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Boström, I. M., Viberg, A., Golovleva, I. & Byström, B. (2024). CTG18.1 expansion in transcription factor 4 (TCF4) in corneal graft failure: preliminary study. Cell and Tissue Banking
Open this publication in new window or tab >>CTG18.1 expansion in transcription factor 4 (TCF4) in corneal graft failure: preliminary study
2024 (English)In: Cell and Tissue Banking, ISSN 1389-9333, E-ISSN 1573-6814Article in journal (Refereed) Epub ahead of print
Abstract [en]

Fuchs endothelial corneal dystrophy (FECD) is caused by a corneal endothelial cell loss, leading to corneal edema and visual impairment. The most significant genetic risk factor for FECD is an expansion of the CTG18.1 locus in transcription factor 4 (TCF4). The current treatment for severe FECD is corneal transplantation, with Descemet stripping automated keratoplasty (DSAEK) as a common surgical method. Although successful in most cases, the risk for transplant failure due to diverse causes must be considered. In this study, we investigated if presence of TCF4 CTG18.1 expansion with more than 31 (n ≥ 31) repeats in donated corneal grafts could be a reason for corneal transplant failure after DSAEK. For this, nine consecutively failed DSAEK corneal grafts were genotyped for CTG18.1 repeat length. One-sided Mann–Whitney U test was performed to evaluate if failed DSAEK corneal grafts had longer CTG18.1 repeats than healthy controls from the same population. All failed corneal grafts had CTG18.1 n ≤ 27 with a median of 18 (IQR 8.0) repeats for the longest allele. There was no statistical difference in CTG18.1 repeat lengths between failed corneal grafts and the geographically matched healthy control group. In conclusion, none of the nine failed corneal grafts in our material had CTG18.1 repeat lengths ≥ 31, a cut-off known to have a biological relevance in FECD. Thus, our results suggest that the assessment of donors and inspection of the corneal tissue before the decision for procurement is sufficient, in terms of recognizing FECD in the donor.

Place, publisher, year, edition, pages
Springer Science+Business Media B.V., 2024
Keywords
CTG18.1, Descemet stripping automated keratoplasty, DSAEK, Fuchs endothelial corneal dystrophy, TCF4, Transcription factor 4
National Category
Ophthalmology
Identifiers
urn:nbn:se:umu:diva-219760 (URN)10.1007/s10561-023-10123-y (DOI)2-s2.0-85181971334 (Scopus ID)
Funder
Umeå UniversityRegion VästerbottenEye FoundationStiftelsen Kronprinsessan Margaretas arbetsnämnd för synskadade
Available from: 2024-01-18 Created: 2024-01-18 Last updated: 2024-01-18
Westin, I. M., Landfors, M., Giannopoulos, A., Viberg, A., Osterman, P., Byström, B., . . . Golovleva, I. (2023). DNA methylation changes and increased mRNA expression of coagulation proteins, factor V and thrombomodulin in Fuchs endothelial corneal dystrophy. Cellular and Molecular Life Sciences (CMLS), 80(3), Article ID 62.
Open this publication in new window or tab >>DNA methylation changes and increased mRNA expression of coagulation proteins, factor V and thrombomodulin in Fuchs endothelial corneal dystrophy
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2023 (English)In: Cellular and Molecular Life Sciences (CMLS), ISSN 1420-682X, E-ISSN 1420-9071, Vol. 80, no 3, article id 62Article in journal (Refereed) Published
Abstract [en]

Late-onset Fuchs endothelial corneal dystrophy (FECD) is a disease affecting the corneal endothelium (CE), associated with a cytosine-thymine-guanine repeat expansion at the CTG18.1 locus in the transcription factor 4 (TCF4) gene. It is unknown whether CTG18.1 expansions affect global methylation including TCF4 gene in CE or whether global CE methylation changes at advanced age. Using genome-wide DNA methylation array, we investigated methylation in CE from FECD patients with CTG18.1 expansions and studied the methylation in healthy CE at different ages. The most revealing DNA methylation findings were analyzed by gene expression and protein analysis. 3488 CpGs had significantly altered methylation pattern in FECD though no substantial changes were found in TCF4. The most hypermethylated site was in a predicted promoter of aquaporin 1 (AQP1) gene, and the most hypomethylated site was in a predicted promoter of coagulation factor V (F5 for gene, FV for protein). In FECD, AQP1 mRNA expression was variable, while F5 gene expression showed a ~ 23-fold increase. FV protein was present in both healthy and affected CE. Further gene expression analysis of coagulation factors interacting with FV revealed a ~ 34-fold increase of thrombomodulin (THBD). THBD protein was detected only in CE from FECD patients. Additionally, we observed an age-dependent hypomethylation in elderly healthy CE.Thus, tissue-specific genome-wide and gene-specific methylation changes associated with altered gene expression were discovered in FECD. TCF4 pathological methylation in FECD because of CTG18.1 expansion was ruled out.

