Evidence map›Paper›PMID 23912084›Full record

ArticleGastroenterology2013

Genetic alterations associated with progression from pancreatic intraepithelial neoplasia to invasive pancreatic tumor.

Stephen J Murphy, Steven N Hart, Joema Felipe Lima, Benjamin R Kipp, Mitchell Klebig, Jennifer L Winters, Csilla Szabo, Lizhi Zhang, Bruce W Eckloff, Gloria M Petersen and 5 more

Abstract read
In one paragraph

Article in Gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing 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

125 citing papers in PubMed.

  1. Article
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  16. Laser capture microdissection.Nature reviews. Methods primers · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. Article

65 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

15 authors.

Stephen J MurphyDepartment of Molecular Medicine, Mayo Clinic, Rochester, Minnesota.
Steven N Hart
Joema Felipe Lima
Benjamin R Kipp
Mitchell Klebig
Jennifer L Winters
Csilla Szabo
Lizhi Zhang
Bruce W Eckloff
Gloria M Petersen
Steven E Scherer
Richard A Gibbs
Robert R McWilliams
George Vasmatzis
Fergus J Couch

Funding

The Human Genome Sequencing CenterU54HG003273 · NHGRI · BAYLOR COLLEGE OF MEDICINE · PI GIBBS, RICHARD A · 2004 to 2015
$341.3M
Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI PETERSEN, GLORIA M. · 2004 to 2018
$32.7M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
Role of Vav1 protooncogene in pancreatic cancerP20CA102701 · NCI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI PETERSEN, GLORIA M. · 2003 to 2003
$1.5M
NCI NIH HHS CA102701NCI NIH HHS P20 CA102701NCI NIH HHS P30 CA015083NCI NIH HHS P50 CA102701NHGRI NIH HHS U54 HG003273NIDDK NIH HHS P30 DK084567NIDDK NIH HHS P30DK084567
6 · The paper itself

Abstract

BACKGROUND &

aimsIncreasing grade of pancreatic intraepithelial neoplasia (PanIN) has been associated with progression to pancreatic ductal adenocarcinoma (PDAC). However, the mechanisms that control progression from PanINs to PDAC are not well understood. We investigated the genetic alterations involved in this process.

methodsGenomic DNA samples from laser-capture microdissected PDACs and adjacent PanIN2 and PanIN3 lesions from 10 patients with pancreatic cancer were analyzed by exome sequencing.

resultsSimilar numbers of somatic mutations were identified in PanINs and tumors, but the mutational load varied greatly among cases. Ten of the 15 isolated PanINs shared more than 50% of somatic mutations with associated tumors. Mutations common to tumors and clonally related PanIN2 and PanIN3 lesions were identified as genes that could promote carcinogenesis. KRAS and TP53 frequently were altered in PanINs and tumors, but few other recurrently modified genes were detected. Mutations in DNA damage response genes were prevalent in all samples. Genes that encode proteins involved in gap junctions, the actin cytoskeleton, the mitogen-activated protein kinase signaling pathway, axon guidance, and cell-cycle regulation were among the earliest targets of mutagenesis in PanINs that progressed to PDAC.

conclusionsEarly stage PanIN2 lesions appear to contain many of the somatic gene alterations required for PDAC development.

Indexed as

Disease ProgressionAdenocarcinomaCarcinogenesisCarcinoma in SituDNA, NeoplasmHumansMutationNeoplasm InvasivenessPancreatic NeoplasmsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsRetrospective StudiesTumor Suppressor Protein p53DNA, NeoplasmKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsTP53 protein, humanTumor Suppressor Protein p53AAFalternate allele frequencyataxia telangiectasia mutatedATMlaser capture microdissectionLCMPPancreaspancreatic ductal adenocarcinomapancreatic intraepithelial neoplasiapancreatic intraepithelial neoplasia alonePanINPDACPxTsingle-nucleotide variantSNVTtumorTumorigenesistumors and adjacent pancreatic intraepithelial neoplasiaWGAwhole-genome amplificationWhole-Genome Amplification

Identifiers

PMID23912084
PMCPMC3926442

What OpenQuestion holds

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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.