Evidence map›Paper›PMID 26114155›Full record

ArticleGenes & diseases2015

Pancreatic cancer stromal biology and therapy.

Dacheng Xie, Keping Xie

Abstract read
In one paragraph

Article in Genes & diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing 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

73 citing papers in PubMed.

  1. Article
  2. Article
  3. Preclinical Fluorescence-Guided Imaging Leveraging Surrounding Sentinel Tumor Microenvironment Identifies High-Risk Premalignant Pancreatic Lesions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Targeting KRAS in pancreatic cancer.Oncology research · 2024
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

13 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.

Dacheng XieDepartment of Medical Oncology and Tumor Institute, Tongji University School of Medicine, Shanghai, People's Republic of China; Department of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Keping XieDepartment of Medical Oncology and Tumor Institute, Tongji University School of Medicine, Shanghai, People's Republic of China; Department of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
SPORE in Pancreatic CancerP20CA101936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABBRUZZESE, JAMES L. · 2003 to 2009
$5.4M
Molecular Mediators of Pancreatic Cancer Invasion and ProgressionR01CA172233 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BRESALIER, ROBERT S · 2013 to 2017
$1.7M
Functional Validation of Pancreatic Cancer Progression BiomarkerR01CA152309 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2010 to 2014
$1.6M
KLF4 Genetic and Epigenetic Changes in Human Pancreatic CancerR01CA129956 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2008 to 2012
$1.3M
Genetic Approaches to Pancreatic Cancer ProgressionR01CA148954 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2010 to 2014
$1.3M
Molecular basis of pancreatic cancer progression and metastsisR21CA140999 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2009 to 2010
$271k
NCI NIH HHS P20 CA101936NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA129956NCI NIH HHS R01 CA148954NCI NIH HHS R01 CA152309NCI NIH HHS R01 CA172233NCI NIH HHS R21 CA140999
6 · The paper itself

Abstract

Pancreatic cancer is one of the most lethal malignancies. Significant progresses have been made in understanding of pancreatic cancer pathogenesis, including appreciation of precursor lesions or premalignant pancreatic intraepithelial neoplasia (PanINs), description of sequential transformation from normal pancreatic tissue to invasive pancreatic cancer and identification of major genetic and epigenetic events and the biological impact of those events on malignant behavior. However, the currently used therapeutic strategies targeting tumor epithelial cells, which are potent in cell culture and animal models, have not been successful in the clinic. Presumably, therapeutic resistance of pancreatic cancer is at least in part due to its drastic desmoplasis, which is a defining hallmark for and circumstantially contributes to pancreatic cancer development and progression. Improved understanding of the dynamic interaction between cancer cells and the stroma is important to better understanding pancreatic cancer biology and to designing effective intervention strategies. This review focuses on the origination, evolution and disruption of stromal molecular and cellular components in pancreatic cancer, and their biological effects on pancreatic cancer pathogenesis.

Indexed as

CytokinesGrowth factorsImmunologyStromaTherapyTranscriptional factors

Identifiers

PMID26114155
PMCPMC4476547

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.