Evidence map›Paper›PMID 30134356›Full record

SynthesisPancreas2018

Pancreatitis-Associated Genes and Pancreatic Cancer Risk: A Systematic Review and Meta-analysis.

Irina Mihaela Cazacu, Nelli Farkas, András Garami, Márta Balaskó, Bernadett Mosdósi, Hussain Alizadeh, Zoltán Gyöngyi, Zoltán Rakonczay, Éva Vigh, Tamás Habon and 5 more

Abstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Pancreas, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Current status of inherited pancreatic cancer.Hereditary cancer in clinical practice · 2022
    Review
  14. CFTR and Gastrointestinal Cancers: An Update.Journal of personalized medicine · 2022
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

15 authors.

Irina Mihaela Cazacu
Nelli FarkasInstitute of Bioanalysis.
András Garami
Márta Balaskó
Bernadett MosdósiDepartment of Pediatrics.
Hussain AlizadehDepartment of Haematology, First Department of Medicine, and.
Zoltán GyöngyiDepartment of Public Health Medicine, Medical School, University of Pécs, Pécs.
Zoltán RakonczayDepartment of Pathophysiology, University of Szeged, Szeged.
Éva VighRadiology and.
Tamás HabonCardiology, First Department of Medicine, Medical School, University of Pécs, Pécs, Hungary.
László CzopfCardiology, First Department of Medicine, Medical School, University of Pécs, Pécs, Hungary.
Marilena Alina Lazarescu
Bálint Erőss
Miklós Sahin-TóthDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, MA.
Péter Hegyi

Funding

Wellcome Trust
6 · The paper itself

Abstract

objectiveThe aim of this study was to evaluate the connection between pancreatic cancer (PC) and genetic variants associated with chronic pancreatitis via systematic review and meta-analysis.

methodsThe data search was performed in 3 major databases (PubMed, Embase, and Cochrane Library). The selected studies have looked into the presence of the pancreatitis-associated genes in patients with PC and in control subjects, the outcome being the frequency of the mutations in the 2 groups. For the binary outcomes, pooled odds ratio (OR) and 95% confidence interval (CI) were calculated.

resultsTen articles proved to be eligible for the qualitative synthesis, and 8 articles were suitable for statistical analysis. Six case-control studies, comprising 929 PC cases and 1890 control subjects for serine protease inhibitor Kazal type 1 (SPINK1) mutations, and 5 case-control studies, comprising 1674 PC cases and 19,036 control subjects for CFTR mutations, were enrolled in our analysis. SPINK1 mutations showed no association with PC (OR, 1.52; 95% CI, 0.67-3.45; P = 0.315), whereas mutations in CFTR modestly increased the risk of PC (OR, 1.41; 95% CI, 1.07-1.84; P = 0.013).

conclusionOur meta-analysis showed that mutations in CFTR modestly increase the risk of PC, whereas no association was found between SPINK1 and PC.

Indexed as

MutationCystic Fibrosis Transmembrane Conductance RegulatorGenetic Predisposition to DiseaseHumansOdds RatioPancreatic NeoplasmsPancreatitis, ChronicRisk FactorsTrypsin Inhibitor, Kazal PancreaticCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorSPINK1 protein, humanTrypsin Inhibitor, Kazal Pancreatic

Identifiers

PMID30134356
PMCPMC6291258

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.