Place, publisher, year, edition, pages
Springer, 2023
Keywords
Coagulation factors; DNA methylation; Factor V; Fuchs dystrophy; Thrombomodulin; Transcription factor 4 (TCF4); Trinucleotide repeat disorder
National Category
Medical Genetics
Research subject
Medical Genetics; Medical Genetics
Identifiers
urn:nbn:se:umu:diva-200178 (URN)10.21203/rs.3.rs-1758860/v1 (DOI)000929515100001 ()36773096 (PubMedID)2-s2.0-85147894855 (Scopus ID)
Funder
Region VästerbottenUmeå UniversityStiftelsen Kronprinsessan Margaretas arbetsnämnd för synskadadeThe Kempe Foundations
Note

Originally included in thesis in manuscript form. 

Available from: 2022-10-12 Created: 2022-10-12 Last updated: 2023-09-05Bibliographically approved
Berglund, E., Barbany, G., Orsmark-Pietras, C., Fogelstrand, L., Abrahamsson, J., Golovleva, I., . . . Rosenquist, R. (2022). A Study Protocol for Validation and Implementation of Whole-Genome and -Transcriptome Sequencing as a Comprehensive Precision Diagnostic Test in Acute Leukemias. Frontiers in Medicine, 9, Article ID 842507.
Open this publication in new window or tab >>A Study Protocol for Validation and Implementation of Whole-Genome and -Transcriptome Sequencing as a Comprehensive Precision Diagnostic Test in Acute Leukemias
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2022 (English)In: Frontiers in Medicine, E-ISSN 2296-858X, Vol. 9, article id 842507Article in journal (Refereed) Published
Abstract [en]

Background: Whole-genome sequencing (WGS) and whole-transcriptome sequencing (WTS), with the ability to provide comprehensive genomic information, have become the focal point of research interest as novel techniques that can support precision diagnostics in routine clinical care of patients with various cancer types, including hematological malignancies. This national multi-center study, led by Genomic Medicine Sweden, aims to evaluate whether combined application of WGS and WTS (WGTS) is technically feasible and can be implemented as an efficient diagnostic tool in patients with acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). In addition to clinical impact assessment, a health-economic evaluation of such strategy will be performed.

Methods and Analysis: The study comprises four phases (i.e., retrospective, prospective, real-time validation, and follow-up) including approximately 700 adult and pediatric Swedish AML and ALL patients. Results of WGS for tumor (90×) and normal/germline (30×) samples as well as WTS for tumors only will be compared to current standard of care diagnostics. Primary study endpoints are diagnostic efficiency and improved diagnostic yield. Secondary endpoints are technical and clinical feasibility for routine implementation, clinical utility, and health-economic impact.

Discussion: Data from this national multi-center study will be used to evaluate clinical performance of the integrated WGTS diagnostic workflow compared with standard of care. The study will also elucidate clinical and health-economic impacts of a combined WGTS strategy when implemented in routine clinical care.

Clinical Trial Registration: [https://doi.org/10.1186/ISRCTN66987142], identifier [ISRCTN66987142].

