Evidence map›Paper›PMID 12610506›Full record

ArticleBritish journal of cancer2003

Methylation status of p14ARF and p16INK4a as detected in pancreatic secretions.

B Klump, C J Hsieh, O Nehls, S Dette, K Holzmann, R Kiesslich, M Jung, U Sinn, M Ortner, R Porschen and 1 more

Open access · hybridAbstract readComparative Study
In one paragraph

Article in British journal of cancer, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Advances in biomarker research for pancreatic cancer.Current pharmaceutical design · 2012
    Review
  10. Article
  11. Epigenetics and epigenetic alterations in pancreatic cancer.International journal of clinical and experimental pathology · 2009
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Detection of oncogenes in chronic pancreatitis.HPB : the official journal of the International Hepato Pancreato Biliary Association · 2003
    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

11 authors at 4 institutions in 1 country.

B KlumpDepartment of Internal Medicine I, University Hospital Tübingen, Germany. bodo.klump@med.uni-tuebingen.de
C J Hsieh
O Nehls
S Dette
K Holzmann
R Kiesslich
M Jung
U Sinn
M Ortner
R Porschen
M Gregor
University Children's Hospital Tübingen · DECharité - Universitätsmedizin Berlin · DEKlinikum Bremen-Mitte · DEUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The clinical management of pancreatic disease is often hampered by a lack of tissue diagnosis. Endoscopic pancreatography offers the opportunity to investigate exfoliated cells. However, the significance of mere cytological investigation is compromised by an insufficient sensitivity. The evaluation of the molecular background of carcinogenesis hopefully is capable of providing more sensitive diagnostic markers. The p16INK4a-/retinoblastoma tumour-suppressive pathway has been shown to be involved in the development of near to all pancreatic neoplasms. p14ARF is another tumour suppressor located in the immediate neighbourhood of p16INK4a. Promoter methylation has been demonstrated to be a major inactivating mechanism of both genes. We sought to further evaluate the role of the gene locus INK4a methylation status in the endoscopic differentiation of chronic inflammatory and neoplastic pancreatic disease. Pancreatic fluid specimens of 61 patients with either pancreatic carcinoma (PCA: 39), chronic pancreatitis (CP: 16) or a normal pancreatogram (NAD: 6) were retrieved. In order to detect methylation of either the p14ARF or the p16INK4a promoter a methylation-specific PCR protocol was applied. While 19 out of 39 patients with PCA showed p16 promoter methylation (49%), none of the 16 patients with CP revealed p16 promoter methylation. p14ARF methylation was found in a lower percentage of PCA specimens and in none of the samples of patients with CP. These results suggest a specific significance of INK4a for the development of malignant pancreatic disease. Our data further indicate a potential role for INK4a methylation as a diagnostic marker in the endoscopic differentiation of benign and malignant pancreatic disease.

Indexed as

DNA MethylationAdenocarcinomaAdultAgedAged, 80 and overBileCase-Control StudiesCholangiopancreatography, Endoscopic RetrogradeChronic DiseaseCyclin-Dependent Kinase Inhibitor p16DNA, NeoplasmDNA PrimersGene Expression Regulation, NeoplasticHumansMiddle AgedMutationCyclin-Dependent Kinase Inhibitor p16DNA, NeoplasmDNA PrimersTumor Suppressor Protein p14ARF

Identifiers

PMID12610506
PMCPMC2377051
OpenAlexW2144140851

What OpenQuestion holds

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LicenceCC BY
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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.