Evidence map›Paper›PMID 23322900›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2013

Molecular pathways: hepatitis C virus, CXCL10, and the inflammatory road to liver cancer.

Jessica Brownell, Stephen J Polyak

Open access · greenAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.8field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Observational
  6. Review
  7. Article
  8. Pathoimmunological analyses of fatal E11 infection in premature infants.Frontiers in cellular and infection microbiology · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. The Protective Role of IL-36/IL-36R Signal in Con A-Induced Acute Hepatitis.Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  14. Article
  15. Article
  16. Identification of CXCR4 and CXCL10 as Potential Predictive Biomarkers in Triple Negative Breast Cancer (TNBC).Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  17. Review
  18. Article
  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

2 authors at 1 institution in 1 country.

Jessica BrownellPathobiology Program, Department of Global Health, University of Washington, Seattle, Washington 98104, USA.
Stephen J Polyak
University of Washington · US

Funding

Suppression of HCV-specific CD4+ T Cells by Core ProteinU19AI066328 · NIAID · UNIVERSITY OF COLORADO DENVER · PI ROSEN, HUGO RAMON · 2005 to 2014
$6.8M
Diseases of Public Health Importance Training GrantT32AI007509 · NIAID · UNIVERSITY OF WASHINGTON · PI LUND, JENNIFER M · 1997 to 2024
$6.3M
NIAID NIH HHS 2T32AI007509NIAID NIH HHS T32 AI007509NIAID NIH HHS U19 AI066328NIAID NIH HHS U19AI066328
6 · The paper itself

Abstract

An estimated 170 million people worldwide are chronically infected with the hepatitis C virus (HCV), which is characterized histologically by a persistent immune and inflammatory response that fails to clear HCV from hepatocytes. This response is recruited to the liver, in part, by the chemokine CXCL10, the serum and intrahepatic levels of which have been inversely linked to the outcome of interferon-based therapies for hepatitis C. Bystander tissue damage from this ineffective response is thought to lead to increased hepatocyte turnover and the development of fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). However, CXCL10 is traditionally viewed as an orchestrator of the angiostatic and antitumor immune response. In this review, we will explore this duality and the pathways by which CXCL10 is produced by hepatocytes during HCV infection, its effects on resident and infiltrating immune cells, and how deregulation of these cell populations within the liver may lead to chronic liver inflammation. We will also discuss potential host-directed therapies to slow or reverse HCV-induced inflammation that leads to fibrosis, cirrhosis, and HCCs.

Indexed as

Hepatitis C, ChronicBystander EffectCarcinoma, HepatocellularChemokine CXCL10FibrosisHepacivirusHepatocytesHumansInflammationInterferonsLiver CirrhosisLiver NeoplasmsChemokine CXCL10CXCL10 protein, humanInterferons

Identifiers

PMID23322900
PMCPMC3602344
OpenAlexW2112473152

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.