Evidence map›Paper›PMID 22465232›Full record

ReviewSeminars in cancer biology2012

What are regulatory T cells (Treg) regulating in cancer and why?

Theresa L Whiteside

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Seminars in cancer biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 2 pooled it
11.3field-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

167 citing papers in PubMed, 2 syntheses or guidelines pooled it, 285 citations in OpenAlex.

  1. Pooled it
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  4. Low-Dose Cyclophosphamide Induces Antitumor T-Cell Responses, which Associate with Survival in Metastatic Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
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  16. The role of exosomes in bladder cancer immunotherapy.Journal of the National Cancer Center · 2025
    Review
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107 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

1 author at 1 institution in 1 country.

Theresa L WhitesideUniversity of Pittsburgh Cancer Institute, Hillman Cancer Center, Pittsburgh, PA 15213, USA. whitesidetl@upmc.edu
UPMC Hillman Cancer Center · US

Funding

Tissue Procurement / ImmunohistologyP01CA109688 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SCHLESSELMAN, JAMES J · 2006 to 2010
$5.9M
NCI NIH HHS P01 CA109688NCI NIH HHS P01-CA109688
6 · The paper itself

Abstract

The role regulatory T cells (Treg) play in cancer development and progression is not clear. Earlier evidence suggested that CD4(+)FOXP3(+)CD25(high) Treg accumulate in tumors and the peripheral blood of patients with cancer and through suppression of anti-tumor immune responses promote tumor growth. However, more recent data indicate that in certain cancers, such as colorectal carcinoma (CRC), Treg suppress bacteria-driven inflammation which promotes carcinogenesis and thus benefit the host. Treg appear to play a dual role in cancer. This might explain why the frequency and functions of Treg are associated with a poor prognosis in some cancers but with favorable outcome in others. The clinical and prognostic significance of Treg in cancer depends on environmental factors, including infectious agents, tumor-derived products and locally-produced cytokines, which shape the nature of immune responses, including Treg generation, recruitment and survival. Adaptive or inducible (i) Treg or Tr1 are the major subset(s) of Treg present in cancer. These iTreg are a distinct subset of regulatory cells that phenotypically and functionally differ from FOXP3(+) natural (n) Treg responsible for peripheral tolerance. They mediate powerful suppression of effector T cells via diverse mechanisms, produce immunosuppressive cytokines, notably TGF-β as well as prostaglandin E2 and adenosine, and are resistant to apoptosis or oncological therapies. Strategies for silencing of Tr1 in patients with cancer will require novel approaches that can selectively deplete these cells or block molecular pathways they utilize.

Indexed as

AnimalsColorectal NeoplasmsHumansImmunotherapyInflammationNeoplasmsPrognosisT-Lymphocytes, Regulatory

Identifiers

PMID22465232
PMCPMC3385925
OpenAlexW2052071472

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.