Place, publisher, year, edition, pages
Frontiers Media S.A., 2022
Keywords
acute lymphoblastic leukemia, acute myeloid leukemia, clinical utility, diagnostic efficiency, health-economic evaluation, technical feasibility, whole-genome sequencing, whole-transcriptome sequencing
National Category
Hematology
Identifiers
urn:nbn:se:umu:diva-196179 (URN)10.3389/fmed.2022.842507 (DOI)000789699000001 ()35402448 (PubMedID)2-s2.0-85130851065 (Scopus ID)
Funder
VinnovaSwedish Childhood Cancer FoundationSwedish Cancer SocietySwedish Research CouncilRegion SkåneKarolinska InstituteScience for Life Laboratory, SciLifeLab, NP00043
Available from: 2022-06-13 Created: 2022-06-13 Last updated: 2023-05-23Bibliographically approved
Solaki, M., Baumann, B., Reuter, P., Andreasson, S., Audo, I., Ayuso, C., . . . Kohl, S. (2022). Comprehensive variant spectrum of the CNGA3 gene in patients affected by achromatopsia. Human Mutation, 43(7), 832-858
Open this publication in new window or tab >>Comprehensive variant spectrum of the CNGA3 gene in patients affected by achromatopsia
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2022 (English)In: Human Mutation, ISSN 1059-7794, E-ISSN 1098-1004, Vol. 43, no 7, p. 832-858Article in journal (Refereed) Published
Abstract [en]

Achromatopsia (ACHM) is a congenital cone photoreceptor disorder characterized by impaired color discrimination, low visual acuity, photosensitivity, and nystagmus. To date, six genes have been associated with ACHM (CNGA3, CNGB3, GNAT2, PDE6C, PDE6H, and ATF6), the majority of these being implicated in the cone phototransduction cascade. CNGA3 encodes the CNGA3 subunit of the cyclic nucleotide-gated ion channel in cone photoreceptors and is one of the major disease-associated genes for ACHM. Herein, we provide a comprehensive overview of the CNGA3 variant spectrum in a cohort of 1060 genetically confirmed ACHM patients, 385 (36.3%) of these carrying “likely disease-causing” variants in CNGA3. Compiling our own genetic data with those reported in the literature and in public databases, we further extend the CNGA3 variant spectrum to a total of 316 variants, 244 of which we interpreted as “likely disease-causing” according to ACMG/AMP criteria. We report 48 novel “likely disease-causing” variants, 24 of which are missense substitutions underlining the predominant role of this mutation class in the CNGA3 variant spectrum. In addition, we provide extensive in silico analyses and summarize reported functional data of previously analyzed missense, nonsense and splicing variants to further advance the pathogenicity assessment of the identified variants.

Place, publisher, year, edition, pages
John Wiley & Sons, 2022
Keywords
achromatopsia, CNGA3, cyclic nucleotide-gated ion channel, in silico analysis, variant classification, variant spectrum
National Category
Medical Genetics
Research subject
Medical Genetics
Identifiers
urn:nbn:se:umu:diva-194641 (URN)10.1002/humu.24371 (DOI)000782385300001 ()35332618 (PubMedID)2-s2.0-85129080727 (Scopus ID)
Available from: 2022-05-13 Created: 2022-05-13 Last updated: 2023-03-24Bibliographically approved
Viberg, A., Westin, I. M., Golovleva, I. & Byström, B. (2022). TCF4 trinucleotide repeat expansion in Swedish cases with Fuchs’ endothelial corneal dystrophy. Acta Ophthalmologica, 100(5), 541-548
Open this publication in new window or tab >>TCF4 trinucleotide repeat expansion in Swedish cases with Fuchs’ endothelial corneal dystrophy
2022 (English)In: Acta Ophthalmologica, ISSN 1755-375X, E-ISSN 1755-3768, Vol. 100, no 5, p. 65p. 541-548Article in journal (Refereed) Published
Abstract [en]

Purpose: Fuchs' endothelial corneal dystrophy (FECD) has been considered a genetically heterogeneous disease but is increasingly associated with the transcription factor 4 (TCF4) gene. This study investigates the prevalence of the cytosine-thymine-guanine (CTG)n repeat expansion in TCF4 among FECD patients in northern Sweden coupled to the phenotype.

Methods: Blood samples were collected from 85 FECD cases at different stages. Short tandem repeat PCR and triplet repeat-primed PCR were applied in order to determine TCF4 (CTG)n genotype.

Results: A (CTG)n repeat expansion (n > 50) in TCF4 was identified in 76 of 85 FECD cases (89.4%) and in four of 102 controls (3.9%). The median (CTG)n repeat length was 81 (IQR 39.3) in mild FECD and 87 (IQR 13.0) in severe FECD (p = 0.01). A higher number of (CTG)n repeats in an expanded TCF4 allele increased the probability of severe FECD. Other ocular surgery was overrepresented in FECD cases without a (CTG)n repeat expansion (44.4%, n = 4) compared with 3.9% (n = 3) in FECD cases with an (CTG)n repeat expansion (p < 0.001).

