Evidence map›Paper›PMID 30154786›Full record

ReviewFrontiers in immunology2018

Cancer Cells Exploit Notch Signaling to Redefine a Supportive Cytokine Milieu.

Michela Colombo, Leonardo Mirandola, Maurizio Chiriva-Internati, Andrea Basile, Massimo Locati, Elena Lesma, Raffaella Chiaramonte, Natalia Platonova

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Contribution of Keratinocytes in Skin Cancer Initiation and Progression.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. γ-Secretase fanning the fire of innate immunity.Biochemical Society transactions · 2023
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. The MITF regulatory network in melanoma.Pigment cell & melanoma research · 2022
    Article
  18. Article
  19. Review
  20. p73α1, a p73 C-terminal isoform, regulates tumor suppression and the inflammatory response via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2022
    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

8 authors at 2 institutions in 2 countries.

Michela ColomboDepartment of Health Sciences, Università degli Studi di Milano, Milano, Italy.
Leonardo MirandolaKiromic Biopharma Inc., Houston, TX, United States.
Maurizio Chiriva-InternatiKiromic Biopharma Inc., Houston, TX, United States.
Andrea BasileDepartment of Oncology and Hemato-Oncology, Università degli Studi di Milano, Milano, Italy.
Massimo LocatiDepartment of Medical Biotechnologies and Translational Medicine, Università degli Studi di Milano, Milano, Italy.
Elena LesmaDepartment of Health Sciences, Università degli Studi di Milano, Milano, Italy.
Raffaella ChiaramonteDepartment of Health Sciences, Università degli Studi di Milano, Milano, Italy.
Natalia PlatonovaDepartment of Health Sciences, Università degli Studi di Milano, Milano, Italy.
University of Milan · ITThe University of Texas MD Anderson Cancer Center · US

Funding

(PQC2) Niche-responsive RNA editing by ADAR1 in dormant multiple myeloma initiating cell maintenanceR21CA194679 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JAMIESON, CATRIONA HELEN MACLEOD · 2015 to 2016
$366k
NCI NIH HHS R21 CA194679
6 · The paper itself

Abstract

Notch signaling is a well-known key player in the communication between adjacent cells during organ development, when it controls several processes involved in cell differentiation. Notch-mediated communication may occur through the interaction of Notch receptors with ligands on adjacent cells or by a paracrine/endocrine fashion, through soluble molecules that can mediate the communication between cells at distant sites. Dysregulation of Notch pathway causes a number of disorders, including cancer. Notch hyperactivation may be caused by mutations of Notch-related genes, dysregulated upstream pathways, or microenvironment signals. Cancer cells may exploit this aberrant signaling to "educate" the surrounding microenvironment cells toward a pro-tumoral behavior. This may occur because of key cytokines secreted by tumor cells or it may involve the microenvironment through the activation of Notch signaling in stromal cells, an event mediated by a direct cell-to-cell contact and resulting in the increased secretion of several pro-tumorigenic cytokines. Up to now, review articles were mainly focused on Notch contribution in a specific tumor context or immune cell populations. Here, we provide a comprehensive overview on the outcomes of Notch-mediated pathological interactions in different tumor settings and on the molecular and cellular mediators involved in this process. We describe how Notch dysregulation in cancer may alter the cytokine network and its outcomes on tumor progression and antitumor immune response.

Indexed as

Signal TransductionAdaptive ImmunityAnimalsBiomarkersCell Line, TumorCellular SenescenceCytokinesHumansImmunity, InnateImmunomodulationInflammation MediatorsNeoplasmsRANK LigandReceptors, NotchBiomarkersCytokinesInflammation MediatorsRANK LigandReceptors, Notchcancerchemokinecytokineimmune responseinflammationNotchsenescenceVEGF

Identifiers

PMID30154786
PMCPMC6102368
OpenAlexW2886488254

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.