Evidence map›Paper›PMID 26315515›Full record

ReviewThe Surgical clinics of North America2015

The Triple-Code Model for Pancreatic Cancer: Cross Talk Among Genetics, Epigenetics, and Nuclear Structure.

Gwen A Lomberk, Raul Urrutia

Abstract readReview
In one paragraph

Review in The Surgical clinics of North America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. MLH1 promoter methylation in pancreatic ductal adenocarcinoma: frequent but not prognostic.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. KrasGenome biology · 2021
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Pancreatic Cancer, A Mis-interpreter of the Epigenetic Language.The Yale journal of biology and medicine · 2016
    Review
  14. Review
  15. MicroRNA in pancreatic ductal adenocarcinoma and its precursor lesions.World journal of gastrointestinal oncology · 2016
    Review
  16. Article
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.

Gwen A LomberkLaboratory of Epigenetics and Chromatin Dynamics, Gastroenterology Research Unit, Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic, 200 First Street Southwest, Guggenheim 10-24A, Rochester, MN 55905, USA. Electronic address: lomberk.gwen@mayo.edu.
Raul UrrutiaLaboratory of Epigenetics and Chromatin Dynamics, Gastroenterology Research Unit, Department of Biochemistry and Molecular Biology, Mayo Clinic, Guggenheim 10-42C, Rochester, MN 55905, USA; Laboratory of Epigenetics and Chromatin Dynamics, Gastroenterology Research Unit, Department of Biophysics, Mayo Clinic, Guggenheim 10-42C, Rochester, MN 55905, USA; Laboratory of Epigenetics and Chromatin Dynamics, Gastroenterology Research Unit, Department of Medicine, Mayo Clinic, Guggenheim 10-42C, Rochester, MN 55905, USA. Electronic address: urrutia.raul@mayo.edu.

Funding

Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI MUKHOPADHYAY, DEBABRATA · 2004 to 2018
$32.7M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI Nicholas F. LaRusso · 2009 to 2026
$22.2M
ZINC FINGER GENES AND PANCREATIC CELL GROWTHR01DK052913 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI LOMBERK, GWEN, URRUTIA, RAUL A. · 1998 to 2023
$7.0M
Novel Experimental Therapeutics for Pancreatic CancerR01CA178627 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI LOMBERK, GWEN · 2014 to 2018
$1.6M
NCI NIH HHS P50 CA102701NCI NIH HHS R01 CA178627NIDDK NIH HHS P30 DK084567NIDDK NIH HHS P30DK084567NIDDK NIH HHS R01 DK052913NIDDK NIH HHS R01 DK52913
6 · The paper itself

Abstract

Pancreatic adenocarcinoma is painful, generally incurable, and frequently lethal. The current progression model indicates that this cancer evolves by mutations and deletions in key oncogenes and tumor suppressor genes. This article describes an updated, more comprehensive model that includes concepts from the fields of epigenetics and nuclear architecture. Widespread use of next-generation sequencing for identifying genetic and epigenetic changes genome-wide will help identify and validate more and better markers for this disease. Epigenetic alterations are amenable to pharmacologic manipulations, thus this new integrated paradigm will contribute to advance this field from a mechanistic and translational point of view.

Indexed as

Epigenesis, GeneticModels, GeneticNucleosomesAdenocarcinomaBiomarkers, TumorHumansMutationPancreatic NeoplasmsBiomarkers, TumorNucleosomesEpigeneticsPancreatic adenocarcinomaTriple-code hypothesis

Identifiers

PMID26315515
PMCPMC4556141

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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.