Conclusion: In northern Sweden, the FECD phenotype is associated with (CTG)n expansion in the TCF4 gene, with nearly 90% of patients being hetero- or homozygous for (CTG)n expansion over 50 repeats. Furthermore, the severity of FECD was associated with the repeat length in the TCF4 gene. Ocular surgery might act as an environmental factor explaining the clinical disease in FECD without a repeat expansion in TCF4.

Place, publisher, year, edition, pages
John Wiley & Sons, 2022. p. 65
Keywords
cornea, Fuchs’ endothelial corneal dystrophy, genetic aetiology, TCF4, trinucleotide repeat disorders
National Category
Ophthalmology
Research subject
ophthalmology; Medical Genetics
Identifiers
urn:nbn:se:umu:diva-187710 (URN)10.1111/aos.15032 (DOI)000706786900001 ()34644448 (PubMedID)2-s2.0-85116925455 (Scopus ID)978-91-7855-588-8 (ISBN)978-91-7855-589-5 (ISBN)
Funder
Stiftelsen Kronprinsessan Margaretas arbetsnämnd för synskadadeRegion Västerbotten
Note

Previously included in thesis in manuscript form.

Available from: 2021-09-18 Created: 2021-09-18 Last updated: 2022-11-29Bibliographically approved
Westin, I. M., Jonsson, F., Österman, L., Holmberg, M., Burstedt, M. & Golovleva, I. (2021). EYS mutations and implementation of minigene assay for variant classification in EYS-associated retinitis pigmentosa in northern Sweden. Scientific Reports, 11(1), Article ID 7696.
Open this publication in new window or tab >>EYS mutations and implementation of minigene assay for variant classification in EYS-associated retinitis pigmentosa in northern Sweden
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2021 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 11, no 1, article id 7696Article in journal (Refereed) Published
Abstract [en]

Retinitis pigmentosa (RP) is a clinically and genetically heterogeneous group of inherited retinal degenerations. The ortholog of Drosophila eyes shut/spacemaker, EYS on chromosome 6q12 is a major genetic cause of recessive RP worldwide, with prevalence of 5 to 30%. In this study, by using targeted NGS, MLPA and Sanger sequencing we uncovered the EYS gene as one of the most common genetic cause of autosomal recessive RP in northern Sweden accounting for at least 16%. The most frequent pathogenic variant was c.8648_8655del that in some patients was identified in cis with c.1155T>A, indicating Finnish ancestry. We also showed that two novel EYS variants, c.2992_2992+6delinsTG and c.3877+1G>A caused exon skipping in human embryonic kidney cells, HEK293T and in retinal pigment epithelium cells, ARPE-19 demonstrating that in vitro minigene assay is a straightforward tool for the analysis of intronic variants. We conclude, that whenever it is possible, functional testing is of great value for classification of intronic EYS variants and the following molecular testing of family members, their genetic counselling, and inclusion of RP patients to future treatment studies.

Place, publisher, year, edition, pages
Nature Publishing Group, 2021
National Category
Medical Genetics Ophthalmology
Identifiers
urn:nbn:se:umu:diva-182475 (URN)10.1038/s41598-021-87224-9 (DOI)000639562100016 ()2-s2.0-85104048909 (Scopus ID)
Available from: 2021-04-29 Created: 2021-04-29 Last updated: 2023-09-05Bibliographically approved
Westin, I. M., Viberg, A., Byström, B. & Golovleva, I. (2021). Lower fractions of TCF4 transcripts spanning over the CTG18.1 trinucleotide repeat in human corneal endothelium. Genes, 12(12), Article ID 2006.
Open this publication in new window or tab >>Lower fractions of TCF4 transcripts spanning over the CTG18.1 trinucleotide repeat in human corneal endothelium
2021 (English)In: Genes, ISSN 2073-4425, E-ISSN 2073-4425, Vol. 12, no 12, article id 2006Article in journal (Refereed) Published
Abstract [en]

