Evidence map›Paper›PMID 11729383›Full record

ArticleAnnals of surgery2001

Identification of disease-specific genes in chronic pancreatitis using DNA array technology.

H Friess, J Ding, J Kleeff, Q Liao, P O Berberat, J Hammer, M W Büchler

Open access · greenAbstract read
In one paragraph

Article in Annals of surgery, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Epigenetics insights · 2019
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  7. What is personalized medicine and what should it replace?Nature reviews. Gastroenterology & hepatology · 2012
    Review
  8. Unraveling the mystery of pain in chronic pancreatitis.Nature reviews. Gastroenterology & hepatology · 2012
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Transcriptional network governing the angiogenic switch in human pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  17. Association of cysteine-rich secretory protein 3 and beta-microseminoprotein with outcome after radical prostatectomy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2007
    Article
  18. Article
  19. Review
  20. 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

7 authors at 3 institutions in 2 countries.

H FriessDepartment of Visceral and Transplantation Surgery, Inselspital, University of Bern, Bern, Switzerland. helmut_friess@med.uni-heidelberg.de
J Ding
J Kleeff
Q Liao
P O Berberat
J Hammer
M W Büchler
University Hospital of Bern · CHUniversity of Bern · CHHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo use DNA arrays to analyze the differential gene expression patterns in the normal pancreas and in pancreatic diseases. SUMMARY BACKGROUND DATA: Genome-wide gene expression analysis will provide new insights into gene function and cause of disease.

methodsRNA was extracted from eight normal pancreatic specimens, eight specimens with chronic pancreatitis (CP), and eight pancreatic cancer (PCa) tissues. Poly A(+) RNA was purified, reverse-transcribed, and converted into cRNA using biotinylated nucleotides. The HuGeneFL DNA array containing 5,600 full-length human genes was used for analysis.

resultsFirst, normal pancreatic tissues were analyzed in comparison with a panel of other normal tissues (colon, liver, prostate, lung, lymph node). This analysis revealed 11 signature genes that were selectively expressed in the pancreas (e.g., pancreatic elastase-IIA). Comparison of the expression of 5,600 genes between the normal pancreas, CP, and PCa specimens showed that the expression of 34 genes was decreased in CP tissues compared with normal pancreatic tissues, and that the expression of all of these genes was simultaneously decreased in PCa. In addition, the expression of 157 genes was increased in CP tissues compared with the normal pancreas. Of those, 152 genes were simultaneously increased in PCa. Thus, only 5 of 5,600 genes were significantly overexpressed in CP compared with both normal pancreas and PCa.

conclusionsThe majority of alterations observed in CP are present in PCa, and the number of genes whose expression is selectively deregulated in CP is surprisingly small. These results may provide new insight into the pathobiology of CP and help identify certain molecular alterations that might serve as targets for new diagnostic tools and disease-specific therapy.

Indexed as

Gene Expression ProfilingOligonucleotide Array Sequence AnalysisAdultAgedAged, 80 and overBlotting, NorthernCartilage Oligomeric Matrix ProteinChronic DiseaseExtracellular Matrix ProteinsFemaleGene RearrangementGlycoproteinsHumansImmunoglobulin lambda-ChainsMaleMatrilin ProteinsCartilage Oligomeric Matrix ProteinCRISP3 protein, humanExtracellular Matrix ProteinsGlycoproteinsImmunoglobulin lambda-ChainsMatrilin ProteinsMucinsSalivary Proteins and PeptidesSeminal Plasma ProteinsSerine EndopeptidasesTryptasesTSP5 protein, human

Identifiers

PMID11729383
PMCPMC1422136
OpenAlexW2035777674

What OpenQuestion holds

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Registered trials

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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.