Evidence map›Paper›PMID 21744007›Full record

ArticlePathology oncology research : POR2012

Variations in suppressor molecule ctla-4 gene are related to susceptibility to multiple myeloma in a polish population.

Lidia Karabon, Edyta Pawlak-Adamska, Anna Tomkiewicz, Anna Jedynak, Marek Kielbinski, Dariusz Woszczyk, Stanisław Potoczek, Anna Jonkisz, Kazimierz Kuliczkowski, Irena Frydecka

Open access · hybridAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Pathology oncology research : POR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 4 pooled it
0.6field-weighted citation impact, top 34% 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

20 citing papers in PubMed, 4 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  3. Meta-analysis of the cytotoxic T-lymphocyte antigen 4 gene +6230G/A polymorphism and cancer risk.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
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  18. Checkpoint inhibition in myeloma.Hematology. American Society of Hematology. Education Program · 2016
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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 3 institutions in 1 country.

Lidia KarabonDepartment of Experimental Therapy, Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Weigla 12, 53-114, Wroclaw, Poland. lkarabon@iitd.pan.wroc.pl
Edyta Pawlak-Adamska
Anna Tomkiewicz
Anna Jedynak
Marek Kielbinski
Dariusz Woszczyk
Stanisław Potoczek
Anna Jonkisz
Kazimierz Kuliczkowski
Irena Frydecka
Polish Academy of Sciences · PLWroclaw Medical University · PLUniversity of Opole · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various phenotype and functional T-cell abnormalities are observed in multiple myeloma (MM) patients. The aim of this study was to investigate the association between polymorphisms in the gene encoding cytotoxic T-lymphocyte antigen-4 (CTLA-4), a negative regulator of the T-lymphocyte immune response and susceptibility to multiple myeloma in a Polish population. Two hundred MM patients and 380 healthy subjects were genotyped for the following polymorphisms: CTLA-4c.49A>G, CTLA-4g.319C>T, CTLA-4g.*642AT(8_33), CT60 (CTLA-4g.*6230G>A), Jo31 (CTLA-4g.*10223G>T). Our study is the largest and most comprehensive evaluation to date of the association between genetic polymorphisms in the CTLA-4 molecule and multiple myeloma. It was found that CTLA-4c.49A>G[G], CT60[G], and Jo31[G] alleles were more frequently observed in MM patients than in controls (0.50 vs. 0.44, p = 0.03, 0.65 vs. 0.58, p = 0.04, and 0.63 vs. 0.57, p = 0.03, respectively). Moreover, the haplotype CTLA-4c.49A>G[G], CTLA-4g.319C>T[C], CTLA-4g.*642AT(8_33) [8], CT60[G], Jo31[G] including all susceptibility alleles increases the risk of MM about fourfold (OR: 3.79, 95%CI: 2.08-6.89, p = 0.00001). These findings indicate that genetic variations in the CTLA-4 gene play role in susceptibility to multiple myeloma and warrant further investigation through replication studies.

Indexed as

Genetic Predisposition to DiseaseAdultAgedAged, 80 and overAllelesCase-Control StudiesCTLA-4 AntigenDNAFemaleGene FrequencyHaplotypesHumansMaleMiddle AgedMultiple MyelomaPhenotypeCTLA-4 AntigenDNA

Identifiers

PMID21744007
PMCPMC3313022
OpenAlexW1992628481

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.