Evidence map›Paper›PMID 36446904›Full record

ReviewNature reviews. Cancer2023

Epithelial and stromal co-evolution and complicity in pancreatic cancer.

Sunil R Hingorani

Abstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing 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

71 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Ibrutinib and PD-1 Blockade Potentiate Mesothelin-Targeting CAR T-cell Therapy in Preclinical Models of Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. A Darwinian Perspective on Tumor Evolution.International journal of biological sciences · 2026
    Review
  20. Review

11 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

1 author.

Sunil R HingoraniDivision of Hematology and Oncology, Department of Medicine, University of Nebraska Medical Center, Omaha, NE, USA. shingorani@unmc.edu.ORCID 0000-0002-3869-8729

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
OVERCOMING STROMAL BARRIERS TO THERAPEUTICS IN PANCREAS CANCERR01CA161112 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Sunil R Hingorani · 2011 to 2026
$7.6M
Stopping PDA progression using inhibitors of CSC dissemination and immunotherapyU01CA224193 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HINGORANI, SUNIL R · 2017 to 2021
$3.3M
Investigating the metastatic drive in pancreas cancerR01CA223483 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI HINGORANI, SUNIL R · 2018 to 2022
$2.4M
NCI NIH HHS P30 CA015704NCI NIH HHS R01 CA161112NCI NIH HHS R01 CA223483NCI NIH HHS U01 CA224193
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinomas are distinguished by their robust desmoplasia, or fibroinflammatory response. Dominated by non-malignant cells, the mutated epithelium must therefore combat, cooperate with or co-opt the surrounding cells and signalling processes in its microenvironment. It is proposed that an invasive pancreatic ductal adenocarcinoma represents the coordinated evolution of malignant and non-malignant cells and mechanisms that subvert and repurpose normal tissue composition, architecture and physiology to foster tumorigenesis. The complex kinetics and stepwise development of pancreatic cancer suggests that it is governed by a discrete set of organizing rules and principles, and repeated attempts to target specific components within the microenvironment reveal self-regulating mechanisms of resistance. The histopathological and genetic progression models of the transforming ductal epithelium must therefore be considered together with a programme of stromal progression to create a comprehensive picture of pancreatic cancer evolution. Understanding the underlying organizational logic of the tumour to anticipate and pre-empt the almost inevitable compensatory mechanisms will be essential to eradicate the disease.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsComplicityHumansPancreasStromal CellsTumor Microenvironment

Identifiers

PMID36446904
PMCPMC10470605

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.