Evidence map›Paper›PMID 28555083›Full record

ArticleLeukemia2018

PPAR-delta modulates membrane cholesterol and cytokine signaling in malignant B cells.

L Sun, Y Shi, G Wang, X Wang, S Zeng, S E Dunn, G D Fairn, Y-J Li, D E Spaner

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 27% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Metabolic Reprogramming and Potential Therapeutic Targets in Lymphoma.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Metabolism and Transcription in Cancer: Merging Two Classic Tales.Frontiers in cell and developmental biology · 2017
    Review
  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

9 authors at 6 institutions in 2 countries.

L SunBiology Platform, Sunnybrook Research Institute, Toronto, Ontario, Canada.
Y ShiBiology Platform, Sunnybrook Research Institute, Toronto, Ontario, Canada.
G WangBiology Platform, Sunnybrook Research Institute, Toronto, Ontario, Canada.
X WangBiology Platform, Sunnybrook Research Institute, Toronto, Ontario, Canada.
S ZengBiology Platform, Sunnybrook Research Institute, Toronto, Ontario, Canada.
S E DunnDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada.
G D FairnKeenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada.
Y-J LiBiology Platform, Sunnybrook Research Institute, Toronto, Ontario, Canada.
D E SpanerBiology Platform, Sunnybrook Research Institute, Toronto, Ontario, Canada.
Sunnybrook Research InstituteSunnybrook Hospital · CAJilin University · CNSt. Michael's Hospital · CAToronto General Hospital · CAUniversity of Toronto · CA

Funding

CIHR MOP 110952CIHR MOP1304CIHR MOP133656
6 · The paper itself

Abstract

A deeper understanding of the mechanisms that underlie aberrant signal transduction in B-cell cancers such as chronic lymphocytic leukemia (CLL) may reveal new treatment strategies. The lipid-activated nuclear receptor peroxisome proliferator-activated receptor delta (PPARδ) accounts for a number of properties of aggressive cancers and was found to enhance Janus kinase (JAK)-mediated phosphorylation of signal transducer and activator of transcription (STAT) proteins in B lymphoma cell lines and primary CLL cells. Autocrine production of cytokines such as IL10 and interferon-beta was not increased by PPARδ but signaling responses to these cytokines were amplified and associated with increased cholesterol biosynthesis and plasma membrane levels. Plasmalemmal cholesterol and STAT phosphorylation from type 1 interferons (IFNs) were increased by PPARδ agonists, transgenes and exogenous cholesterol, and decreased by cyclodextrin, PPARD deletion and chemical PPARδ inhibitors. Functional consequences of PPARδ-mediated perturbation of IFN signaling included impaired upregulation of co-stimulatory molecules. These observations suggest PPARδ modulates signaling processes in malignant B cells in part by altering cholesterol metabolism and changes the outcomes of signaling from cytokines such as IFNs. PPARδ antagonists may have therapeutic activity as anti-leukemic signal transduction modulators.

Indexed as

AnimalsB-LymphocytesCell Line, TumorCell MembraneCell ProliferationCholesterolCytokinesHumansLeukemia, Lymphocytic, Chronic, B-CellMCF-7 CellsMiceMice, Inbred C57BLPhosphorylationPPAR deltaSignal TransductionCholesterolCytokinesPPAR delta

Identifiers

PMID28555083
OpenAlexW2617245115

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.