Circulating MACC1 Transcripts in Glioblastoma Patients Predict Prognosis and Treatment Response.
glioblastoma multiforme
liquid biopsy
metastasis-associated in colon cancer 1 (MACC1)
prognostic marker
therapy response
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
13 Jun 2019
13 Jun 2019
Historique:
received:
27
05
2019
revised:
10
06
2019
accepted:
11
06
2019
entrez:
16
6
2019
pubmed:
16
6
2019
medline:
16
6
2019
Statut:
epublish
Résumé
Glioblastoma multiforme is the most aggressive primary brain tumor of adults, but lacks reliable and liquid biomarkers. We evaluated circulating plasma transcripts of metastasis-associated in colon cancer-1 (MACC1), a prognostic biomarker for solid cancer entities, for prediction of clinical outcome and therapy response in glioblastomas. MACC1 transcripts were significantly higher in patients compared to controls. Low MACC1 levels clustered together with other prognostically favorable markers. It was associated with patients' prognosis in conjunction with the isocitrate dehydrogenase (IDH) mutation status: IDH1 R132H mutation and low MACC1 was most favorable (median overall survival (OS) not yet reached), IDH1 wildtype and high MACC1 was worst (median OS 8.1 months), while IDH1 wildtype and low MACC1 was intermediate (median OS 9.1 months). No patients displayed IDH1 R132H mutation and high MACC1. Patients with low MACC1 levels receiving standard therapy survived longer (median OS 22.6 months) than patients with high MACC1 levels (median OS 8.1 months). Patients not receiving the standard regimen showed the worst prognosis, independent of MACC1 levels (low: 6.8 months, high: 4.4 months). Addition of circulating MACC1 transcript levels to the existing prognostic workup may improve the accuracy of outcome prediction and help define more precise risk categories of glioblastoma patients.
Identifiants
pubmed: 31200581
pii: cancers11060825
doi: 10.3390/cancers11060825
pmc: PMC6627447
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : German Cancer Consortium (DKTK), Heidelberg, Germany
ID : DKTK
Organisme : Deutsche Forschungsgemeinschaft
ID : Open Access Publishing
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