Evidence map›Paper›PMID 27811314›Full record

ReviewGut2017

Epigenetic treatment of pancreatic cancer: is there a therapeutic perspective on the horizon?

Elisabeth Hessmann, Steven A Johnsen, Jens T Siveke, Volker Ellenrieder

Open access · hybridAbstract readReview
In one paragraph

Review in Gut, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 146 citations in OpenAlex.

  1. Review
  2. Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Epigenetic regulation of the tumor microenvironment: A leading force driving pancreatic cancer.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

14 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

4 authors at 2 institutions in 1 country.

Elisabeth HessmannDepartment of Gastroenterology and Gastrointestinal Oncology, University Medical Center Goettingen, Goettingen, Germany.
Steven A JohnsenDepartment of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, Goettingen, Germany.
Jens T SivekeDivision of Solid Tumor Translational Oncology, German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Volker EllenriederDepartment of Gastroenterology and Gastrointestinal Oncology, University Medical Center Goettingen, Goettingen, Germany.
German Cancer Research Center · DEUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) constitutes one of the most aggressive malignancies with a 5-year survival rate of <7%. Due to growing incidence, late diagnosis and insufficient treatment options, PDAC is predicted to soon become one of the leading causes of cancer-related death. Although intensified cytostatic combinations, particularly gemcitabine plus nab-paclitaxel and the folinic acid, fluorouracil, irinotecan, oxaliplatin (FOLFIRINOX) protocol, provide some improvement in efficacy and survival compared with gemcitabine alone, a breakthrough in the treatment of metastatic pancreatic cancer remains out of sight. Nevertheless, recent translational research activities propose that either modulation of the immune response or pharmacological targeting of epigenetic modifications alone, or in combination with chemotherapy, might open highly powerful therapeutic avenues in GI cancer entities, including pancreatic cancer. Deregulation of key epigenetic factors and chromatin-modifying proteins, particularly those responsible for the addition, removal or recognition of post-translational histone modifications, are frequently found in human pancreatic cancer and hence constitute particularly exciting treatment opportunities. This review summarises both current clinical trial activities and discovery programmes initiated throughout the biopharma landscape, and critically discusses the chances, hurdles and limitations of epigenetic-based therapy in future PDAC treatment.

Indexed as

Molecular Targeted TherapyAcetylationBromodomain Containing ProteinsCarcinoma, Pancreatic DuctalCell Cycle ProteinsEpigenesis, GeneticHistonesHumansNuclear ProteinsPancreatic NeoplasmsPolycomb-Group ProteinsProtein Serine-Threonine KinasesRNA-Binding ProteinsTranscription FactorsBRD2 protein, humanBRD3 protein, humanBRD4 protein, humanBRDT protein, humanBromodomain Containing ProteinsCell Cycle ProteinsHistonesNuclear ProteinsPolycomb-Group ProteinsProtein Serine-Threonine KinasesRNA-Binding ProteinsTranscription FactorsPANCREATIC CANCER

Identifiers

PMID27811314
PMCPMC5256386
OpenAlexW2548379965

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.