Evidence map›Paper›PMID 28101800›Full record

ArticlePathology oncology research : POR2017

Is the Genetic Background of Co-Stimulatory CD28/CTLA-4 Pathway the Risk Factor for Prostate Cancer?

Lidia Karabon, K Tupikowski, A Tomkiewicz, A Partyka, E Pawlak-Adamska, A Wojciechowski, A Kolodziej, J Dembowski, R Zdrojowy, I Frydecka

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In one paragraph

Article in Pathology oncology research : POR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Association Between the CD28 c.17 +3 T>C Polymorphism (rs3116496) and Cancer Risk: An Updated Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Pooled it
  2. CTLA-4: a promising immunosuppressive immune checkpoint in prostate cancer therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  3. Association ofCurrent issues in molecular biology · 2024
    Article
  4. Article
  5. 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

10 authors at 2 institutions in 1 country.

Lidia KarabonDepartment of Urology and Oncological Urology, Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland. lkarabon@iitd.pan.wroc.pl.ORCID http://orcid.org/0000-0001-8172-0971
K TupikowskiDepartment of Urology and Oncological Urology, Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
A TomkiewiczDepartment of Experimental Therapy, Hirszfeld Institute of Immunology and Experimental Therapy, Weigla 12, 53-114, Wroclaw, Poland.
A PartykaDepartment of Experimental Therapy, Hirszfeld Institute of Immunology and Experimental Therapy, Weigla 12, 53-114, Wroclaw, Poland.
E Pawlak-AdamskaDepartment of Experimental Therapy, Hirszfeld Institute of Immunology and Experimental Therapy, Weigla 12, 53-114, Wroclaw, Poland.
A WojciechowskiDepartment of Urology and Oncological Urology, Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
A KolodziejDepartment of Urology and Oncological Urology, Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
J DembowskiDepartment of Urology and Oncological Urology, Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
R ZdrojowyDepartment of Urology and Oncological Urology, Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
I FrydeckaDepartment of Experimental Therapy, Hirszfeld Institute of Immunology and Experimental Therapy, Weigla 12, 53-114, Wroclaw, Poland.
Wroclaw Medical University · PLLudwik Hirszfeld Institute of Immunology and Experimental Therapy · PL

Funding

Narodowe Centrum Nauki N403 172339Narodowe Centrum Nauki N N402 454339
6 · The paper itself

Abstract

The impairment of immunological surveillance caused by aberrant T cell activation can lead to an inadequate anti-tumor response. Therefore, deregulation in co-stimulatory pathway might be associated with cancer susceptibility. Here we undertook a prospective study to investigate whether genetic variations in gene encoding molecule CD28 and CTLA-4 playing pivotal role in regulating adoptive immune response can influence susceptibility to prostate cancer. Single nucleotide polymorphisms (SNPs) in CTLA-4 and CD28 genes were genotyped in 301 prostate cancer (PCa) patients and 301 controls. The distributions of the genotypes and haplotypes in the CTLA-4/CD28 SNPs were similar in both studied groups. However, the overrepresentation of carriers of CTLA-4c.49A>G[A] allele and carriers of CTLA-4g.319C>T[T] allele in PCa as compared to controls was observed (p = 0.082 and p = 0.13, respectively). The risk of disease was higher (OR 1.78) for carriers of both susceptibility alleles as compared to carriers of protective genotypes (p = 0.03). The CTLA-4c.49A>G and CTLA-4g.319C>T SNPs might be considered as low risk susceptibility locus for PCa.

Indexed as

CD28 AntigensCTLA-4 AntigenGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedPolymorphism, Single NucleotideProstatic NeoplasmsRisk FactorsCD28 AntigensCTLA-4 AntigenCTLA4 protein, humanCD28CTLA-4Gene polymorphismsProstate cancer

Identifiers

PMID28101800
OpenAlexW2573637414

What OpenQuestion holds

Textmetadata
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.