Fuchs’ endothelial corneal dystrophy (FECD) is a bilateral disease of the cornea caused by gradual loss of corneal endothelial cells. Late-onset FECD is strongly associated with the CTG18.1 trinucleotide repeat expansion in the Transcription Factor 4 gene (TCF4), which forms RNA nuclear foci in corneal endothelial cells. To date, 46 RefSeq transcripts of TCF4 are annotated by the National Center of Biotechnology information (NCBI), however the effect of the CTG18.1 expansion on expression of alternative TCF4 transcripts is not completely understood. To investigate this, we used droplet digital PCR for quantification of TCF4 transcripts spanning over the CTG18.1 and transcripts with transcription start sites immediately downstream of the CTG18.1. TCF4 expression was analysed in corneal endothelium and in whole blood of FECD patients with and without CTG18.1 expansion, in non-FECD controls without CTG18.1 expansion, and in five additional control tissues. Subtle changes in transcription levels in groups of TCF4 transcripts were detected. In corneal endothelium, we found a lower fraction of transcripts spanning over the CTG18.1 tract compared to all other tissues investigated.

Place, publisher, year, edition, pages
MDPI, 2021
Keywords
Alternative transcripts, DdPCR, Fuchs corneal dystrophy, MRNA expression, Transcription Factor 4 (TCF4)
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-190871 (URN)10.3390/genes12122006 (DOI)000737561800001 ()2-s2.0-85121416878 (Scopus ID)
Funder
Region VästerbottenStiftelsen Kronprinsessan Margaretas arbetsnämnd för synskadade
Available from: 2021-12-30 Created: 2021-12-30 Last updated: 2023-09-05Bibliographically approved
Vikberg, A.-L., Malla, S. & Golovleva, I. (2020). Differential tissue specific expression of Kif23 alternative transcripts in mice with the human mutation causing congenital dyserythropoietic anemia type III. Blood Cells, Molecules & Diseases, 85, Article ID 102483.
Open this publication in new window or tab >>Differential tissue specific expression of Kif23 alternative transcripts in mice with the human mutation causing congenital dyserythropoietic anemia type III
2020 (English)In: Blood Cells, Molecules & Diseases, ISSN 1079-9796, E-ISSN 1096-0961, Vol. 85, article id 102483Article in journal (Refereed) Published
Abstract [en]

Kinesin Family Member 23 (KIF23), a cell cycle regulator, has a key task in cytokinesis. KIF23 over-expression in cancer has been associated with tumor growth, progression, and poor prognosis, indicating a potential to be a cancer biomarker. A mutation in KIF23 (c.2747C > G, p.P916R) was shown to cause congenital dyserythropoietic anemia, type III (CDA III). To-date, fifteen KIF23 transcripts have been annotated, but their expression is poorly investigated. We hypothesized that tissue specific expression of a particular transcript can be critical for CDA III phenotype. In this study, we quantified expression of alternative Kif23 transcripts in a mouse model with human KIF23 mutation and investigated its association with a regulator of alternative splicing, serine/arginine-rich splicing factor 3 (Srsf3). We confirmed presence of an additional exon 8 in both human and mouse KIF23 transcripts. A transcript lacking exons 17 and 18 was ubiquitously expressed in mice while other isoforms were common in human tissues however in bone marrow of knock-in mice a transcript without exon 18 was prevalent as it was in bone marrow of a CDA III patient. We conclude that the possibility that the tissue specific expression of KIF23 alternative transcripts influence the CDA III phenotype cannot be neglected.

Place, publisher, year, edition, pages
Elsevier, 2020
Keywords
KIF23, Srsf3, CDA III, Expression, Alternative splicing, Droplet digital PCR (ddPCR), Knock-in (KI) mice
National Category
Hematology
Identifiers
urn:nbn:se:umu:diva-175847 (URN)10.1016/j.bcmd.2020.102483 (DOI)000571001800002 ()32818800 (PubMedID)2-s2.0-85089430369 (Scopus ID)
Available from: 2020-10-15 Created: 2020-10-15 Last updated: 2023-03-24Bibliographically approved
Haider, Z., Landfors, M., Golovleva, I., Erlanson, M., Schmiegelow, K., Flaegstad, T., . . . Degerman, S. (2020). DNA methylation and copy number variation profiling of T-cell lymphoblastic leukemia and lymphoma. Blood Cancer Journal, 10(4), Article ID 45.
Open this publication in new window or tab >>DNA methylation and copy number variation profiling of T-cell lymphoblastic leukemia and lymphoma
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2020 (English)In: Blood Cancer Journal, E-ISSN 2044-5385, Vol. 10, no 4, article id 45Article in journal (Refereed) Published
Abstract [en]

