Evidence map›Paper›PMID 32199881›Full record

ReviewGastroenterology2020

Carcinogenesis of Pancreatic Ductal Adenocarcinoma.

Peter Storz, Howard C Crawford

Open access · bronzeAbstract readReview
In one paragraph

Review in Gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Vorinostat Potentiates Chemoimmunotherapy in Immune-Enriched Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Pancreatic cancer.Nature reviews. Disease primers · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Challenges of early detection of pancreatic cancer.The Journal of clinical investigation · 2025
    Review
  18. Review
  19. Review
  20. Article

36 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Peter StorzDepartment of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Jacksonville, Florida. Electronic address: storz.peter@mayo.edu.
Howard C CrawfordDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan. Electronic address: howcraw@umich.edu.
Mayo Clinic in Florida · USUniversity of Michigan–Ann Arbor · US

Funding

Interrupting Cellular Crosstalk in the Immunosuppressive Microenvironment of Pancreas CancerU01CA224145 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CRAWFORD, HOWARD C., PASCA DI MAGLIANO, MARINA · 2017 to 2021
$2.6M
Metaplastic Tuft Cells in Pancreatic CancerR01CA247516 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CRAWFORD, HOWARD C. · 2020 to 2024
$2.3M
PKD1 signaling in the initiation of pancreatic cancerR01CA200572 · NCI · MAYO CLINIC JACKSONVILLE · PI STORZ, PETER · 2016 to 2021
$1.8M
Role of ICAM1 in development and progression of pancreatic cancerR01CA229560 · NCI · MAYO CLINIC JACKSONVILLE · PI STORZ, PETER · 2019 to 2023
$1.8M
NCI NIH HHS R01 CA200572NCI NIH HHS R01 CA229560NCI NIH HHS R01 CA247516NCI NIH HHS U01 CA224145
6 · The paper itself

Abstract

Although the estimated time for development of pancreatic ductal adenocarcinoma (PDA) is more than 20 years, PDAs are usually detected at late, metastatic stages. PDAs develop from duct-like cells through a multistep carcinogenesis process, from low-grade dysplastic lesions to carcinoma in situ and eventually to metastatic disease. This process involves gradual acquisition of mutations in oncogenes and tumor suppressor genes, as well as changes in the pancreatic environment from a pro-inflammatory microenvironment that favors the development of early lesions, to a desmoplastic tumor microenvironment that is highly fibrotic and immune suppressive. This review discusses our current understanding of how PDA originates.

Indexed as

Carcinoma, Pancreatic DuctalCell Transformation, NeoplasticPancreatic NeoplasmsTumor MicroenvironmentAnimalsBiomarkers, TumorCell LineageDisease ProgressionGenetic Predisposition to DiseaseHumansMutationTime FactorsBiomarkers, TumorCarcinogenesisDesmoplastic ReactionMicroenvironmentPancreatic Ductal AdenocarcinomaPancreatic Intraepithelial Neoplasia

Identifiers

PMID32199881
PMCPMC7282937
OpenAlexW3012136543

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.