Evidence map›Paper›PMID 35961707›Full record

ReviewAdvances in cancer research2022

Inflammatory pathways and cholangiocarcinoma risk mechanisms and prevention.

Massimiliano Cadamuro, Mario Strazzabosco

Abstract readReview
In one paragraph

Review in Advances in cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
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  9. 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.

Massimiliano CadamuroDepartment of Molecular Medicine (DMM), University of Padova, Padova, Italy.
Mario StrazzaboscoLiver Center, Department of Internal Medicine, Yale University, New Haven, CT, United States. Electronic address: mario.strazzabosco@yale.edu.

Funding

Yale Liver CenterP30DK034989 · NIDDK · YALE UNIVERSITY · PI YASUKO IWAKIRI · 1986 to 2026
$31.1M
Cross talk between epithelial, inflammatory and mesenchymal cells in the development of portal fibrosisR01DK101528 · NIDDK · YALE UNIVERSITY · PI STRAZZABOSCO, MARIO · 2015 to 2023
$3.5M
NIDDK NIH HHS P30 DK034989NIDDK NIH HHS R01 DK101528
6 · The paper itself

Abstract

Cholangiocarcinoma (CCA), a neoplasm burdened by a poor prognosis and currently lacking adequate therapeutic treatments, can originate at different levels of the biliary tree, in the intrahepatic, hilar, or extrahepatic area. The main risk factors for the development of CCA are the presence of chronic cholangiopathies of various etiology. To date, the most studied prodromal diseases of CCA are primary sclerosing cholangitis, Caroli's disease and fluke infestations, but other conditions, such as metabolic syndrome, nonalcoholic fatty liver disease and obesity, are emerging as associated with an increased risk of CCA development. In this review, we focused on the analysis of the pro-inflammatory mechanisms that induce the development of CCA and on the role of cells of the immune response in cholangiocarcinogenesis. In very recent times, these cellular mechanisms have been the subject of emerging studies aimed at verifying how the modulation of the inflammatory and immunological responses can have a therapeutic significance and how these can be used as therapeutic targets.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaCholangitis, SclerosingBile Ducts, IntrahepaticHumansRisk FactorsCholangiocarcinogenesisCongenital hepatic fibrosisFluke infestationsIntrahepatic cholangiocarcinomaPrimary sclerosing cholangitisTherapeutic targets

Identifiers

PMID35961707
PMCPMC10916841

What OpenQuestion holds

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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.