Evidence map›Paper›PMID 35525794›Full record

ReviewTrends in cancer2022

The interactive role of inflammatory mediators and metabolic reprogramming in pancreatic cancer.

Yuuki Ohara, Paloma Valenzuela, S Perwez Hussain

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  5. Dynamic feedback between IL-6 and TWIST1 drives pancreatic cancer progression.Translational gastroenterology and hepatology · 2026
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  18. Hypermetabolic state is associated with circadian rhythm disruption in mouse and human cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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

3 authors at 2 institutions in 1 country.

Yuuki OharaPancreatic Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Paloma ValenzuelaPancreatic Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
S Perwez HussainPancreatic Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: hussainp@mail.nih.gov.
National Cancer Institute · USCenter for Cancer Research · US

Funding

Molecular Profiling of Pancreatic CancerZIABC011162 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUSSAIN, SYED PERWEZ · 2009 to 2023
$11.1M
Role of Inflammation in the Development and Progression of Pancreatic CancerZIABC011185 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUSSAIN, SYED PERWEZ · 2009 to 2023
$10.4M
Intramural NIH HHS ZIA BC011185
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is characterized by its highly reactive inflammatory desmoplastic stroma with evidence of an extensive tumor stromal interaction largely mediated by inflammatory factors. KRAS mutation and inflammatory signaling promote protumorigenic events, including metabolic reprogramming with several inter-regulatory crosstalks to fulfill the high demand of energy and regulate oxidative stress for tumor growth and progression. Notably, the more aggressive molecular subtype of PDAC enhances influx of glycolytic intermediates. This review focuses on the interactive role of inflammatory signaling and metabolic reprogramming with emerging evidence of crosstalk, which supports the development, progression, and therapeutic resistance of PDAC. Understanding the emerging crosstalk between inflammation and metabolic adaptations may identify potential targets and develop novel therapeutic approaches for PDAC.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsHumansInflammation MediatorsSignal TransductionInflammation Mediatorsautophagyinflammatory mediatorsmetabolic reprogrammingmolecular subtypepancreatic ductal adenocarcinoma (PDAC)

Identifiers

PMID35525794
PMCPMC9233125
OpenAlexW4229042767

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.