Evidence map›Paper›PMID 22734672›Full record

ArticleHuman gene therapy2012

Adoptive transfer of cytotoxic T lymphocytes targeting two different antigens limits antigen loss and tumor escape.

Karen M Kaluza, Timothy Kottke, Rosa Maria Diaz, Diana Rommelfanger, Jill Thompson, Richard Vile

Abstract read
In one paragraph

Article in Human gene therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Adoptive cell therapies in thoracic malignancies.Cancer immunology, immunotherapy : CII · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Genetic Modification of CD8Frontiers in immunology · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Karen M KaluzaDepartment of Immunology, Mayo Clinic, Rochester, MN 55905, USA.
Timothy Kottke
Rosa Maria Diaz
Diana Rommelfanger
Jill Thompson
Richard Vile
WinnMed · US

Funding

T Cell Based Carriers for In Vivo Gene Therapy of CancerR01CA107082 · NCI · MAYO CLINIC ROCHESTER · PI VILE, RICHARD G. · 2005 to 2014
$2.5M
Predoctoral Training Program in Molecular PharmacologyT32GM072474 · NIGMS · MAYO CLINIC ROCHESTER · PI KARNITZ, LARRY M · 2005 to 2020
$2.4M
Autoimmunity and anti tumor immunity outside of the melanocyte/melanoma paradigmR01CA132734 · NCI · MAYO CLINIC ROCHESTER · PI VILE, RICHARD G. · 2008 to 2012
$1.5M
Enhancing Systemic Delivery of Oncolytic Viruses for Cancer TherapyR01CA130878 · NCI · MAYO CLINIC ROCHESTER · PI VILE, RICHARD G. · 2009 to 2013
$1.4M
NCI NIH HHS R01 CA107082NCI NIH HHS R01 CA130878NCI NIH HHS R01 CA132734NIGMS NIH HHS T32 GM072474
6 · The paper itself

Abstract

An antitumor T-cell response can lead to tumor control without clearing all tumor cells. As long as residual tumor cells remain, there is a constant risk of escape from that T-cell response. We previously showed that adoptive transfer of anti-ova OT-I T cells into B16ova-bearing mice led to tumor regression followed by escape of tumors that had lost the ova gene, rendering the OT-I T cells ineffective. In this study, we hypothesized that simultaneous transfer of cytotoxic T lymphocytes targeted against two independent antigens would reduce selection for single-antigen-loss cells, thereby limiting tumor escape. Using OT-I and Pmel T cells to treat B16ova tumors, we found that early cotransfer could prevent tumor emergence in most mice, whereas neither T-cell specificity alone was able to do so. When combined with total body irradiation for the treatment of larger 7-day tumors, cotransfer was also better at limiting tumor recurrence, and the tumors that did escape combination therapy continued to express both target antigens. As adoptively transferred T cells also persisted in vivo, even in mice with recurrent tumors, we hypothesized that restimulation of these antitumor T cells would prolong survival of mice with recurrent tumors. Consistent with this hypothesis, administration of a low-dose regimen of cyclophosphamide following tumor escape slowed tumor growth in mice that had previously received T-cell therapy, but not in control-treated mice, an effect that was associated with increased activation of T cells in vitro by low- but not high-dose cyclophosphamide.

Indexed as

Adoptive TransferAnimalsAntigens, NeoplasmCombined Modality TherapyCyclophosphamideFemaleMelanoma, ExperimentalMiceMice, Inbred C57BLMice, TransgenicOvalbuminReceptors, Antigen, T-CellSurvival AnalysisT-Lymphocytes, CytotoxicTumor EscapeWhole-Body IrradiationAntigens, NeoplasmCyclophosphamideOvalbuminReceptors, Antigen, T-Cell

Identifiers

PMID22734672
PMCPMC3472520
OpenAlexW2092585728

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.