Evidence map›Paper›PMID 27248578›Full record

ArticleCurrent protocols in pharmacology2016

Genetically Engineered Mouse Models of Pancreatic Cancer: The KPC Model (LSL-Kras(G12D/+) ;LSL-Trp53(R172H/+) ;Pdx-1-Cre), Its Variants, and Their Application in Immuno-oncology Drug Discovery.

Jae W Lee, Chad A Komar, Fee Bengsch, Kathleen Graham, Gregory L Beatty

Abstract read
In one paragraph

Article in Current protocols in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.

0numbers the graph read from it
0cells of the map it votes in
163citing 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

163 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. FGFR Inhibitor AZD4547 Disrupts Inflammatory CAF Crosstalk With Cancer Cells and Macrophages and Attenuates Metastasis in Pancreatic Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. PHGDH is a targetable driver of PDAC progression.bioRxiv : the preprint server for biology · 2026
    Article
  16. Article
  17. Enhancing nanomedicine efficacy in KPC pancreatic tumors through ketotifen-mediated tumor microenvironment remodeling.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Article
  18. Article
  19. Article
  20. Article

103 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

5 authors.

Jae W LeeAbramson Cancer Center; University of Pennsylvania, Philadelphia, Pennsylvania.
Chad A KomarAbramson Cancer Center; University of Pennsylvania, Philadelphia, Pennsylvania.
Fee BengschAbramson Cancer Center; University of Pennsylvania, Philadelphia, Pennsylvania.
Kathleen GrahamAbramson Cancer Center; University of Pennsylvania, Philadelphia, Pennsylvania.
Gregory L BeattyAbramson Cancer Center; University of Pennsylvania, Philadelphia, Pennsylvania.

Funding

TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI DOUGLAS J EPSTEIN · 1997 to 2026
$32.5M
CD40 Pathway in Pancreatic AdenocarcinomaK08CA138907 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BEATTY, GREGORY L · 2011 to 2015
$812k
A role for macrophage phenotype in regulating metastasis in pancreatic carcinomaF30CA196106 · NCI · UNIVERSITY OF PENNSYLVANIA · PI LEE, JAE WON · 2015 to 2016
$95k
NCI NIH HHS F30 CA196106NCI NIH HHS K08 CA138907NIDDK NIH HHS P30 DK050306
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) ranks fourth among cancer-related deaths in the United States. For patients with unresectable disease, treatment options are limited and lack curative potential. Preclinical mouse models of PDAC that recapitulate the biology of human pancreatic cancer offer an opportunity for the rational development of novel treatment approaches that may improve patient outcomes. With the recent success of immunotherapy for subsets of patients with solid malignancies, interest is mounting in the possible use of immunotherapy for the treatment of PDAC. Considered in this unit is the value of genetic mouse models for characterizing the immunobiology of PDAC and for investigating novel immunotherapeutics. Several variants of these models are described, all of which may be used in drug development and for providing information on unique aspects of disease biology and therapeutic responsiveness. © 2016 by John Wiley & Sons, Inc.

Indexed as

Animals, Genetically ModifiedCarcinoma, Pancreatic DuctalDisease Models, AnimalMicePancreatic NeoplasmsAnimalsDrug DiscoveryHumansImmunotherapyMacrophagesT-Lymphocytesgenetically engineered mouse modelimmunotherapyinflammationKPCmacrophagepancreatic ductal adenocarcinomaT cell exclusion

Identifiers

PMID27248578
PMCPMC4915217

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.