Evidence map›Paper›PMID 37122695›Full record

ArticleFrontiers in immunology2023

Genetic variants of CTLA4 are associated with clinical outcome of patients with multiple myeloma.

Yolanda Gonzalez-Montes, Rocío Rodriguez-Romanos, Alicia Villavicencio, Gemma Osca-Gelis, Marta González-Bártulos, Francesca Llopis, Victòria Clapes, Albert Oriol, Anna Sureda, Lourdes Escoda and 6 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
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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

16 authors.

Yolanda Gonzalez-MontesHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Rocío Rodriguez-RomanosHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Alicia VillavicencioHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Gemma Osca-GelisHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Marta González-BártulosHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Francesca LlopisHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Victòria ClapesClinical Hematology Department, Institut Català d'Oncologia, L'Hospitalet, IDIBELL, Universitat de Barcelona, Hospitalet de LLobregat, Spain.
Albert OriolHematology Department, Institut Català d'Oncologia, Hospital Germans Trias i Pujol, Josep Carreras Research Institute, Badalona, Barcelona, Spain.
Anna SuredaClinical Hematology Department, Institut Català d'Oncologia, L'Hospitalet, IDIBELL, Universitat de Barcelona, Hospitalet de LLobregat, Spain.
Lourdes EscodaHematology Department, Institut Català d'Oncologia, Hospital Joan XXIII, Universitat Rovira i Virgili (URV), Tarragona, Spain.
Josep SarràHematology Department, Institut Català d'Oncologia, Hospital Joan XXIII, Universitat Rovira i Virgili (URV), Tarragona, Spain.
Ana GarzóHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Natàlia LloverasHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Isabel DíezHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.
Isabel GranadaHematology Department, Institut Català d'Oncologia, Hospital Germans Trias i Pujol, Josep Carreras Research Institute, Badalona, Barcelona, Spain.
David GallardoHematology Department, Institut Català d'Oncologia, Hospital Dr. Josep Trueta, Institut d'Investigació Biomèdica de Girona (IDIBGI), Josep Carreras Research Institute, Girona, Universitat de Girona, Girona, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune dysfunction in patients with multiple myeloma (MM) affects both the innate and adaptive immune system. Molecules involved in the immune checkpoint pathways are essential to determine the ability of cancer cells to escape from the immune system surveillance. However, few data are available concerning the role of these molecules in predicting the kinetics of progression of MM. We retrospectively analysed polymorphisms of CTLA4 (rs231775 and rs733618), BTLA (rs9288953), CD28 (rs3116496), PD-1 (rs36084323 and rs11568821) and LAG-3 (rs870849) genes in 239 patients with newly diagnosed MM. Patients with a CTLA4 rs231775 AA/AG genotype showed a median progression-free survival (PFS) significantly lower than those with GG genotype (32.3 months versus 96.8 months respectively; p: 0.008). The 5-year PFS rate was 25% for patients with grouped AA and AG genotype vs 55.4% for patients with GG genotype. Multivariate analysis confirmed the CTLA4 rs231775 genotype as an independent risk factor for PFS (Hazard Ratio (HR): 2.05; 95% CI: 1.0-6.2; p: 0.047). Our results suggest that the CTLA4 genotype may identify patients with earlier progression of MM. This polymorphism could potentially be used as a prognostic biomarker.

Indexed as

Multiple MyelomaCTLA-4 AntigenGenotypeHumansPolymorphism, Single NucleotideRetrospective StudiesCTLA-4 AntigenCTLA4 protein, humanbone marrow microenvironmentCTLA4 polymorphismscytogenetics and molecular geneticsimmune checkpointmultiple myeloma

Identifiers

PMID37122695
PMCPMC10143497

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