Evidence map›Paper›PMID 29054417›Full record

ReviewAdvances in cancer research2017

The Regulation of Pathways of Inflammation and Resolution in Immune Cells and Cancer Stem Cells by Selenium.

Bastihalli T Diwakar, Arvind M Korwar, Robert F Paulson, K Sandeep Prabhu

Open access · greenAbstract readReview
In one paragraph

Review in Advances in cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Nanoselenium attenuates renal ischemia-reperfusion injury in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. 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

4 authors at 1 institution in 1 country.

Bastihalli T DiwakarCenter for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA, United States.
Arvind M KorwarCenter for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA, United States.
Robert F PaulsonCenter for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA, United States.
K Sandeep PrabhuCenter for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA, United States. Electronic address: ksprabhu@psu.edu.
Pennsylvania State University · US

Funding

Cellular Selenium Status and PGJ2 Metabolism (PA-17-078 supplement 2017)R01DK077152 · NIDDK · PENNSYLVANIA STATE UNIVERSITY, THE · PI PRABHU, KUMBLE SANDEEP · 2008 to 2018
$2.5M
Targeting Leukemia Stem Cells with Dietary SeleniumR01CA162665 · NCI · PENNSYLVANIA STATE UNIVERSITY, THE · PI PRABHU, KUMBLE SANDEEP · 2012 to 2016
$1.5M
NCI NIH HHS R01 CA162665NIDDK NIH HHS R01 DK077152
6 · The paper itself

Abstract

Cancer is a complex disease where cancer stem cells (CSCs) maintain unlimited replicative potential, but evade chemotherapy drugs through cellular quiescence. CSCs are able to give rise to bulk tumor cells that have the capability to override antiproliferative signals and evade apoptosis. Numerous pathways are dysregulated in tumor cells, where increased levels of prooxidant reactive oxygen and nitrogen species can lead to localized inflammation to exacerbate all three stages of tumorigenesis: initiation, progression, and metastasis. Modulation of cellular metabolism in tumor cells as well as immune cells in the tumor microenvironment (TME) can impact inflammatory networks. Altering these pathways can potentially serve as a portal for therapy. It is well known that selenium, through selenoproteins, modulates inflammatory pathways in addition to regulating redox homeostasis in cells. Therefore, selenium has the potential to impact the interaction between tumor cells, CSCs, and immune cells. In the sections later, we review the current status of knowledge regarding this interaction, with reference to leukemia stem cells, and the importance of selenium-dependent regulation of inflammation as a potential mechanism to affect the TME and tumor cell survival.

Indexed as

AnimalsApoptosisCarcinogenesisDisease ProgressionHumansInflammationNeoplasmsNeoplastic Stem CellsOxidation-ReductionReactive Oxygen SpeciesSeleniumSelenoproteinsSignal TransductionTumor MicroenvironmentReactive Oxygen SpeciesSeleniumSelenoproteinsBreast cancerCellular and molecular mechanismsNutritionPreventionSelenium

Identifiers

PMID29054417
PMCPMC5852671
OpenAlexW2753738234

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.