Evidence map›Paper›PMID 26646278›Full record

ArticlePancreas2016

A Common CCK-B Receptor Intronic Variant in Pancreatic Adenocarcinoma in a Hungarian Cohort.

Anita Balázs, Balázs Csaba Németh, Balázs Ördög, Eszter Hegyi, István Hritz, László Czakó, József Czimmer, Szilárd Gódi, Adrienn Csiszkó, Zoltán Rakonczay and 7 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pancreas, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 44% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

17 authors at 7 institutions in 3 countries.

Anita BalázsFrom the *First Department of Medicine, University of Szeged, Szeged, Hungary; †Department of Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA; ‡Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Szeged, Szeged, Hungary; §2nd Department of Pediatrics, Comenius University Medical School, University Children's Hospital, Bratislava, Slovakia; ∥First Department of Internal Medicine, University of Pécs, Hungary; ¶Institute of Surgery, University of Debrecen, Clinical Center, Debrecen, Hungary; #Heim Pál Children's Hospital, Budapest, Hungary; **First Department of Medicine, Szent György Teaching Hospital of County Fejér, Székesfehérvár, Hungary; ††Department of Oncotherapy, University of Szeged, Szeged, Hungary; and ‡‡MTA-SZTE Translational Gastroenterology Research Group, Szeged, Hungary.
Balázs Csaba Németh
Balázs Ördög
Eszter Hegyi
István Hritz
László Czakó
József Czimmer
Szilárd Gódi
Adrienn Csiszkó
Zoltán Rakonczay
Andrea Párniczky
Ferenc Izbéki
Adrienn Halász
Zsuzsanna Kahán
Péter Hegyi
Miklós Sahin-Tóth
Hungarian Pancreatic Study Group
Boston University · USUniversity of Debrecen · HUComenius University Bratislava · SKHeim Pál Gyermekkórház · HUUniversity of Pecs · HUFejér Megyei Szent György Egyetemi Oktató Kórház · HUUniversity of Szeged · HU

Funding

Chymotrypsin in pancreatitisR01DK082412 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2009 to 2024
$5.8M
Molecular Pathomechanism of Hereditary PancreatitisR01DK058088 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2001 to 2019
$5.3M
Pancreatic elastasesR01DK095753 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SAHIN-TOTH, MIKLOS · 2013 to 2016
$1.4M
NIDDK NIH HHS R01 DK058088NIDDK NIH HHS R01DK058088NIDDK NIH HHS R01 DK082412NIDDK NIH HHS R01DK082412NIDDK NIH HHS R01 DK095753NIDDK NIH HHS R01DK095753
6 · The paper itself

Abstract

objectivesVariant c.811+32C>A in intron 4 of the cholecystokinin-B receptor gene (CCKBR) was reported to correlate with higher pancreatic cancer risk and poorer survival. The variant was suggested to induce retention of intron 4, resulting in a new splice form with enhanced receptor activity. Our objective was to validate the c.811+32C>A variant as an emerging biomarker for pancreatic cancer risk and prognosis.

methodsWe genotyped variant c.811+32C>A in 122 pancreatic adenocarcinoma case patients and 106 control subjects by sequencing and examined its association with cancer risk and patient survival. We tested the functional effect of variant c.811+32C>A on pre-messenger RNA splicing in human embryonic kidney 293T and Capan-1 cells transfected with CCKBR minigenes.

resultsThe allele frequency of the variant was similar between patients and control subjects (18.4% and 17.9%, respectively). Survival analysis showed no significant difference between median survival of patients with the C/C genotype (266 days) and patients with the A/C or A/A genotypes (257 days). CCKBR minigenes with or without variant c.811+32C>A exhibited no difference in expression of the intron-retaining splice variant.

conclusionThese data indicate that variant c.811+32C>A in CCKBR does not have a significant impact on pancreatic cancer risk or survival in a Hungarian cohort.

Indexed as

Point MutationAdenocarcinomaAdolescentAdultAgedAged, 80 and overCell Line, TumorCohort StudiesFemaleGene FrequencyGenotypeHEK293 CellsHumansHungaryIntronsMaleReceptor, Cholecystokinin B

Identifiers

PMID26646278
PMCPMC4783207
OpenAlexW2230480369

What OpenQuestion holds

Textmetadata
LicenceTDM
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.