Drug Administration-approved tyrosine kinase inhibitor, sunitinib, in renal cell carcinoma and melanoma tumor models. Sunitinib inhibited Stat3 in dendritic cells and T cells and reduced conversion of transferred FoxP3(-) T cells to tumor-associated regulatory T cells while increasing transferred CD8(+) T-cell infiltration and activation at the tumor site, leading to inhibition of primary tumor growth. These data show that adoptively transferred T cells can be expanded and activated in vivo either by engineering Stat3-silenced T cells or by targeting Stat3 systemically with small-molecule inhibitors.

Indexed as

Cell ProliferationAnimalsAntineoplastic AgentsCD8-Positive T-LymphocytesCell Line, TumorCombined Modality TherapyDendritic CellsFemaleImmunotherapy, AdoptiveIndolesLymphocytes, Tumor-InfiltratingMaleMelanoma, ExperimentalMiceMice, Inbred BALB CMice, Inbred C57BLAntineoplastic AgentsIndolesPyrrolesSTAT3 Transcription FactorSunitinib

Identifiers

PMID21118964
PMCPMC3017475
OpenAlexW2124973385

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.