Despite having common overlapping immunophenotypic and morphological features, T-cell lymphoblastic leukemia (T-ALL) and lymphoma (T-LBL) have distinct clinical manifestations, which may represent separate diseases. We investigated and compared the epigenetic and genetic landscape of adult and pediatric T-ALL (n = 77) and T-LBL (n = 15) patient samples by high-resolution genome-wide DNA methylation and Copy Number Variation (CNV) BeadChip arrays. DNA methylation profiling identified the presence of CpG island methylator phenotype (CIMP) subgroups within both pediatric and adult T-LBL and T-ALL. An epigenetic signature of 128 differentially methylated CpG sites was identified, that clustered T-LBL and T-ALL separately. The most significant differentially methylated gene loci included the SGCE/PEG10 shared promoter region, previously implicated in lymphoid malignancies. CNV analysis confirmed overlapping recurrent aberrations between T-ALL and T-LBL, including 9p21.3 (CDKN2A/CDKN2B) deletions. A significantly higher frequency of chromosome 13q14.2 deletions was identified in T-LBL samples (36% in T-LBL vs. 0% in T-ALL). This deletion, encompassing the RB1, MIR15A and MIR16-1 gene loci, has been reported as a recurrent deletion in B-cell malignancies. Our study reveals epigenetic and genetic markers that can distinguish between T-LBL and T-ALL, and deepen the understanding of the biology underlying the diverse disease localization.

Place, publisher, year, edition, pages
Nature Publishing Group, 2020
National Category
Hematology
Identifiers
urn:nbn:se:umu:diva-171400 (URN)10.1038/s41408-020-0310-9 (DOI)000531381100002 ()32345961 (PubMedID)2-s2.0-85083959026 (Scopus ID)
Available from: 2020-06-03 Created: 2020-06-03 Last updated: 2023-11-15Bibliographically approved
Wu, W.-Y. Y., Johansson, G., Wibom, C., Brännström, T., Malmström, A., Henriksson, R., . . . Melin, B. S. (2019). The Genetic Architecture of Gliomagenesis-Genetic Risk Variants Linked to Specific Molecular Subtypes. Cancers, 11(12), Article ID 2001.
Open this publication in new window or tab >>The Genetic Architecture of Gliomagenesis-Genetic Risk Variants Linked to Specific Molecular Subtypes
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2019 (English)In: Cancers, ISSN 2072-6694, Vol. 11, no 12, article id 2001Article, review/survey (Refereed) Published
Abstract [en]

Genome-wide association studies have identified 25 germline genetic loci that increase the risk of glioma. The somatic tumor molecular alterations, including IDH-mutation status and 1p/19q co-deletion, have been included into the WHO 2016 classification system for glioma. To investigate how the germline genetic risk variants correlate with the somatic molecular subtypes put forward by WHO, we performed a meta-analysis that combined findings from 330 Swedish cases and 876 controls with two other recent studies. In total, 5,103 cases and 10,915 controls were included. Three categories of associations were found. First, variants in TERT and TP53 were associated with increased risk of all glioma subtypes. Second, variants in CDKN2B-AS1, EGFR, and RTEL1 were associated with IDH-wildtype glioma. Third, variants in CCDC26 (the 8q24 locus), C2orf80 (close to IDH), LRIG1, PHLDB1, ETFA, MAML2 and ZBTB16 were associated with IDH-mutant glioma. We therefore propose three etiopathological pathways in gliomagenesis based on germline variants for future guidance of diagnosis and potential functional targets for therapies. Future prospective clinical trials of patients with suspicion of glioma diagnoses, using the genetic variants as biomarkers, are necessary to disentangle how strongly they can predict glioma diagnosis.

Place, publisher, year, edition, pages
MDPI, 2019
Keywords
glioma, IDH mutant, 1p/19q co-deletion, gliomagenesis, genotype phenotype, etiopathogenesis
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-167615 (URN)10.3390/cancers11122001 (DOI)000507382100178 ()31842352 (PubMedID)2-s2.0-85076550363 (Scopus ID)
Available from: 2020-02-06 Created: 2020-02-06 Last updated: 2020-04-08Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-8741-0616

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