Evidence map›Paper›PMID 22135047›Full record

ReviewCancer prevention research (Philadelphia, Pa.)2012

Nuclear receptors as modulators of the tumor microenvironment.

Mara H Sherman, Michael Downes, Ronald M Evans

Abstract readReview
In one paragraph

Review in Cancer prevention research (Philadelphia, Pa.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. The role of HNF4α in adenocarcinoma.Biochemical Society transactions · 2026
    Review
  2. Article
  3. The Role of REV-ERB Receptors in Cancer Pathogenesis.International journal of molecular sciences · 2023
    Review
  4. Demystifying the Functional Role of Nuclear Receptors in Esophageal Cancer.International journal of molecular sciences · 2022
    Review
  5. Exploring Ligand Binding Domain Dynamics in the NRs Superfamily.International journal of molecular sciences · 2022
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Mara H ShermanGene Expression Laboratory, Howard Hughes Medical Institute, 10010 N Torrey Pines Road, La Jolla, CA, USA
Michael Downes
Ronald M Evans
Salk Institute for Biological Studies · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
ProteomicsU19DK062434 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MANGELSDORF, DAVID J · 2002 to 2011
$37.4M
Salk Institute Cancer Training GrantT32CA009370 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Diana Clare Hargreaves, Jan Karlseder · 1986 to 2026
$8.6M
Molecular Mechanisms of Inflammation, Steatosis and Hepatic Insulin ResistanceR24DK090962 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 2010 to 2011
$1.5M
Howard Hughes Medical InstituteNCI NIH HHS CA009370NCI NIH HHS P30 CA014195NCI NIH HHS T32 CA009370NIDDK NIH HHS DK062434NIDDK NIH HHS DK090962NIDDK NIH HHS R24 DK090962NIDDK NIH HHS U19 DK062434
6 · The paper itself

Abstract

Over the past several decades of cancer research, the inherent complexity of tumors has become increasingly appreciated. In addition to acquired cell-intrinsic properties, tumor initiation and growth is supported by an abundance of parenchymal, inflammatory, and stromal cell types, which infiltrate and surround the tumor. Accumulating evidence shows that numerous components of this supportive milieu, referred to collectively as the tumor microenvironment, are indeed critical during the process of multistep tumorigenesis. These findings highlight the important interplay between neoplastic cells and tumor-associated cell types, and suggest that therapy should target both neoplastic cells and supportive stromal cells to effectively attenuate tumor growth. The nuclear receptor superfamily encompasses a druggable class of molecules expressed in numerous stromal and parenchymal cell types, whose established physiologic roles suggest their potential as therapeutic and preventive targets in the context of the reactive tumor microenvironment. In this minireview, we discuss recent evidence that tumor-associated inflammation, angiogenesis, and fibrosis can be modulated at the transcriptional level by nuclear receptors and their ligands. As these processes have been widely implicated in cancer initiation, progression, and resistance to current therapy, nuclear receptor ligands targeting the tumor microenvironment may be potent antitumor agents in combination therapies, including for preventing cancer development within high-risk populations.

Indexed as

Tumor MicroenvironmentAnimalsHumansImmune SystemInflammationLigandsMiceModels, BiologicalNeoplasmsNeovascularization, PathologicReceptors, Cytoplasmic and NuclearRiskLigandsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID22135047
PMCPMC3408218
OpenAlexW2141034621

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.