Epigenetic Suppression of the IL-7 Pathway in Progressive Glioblastoma.

CpG methylation epigenomics glioblastoma immune evasion interleukin 7 pathway

Journal

Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304

Informations de publication

Date de publication:
02 Sep 2022
Historique:
received: 13 08 2022
revised: 26 08 2022
accepted: 30 08 2022
entrez: 23 9 2022
pubmed: 24 9 2022
medline: 24 9 2022
Statut: epublish

Résumé

Immune evasion in glioblastoma (GBM) shields cancer cells from cytotoxic immune response. We investigated CpG methylation in promoters, genes, and pathways in 22 pairs of formalin-fixed paraffin-embedded sequential (FFPE) GBM using restricted resolution bisulfite sequencing (RRBS) and bioinformatic analyses. Gene ontology revealed hypermethylation in elements of the innate and adaptive immune system when recurrent GBM samples (GBM This study revealed the progressive suppression of the IL-7 receptor-mediated pathway as a means of immune evasion by GBM and thereby highlighted it as a new treatment target.

Sections du résumé

BACKGROUND BACKGROUND
Immune evasion in glioblastoma (GBM) shields cancer cells from cytotoxic immune response.
METHODS METHODS
We investigated CpG methylation in promoters, genes, and pathways in 22 pairs of formalin-fixed paraffin-embedded sequential (FFPE) GBM using restricted resolution bisulfite sequencing (RRBS) and bioinformatic analyses.
RESULTS RESULTS
Gene ontology revealed hypermethylation in elements of the innate and adaptive immune system when recurrent GBM samples (GBM
CONCLUSIONS CONCLUSIONS
This study revealed the progressive suppression of the IL-7 receptor-mediated pathway as a means of immune evasion by GBM and thereby highlighted it as a new treatment target.

Identifiants

pubmed: 36140275
pii: biomedicines10092174
doi: 10.3390/biomedicines10092174
pmc: PMC9496096
pii:
doi:

Types de publication

Journal Article

Langues

eng

Subventions

Organisme : Elixir Converge
ID : Nr. 871075
Organisme : Natikonal Research, Development and Innovation Fund, Hungary
ID : TKP2020-4.1.1
Organisme : Ginop
ID : GINOP-2.3.4-15-2020-00010
Organisme : Ginop
ID : GINOP-2.3.1-20-2020- 00001
Organisme : Erasmus+
ID : 2019-0-HU01-KA203-061251
Organisme : H2020-MSCA-COFUND Marie Skłodowska-Curie
ID : Nr. 754432

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Auteurs

Marton Tompa (M)

Szentagothai Research Center, University of Pecs, 7624 Pecs, Hungary.

Zoltan Kraboth (Z)

Department of Laboratory Medicine, University of Pecs, School of Medicine, Clinical Center, 7624 Pecs, Hungary.
Department of Pathology, University of Pecs, School of Medicine, Clinical Center, 7624 Pecs, Hungary.

Bence Galik (B)

Szentagothai Research Center, University of Pecs, 7624 Pecs, Hungary.
Department of Clinical Molecular Biology, Medical University of Bialystok, 15-269 Bialystok, Poland.

Bela Kajtar (B)

Szentagothai Research Center, University of Pecs, 7624 Pecs, Hungary.
Department of Pathology, University of Pecs, School of Medicine, Clinical Center, 7624 Pecs, Hungary.

Attila Gyenesei (A)

Szentagothai Research Center, University of Pecs, 7624 Pecs, Hungary.
Department of Clinical Molecular Biology, Medical University of Bialystok, 15-269 Bialystok, Poland.

Bernadette Kalman (B)

Szentagothai Research Center, University of Pecs, 7624 Pecs, Hungary.
Department of Laboratory Medicine, University of Pecs, School of Medicine, Clinical Center, 7624 Pecs, Hungary.

Classifications MeSH