Evidence map›Paper›PMID 21225475›Full record

ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract2011

High-throughput mutation profiling in intraductal papillary mucinous neoplasm (IPMN).

Nir Lubezky, Menahem Ben-Haim, Sylvia Marmor, Eli Brazowsky, Gideon Rechavi, Joseph M Klausner, Yoram Cohen

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Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. The genetic classification of pancreatic neoplasia.Journal of gastroenterology · 2015
    Review
  7. Review
  8. Genomic landscapes of pancreatic neoplasia.Journal of pathology and translational medicine · 2015
    Review
  9. Article
  10. Article
  11. Loss of PTEN expression is associated with poor prognosis in patients with intraductal papillary mucinous neoplasms of the pancreas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  12. Review
  13. Review
  14. Article
  15. Review
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 1 country.

Nir LubezkyDepartment of Surgery B, Tel-Aviv Sourasky Medical Center, Sackler School of Medicine, Tel-Aviv University, 6 Weitzman St., Tel Aviv 64239, Israel. nirl@tasmc.health.gov.il
Menahem Ben-Haim
Sylvia Marmor
Eli Brazowsky
Gideon Rechavi
Joseph M Klausner
Yoram Cohen
Tel Aviv University · ILSheba Medical Center · ILTel Aviv Sourasky Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSpecific mutations leading to the development of various histological grades of intraductal papillary mucinous neoplasm (IPMN) have been partially characterized.

methodsAnalysis of 323 oncogenic mutations in 22 tumor-related genes was conducted, using a chip-based matrix-assisted laser desorption time-of-flight mass spectrometer of DNA extracted from microdissected cells of low-grade (n = 14), borderline (n = 6), and invasive IPMN (n = 7). Additional assays were performed on the DNA extracted from dyplastic cells found in the background of the adenocarcinoma.

resultsWe identified 9 K-ras mutations (low grade, 2/14; borderline, 1/6; invasive, 6/7), 3 p53 mutations (low grade, 1/14; invasive 2/7), and 2 PIK3CA mutations (low grade, 1/14; invasive, 1/7). K-ras, p53, and PIK3CA mutations present in the invasive cancer were absent in the adjacent precursor cells in 50% of the cases. In one patient, K-ras mutation was present in the precursor lesion and absent in the adjacent invasive lesion.

conclusionsOf the 22 screened tumor-related genes, only K-ras, p53, and PIK3CA mutations were found in IPMN. K-ras mutations are more prevalent in invasive than premalignant IPMN. The variable coexistence of mutations in the invasive cancer and in the adjacent precursor cells may point to the heterogeneous nature of this tumor.

Indexed as

MutationAdenocarcinoma, MucinousAdenocarcinoma, PapillaryAgedAged, 80 and overClass I Phosphatidylinositol 3-KinasesDNA Mutational AnalysisFemaleGenes, p53Genes, rasGenes, Tumor SuppressorGenotypeHumansMaleMiddle AgedPancreatic NeoplasmsClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesPIK3CA protein, human

Identifiers

PMID21225475
OpenAlexW2039451930

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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.