Evidence map›Paper›PMID 30721663›Full record

ReviewGastroenterology2019

Fibroblasts in Pancreatic Ductal Adenocarcinoma: Biological Mechanisms and Therapeutic Targets.

Martin C Whittle, Sunil R Hingorani

Abstract readReview
In one paragraph

Review in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing 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

90 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Pancreatic cancer-derived extracellular vesicles enhance chemoresistance by delivering KRASMolecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  11. HMGA2 Expression Predicts Subtype, Survival, and Treatment Outcome in Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

30 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.

Martin C WhittleClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Electronic address: mwhittle@fhcrc.org.
Sunil R HingoraniClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington; Division of Medical Oncology, University of Washington School of Medicine, Seattle, Washington. Electronic address: srh@fhcrc.org.

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
Defining and targeting mechanisms of pancreas cancer pathogenesisR50CA211425 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI WHITTLE, MARTIN · 2017 to 2021
$697k
NCI NIH HHS P30 CA015704NCI NIH HHS R01 CA161112NCI NIH HHS R50 CA211425NCI NIH HHS U01 CA224193
6 · The paper itself

Abstract

The desmoplastic reaction of pancreas cancer may begin as a wound healing response to the nascent neoplasm, but it soon creates an insidious shelter that can sustain the growing tumor and rebuff therapy. Among the many cell types subverted by transformed epithelial cells, fibroblasts are recruited and activated to lay a foundation of extracellular matrix proteins and glycosaminoglycans that alter tumor biophysics and signaling. Their near-universal presence in pancreas cancer and ostensible support of disease progression make fibroblasts attractive therapeutic targets. More recently, however, it has also become apparent that diverse subpopulations of fibroblasts with distinct phenotypes and secretomes inhabit the stroma, and that targeted depletion of particular fibroblast subsets could either provide substantial therapeutic benefit or accelerate disease progression. An improved characterization of these fibroblast subtypes, along with their potential relationships to tumor subtypes and mutational repertoires, is needed in order to make anti-fibroblast therapies clinically viable.

Indexed as

AnimalsAntineoplastic AgentsCancer-Associated FibroblastsCarcinoma, Pancreatic DuctalHumansPancreatic NeoplasmsPhenotypeSignal TransductionTumor MicroenvironmentAntineoplastic AgentsDesmoplasiaFibroblastGEMMPDA

Identifiers

PMID30721663
PMCPMC6486863

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.