Evidence map›Paper›PMID 29493812›Full record

ReviewJournal of leukocyte biology2018

BET proteins in abnormal metabolism, inflammation, and the breast cancer microenvironment.

Guillaume P Andrieu, Jordan S Shafran, Jude T Deeney, Kishan R Bharadwaj, Annapoorni Rangarajan, Gerald V Denis

Abstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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 2 institutions in 2 countries.

Guillaume P AndrieuCancer Center, Boston University School of Medicine, Boston, Massachusetts, USA.
Jordan S ShafranCancer Center, Boston University School of Medicine, Boston, Massachusetts, USA.
Jude T DeeneyDepartment of Medicine, Section of Endocrinology, Obesity Research Center, Evans Biomedical Research Center, Boston University School of Medicine, Boston, Massachusetts, USA.
Kishan R BharadwajDepartment of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bengaluru, India.
Annapoorni RangarajanDepartment of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bengaluru, India.
Gerald V DenisCancer Center, Boston University School of Medicine, Boston, Massachusetts, USA.ORCID 0000-0001-9886-0401
Boston University · USIndian Institute of Science Bangalore · IN

Funding

Mechanisms of BET bromodomain metabolic reprogramming in triple negative breast cancerR01CA222170 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI DENIS, GERALD V · 2018 to 2022
$3.1M
Uncoupling obesity from breast cancer in African American womenU01CA182898 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI DENIS, GERALD V, PALMER, JULIE R · 2013 to 2017
$3.1M
NCI NIH HHS R01 CA222170NCI NIH HHS U01 CA182898Wellcome Trust
6 · The paper itself

Abstract

Obesity and its associated pathology Type 2 diabetes are two chronic metabolic and inflammatory diseases that promote breast cancer progression, metastasis, and poor outcomes. Emerging critical opinion considers unresolved inflammation and abnormal metabolism separately from obesity; settings where they do not co-occur can inform disease mechanism. In breast cancer, the tumor microenvironment is often infiltrated with T effector and T regulatory cells programmed by metabolic signaling. The pathways by which tumor cells evade immune surveillance, immune therapies, and take advantage of antitumor immunity are poorly understood, but likely depend on metabolic inflammation in the microenvironment. Immune functions are abnormal in metabolic disease, and lessons learned from preclinical studies in lean and metabolically normal environments may not translate to patients with obesity and metabolic disease. This problem is made more urgent by the rising incidence of breast cancer among women who are not obese but who have metabolic disease and associated inflammation, a phenotype common in Asia. The somatic BET proteins, comprising BRD2, BRD3, and BRD4, are new critical regulators of metabolism, coactivate transcription of genes that encode proinflammatory cytokines in immune cell subsets infiltrating the microenvironment, and could be important targets in breast cancer immunotherapy. These transcriptional coregulators are well known to regulate tumor cell progression, but only recently identified as critical for metabolism, metastasis, and expression of immune checkpoint molecules. We consider interrelationships among metabolism, inflammation, and breast cancer aggressiveness relevant to the emerging threat of breast cancer among women with metabolic disease, but without obesity.

Indexed as

AnimalsBreast NeoplasmsFemaleHumansInflammationMetabolic DiseasesNuclear ProteinsProtein Serine-Threonine KinasesRNA-Binding ProteinsTranscription FactorsTumor MicroenvironmentNuclear ProteinsProtein Serine-Threonine KinasesRNA-Binding ProteinsTranscription FactorsBET proteinsbreast cancerchronic inflammationmetabolic diseaseType 2 diabetes

Identifiers

PMID29493812
PMCPMC6134394
OpenAlexW2789381596

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.