Evidence map›Paper›PMID 31158393›Full record

ReviewPharmacology & therapeutics2019

Cellular determinants and therapeutic implications of inflammation in pancreatic cancer.

Meredith L Stone, Gregory L Beatty

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 3 pooled it
3.8field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 3 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Unravelling the pathogenesis and therapeutic approaches of pancreatic ductal adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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  9. Review
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  15. [Therapeutic mechanism of aqueous extract ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  16. Article
  17. New avenues for the treatment of immunotherapy-resistant pancreatic cancer.World journal of gastrointestinal oncology · 2024
    Review
  18. Review
  19. Review
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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

2 authors at 1 institution in 1 country.

Meredith L StoneAbramson Cancer Center, University of Pennsylvania, Philadelphia, PA, United states of America; Division of Hematology-Oncology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.
Gregory L BeattyAbramson Cancer Center, University of Pennsylvania, Philadelphia, PA, United states of America; Division of Hematology-Oncology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America. Electronic address: gregory.beatty@pennmedicine.upenn.edu.
University of Pennsylvania · US

Funding

IMMUNOBIOLOGY OF NORMAL AND NEOPLASTIC LYMPHOCYTEST32CA009140 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Malay Haldar, WARREN S PEAR · 1985 to 2026
$16.1M
Targeting the liver for immunotherapy in pancreatic cancerR01CA197916 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Gregory L Beatty · 2016 to 2026
$3.7M
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
NCI NIH HHS R01 CA197916NCI NIH HHS T32 CA009140NCI NIH HHS U01 CA224193
6 · The paper itself

Abstract

Inflammation is a hallmark of cancer. For pancreatic ductal adenocarcinoma (PDAC), malignant cells arise in the context of a brisk inflammatory cell infiltrate surrounded by dense fibrosis that is seen beginning at the earliest stages of cancer conception. This inflammatory and fibrotic milieu supports cancer cell escape from immune elimination and promotes malignant progression and metastatic spread to distant organs. Targeting this inflammatory reaction in PDAC by inhibiting or depleting pro-tumor elements and by engaging the potential of inflammatory cells to acquire anti-tumor activity has garnered strong research and clinical interest. Herein, we describe the current understanding of key determinants of inflammation in PDAC; mechanisms by which inflammation drives immune suppression; the impact of inflammation on metastasis, therapeutic resistance, and clinical outcomes; and strategies to intervene on inflammation for providing therapeutic benefit.

Indexed as

AnimalsCarcinoma, Pancreatic DuctalHumansImmunotherapyInflammationNeoplasm MetastasisPancreatic NeoplasmsCancerClinical trialsImmune evasionImmunosurveillanceImmunotherapyInflammationMacrophagesMetastasisNeutrophilsPancreatic ductal adenocarcinomaT cellsTherapeutic resistanceTreatment paradigmsTumor microenvironmentVaccines

Identifiers

PMID31158393
PMCPMC6708742
OpenAlexW2947866758

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.