Umeå University's logo

umu.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Genome-wide polygenic risk scores predict risk of glioma and molecular subtypes
Department of Epidemiology and Population Health, Stanford University School of Medicine, Stanford, California, USA.ORCID iD: 0000-0002-3078-098X
Department of Neurological Surgery, University of California San Francisco, San Francisco, California, USA.ORCID iD: 0000-0001-9870-9998
Department of Neurosurgery, Duke University School of Medicine, Durham, North Carolina, USA.
Psychiatric and Neurodevelopmental Genetics Unit, Center for Genomic Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA; Department of Psychiatry, Center for Precision Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA.
Show others and affiliations
2024 (English)In: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 26, no 10, p. 1933-1944Article in journal (Refereed) Published
Abstract [en]

Background: Polygenic risk scores (PRS) aggregate the contribution of many risk variants to provide a personalized genetic susceptibility profile. Since sample sizes of glioma genome-wide association studies (GWAS) remain modest, there is a need to efficiently capture genetic risk using available data.

Methods: We applied a method based on continuous shrinkage priors (PRS-CS) to model the joint effects of over 1 million common variants on disease risk and compared this to an approach (PRS-CT) that only selects a limited set of independent variants that reach genome-wide significance (P < 5 x 10(-8)). PRS models were trained using GWAS stratified by histological (10 346 cases and 14 687 controls) and molecular subtype (2632 cases and 2445 controls), and validated in 2 independent cohorts.

Results: PRS-CS was generally more predictive than PRS-CT with a median increase in explained variance (R-2) of 24% (interquartile range = 11-30%) across glioma subtypes. Improvements were pronounced for glioblastoma (GBM), with PRS-CS yielding larger odds ratios (OR) per standard deviation (SD) (OR = 1.93, P = 2.0 x 10(-54) vs. OR = 1.83, P = 9.4 x 10(-50)) and higher explained variance (R-2 = 2.82% vs. R-2 = 2.56%). Individuals in the 80th percentile of the PRS-CS distribution had a significantly higher risk of GBM (0.107%) at age 60 compared to those with average PRS (0.046%, P = 2.4 x 10(-12)). Lifetime absolute risk reached 1.18% for glioma and 0.76% for IDH wildtype tumors for individuals in the 95th PRS percentile. PRS-CS augmented the classification of IDH mutation status in cases when added to demographic factors (AUC = 0.839 vs. AUC = 0.895, P-Delta AUC = 6.8 x 10(-9)).

Conclusions: Genome-wide PRS has the potential to enhance the detection of high-risk individuals and help distinguish between prognostic glioma subtypes.

Place, publisher, year, edition, pages
Oxford University Press, 2024. Vol. 26, no 10, p. 1933-1944
Keywords [en]
genetic susceptibility, glioma, polygenic risk score (PRS), prediction, risk
National Category
Cancer and Oncology Neurosciences
Identifiers
URN: urn:nbn:se:umu:diva-228687DOI: 10.1093/neuonc/noae112ISI: 001272037500001PubMedID: 38916140Scopus ID: 2-s2.0-85205740777OAI: oai:DiVA.org:umu-228687DiVA, id: diva2:1891169
Funder
NIH (National Institutes of Health), T32CA151022; R01CA266676; R01CA52689; P50CA097257; R01CA126831; R01CA139020; R01AI128775; R25CA112355; R00CA246076; U01CA261339; U01HG011723; R01CA232754Available from: 2024-08-21 Created: 2024-08-21 Last updated: 2024-10-14Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMedScopus

Authority records

Melin, Beatrice S.

Search in DiVA

By author/editor
Nakase, TaishiGuerra, Geno A.Melin, Beatrice S.Kachuri, Linda
By organisation
OncologyDepartment of Diagnostics and Intervention
In the same journal
Neuro-Oncology
Cancer and OncologyNeurosciences

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 455 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf