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  • 1.
    Corell, Alba
    et al.
    Sahlgrens Univ Hosp, Dept Neurosurg, Gothenburg, Sweden.;Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden..
    Vecchio, Tomas Gomez
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden..
    Vega, Sandra Ferreyra
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden..
    Denes, Anna
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden..
    Neimantaite, Alice
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden..
    Hagerius, Alexander
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden..
    Barcheus, Hanna
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden..
    Solheim, Ole
    Norwegian Univ Sci & Technol, Dept Neuromed & Movement Sci, Trondheim, Norway.;St Olavs Univ Hosp, Dept Neurosurg, Trondheim, Norway..
    Lindskog, Cecilia
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Bontell, Thomas Olsson
    Sahlgrens Univ Hosp, Dept Clin Pathol & Cytol, Gothenburg, Sweden.;Univ Gothenburg, Sahlgrenska Acad, Dept Physiol, Inst Neurosci & Physiol, Gothenburg, Sweden..
    Caren, Helena
    Univ Gothenburg, Sahlgrenska Acad, Sahlgrenska Ctr Canc Res, Inst Biomed,Dept Lab Med, Gothenburg, Sweden..
    Jakola, Asgeir S.
    Sahlgrens Univ Hosp, Dept Neurosurg, Gothenburg, Sweden.;Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden.;Norwegian Univ Sci & Technol, Dept Neuromed & Movement Sci, Trondheim, Norway..
    Smits, Anja
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden..
    Stemness and clinical features in relation to the subventricular zone in diffuse lower-grade glioma: an exploratory study2022In: Neuro-Oncology Advances, E-ISSN 2632-2498, Vol. 4, no 1, article id vdac074Article in journal (Refereed)
    Abstract [en]

    Background The subventricular zone (SVZ) of the human brain is a site of adult stem cell proliferation and a microenvironment for neural stem cells (NSCs). It has been suggested that NSCs in the SVZ are potential cells of origin containing driver mutations of glioblastoma, but their role in the origin of diffuse lower-grade gliomas (dLGGs) is not much studied. Methods We included 188 patients >= 18 years with IDH-mutated dLGG (WHO grades 2-3) histologically diagnosed between 2007 and 2020. Tissue microarrays of tumor samples for patients between 2007 and 2016 were used for immunodetection of Nestin, SOX2, SOX9, KLF4, NANOG, CD133 cMYC, and Ki67. DNA methylation profile was used for stemness index (mDNAsi). Tumor contact with the SVZ was assessed and the distance was computed. Results Overall, 70.2% of the dLGG had SVZ contact. Tumors with SVZ contact were larger (102.4 vs 30.9 mL, P < .01), the patients were older (44.3 vs 40.4 years, P = .04) and more often had symptoms related to increased intracranial pressure (31.8% vs 7.1%, P < .01). The expression of SOX2, SOX9, Nestin, and Ki67 showed intersample variability, but no difference was found between tumors with or without SVZ contact, nor with the actual distance to the SVZ. mDNAsi was similar between groups (P = .42). Conclusions We found no statistical relationship between proximity with the SVZ and mDNAsi or expression of SOX2, SOX9, Nestin, and Ki67 in IDH-mutated dLGG. Our data suggest that the potential impact of SVZ on IDH-mutated dLGG is probably not associated with a more stemness-like tumor profile.

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  • 2.
    Fahlström, Andreas
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery. Royal Melbourne Hosp, Dept Neurosurg, Parkville, Vic, Australia..
    Dwivedi, Shourye
    Royal Melbourne Hosp, Dept Neurosurg, Parkville, Vic, Australia..
    Drummond, Katharine
    Royal Melbourne Hosp, Dept Neurosurg, Parkville, Vic, Australia.;Univ Melbourne, Dept Surg, Parkville, Vic, Australia.;Royal Melbourne Hosp, Dept Neurosurg, 4 East,Grattan St, Parkville, Vic 3050, Australia..
    Multiple meningiomas: Epidemiology, management, and outcomes2023In: Neuro-Oncology Advances, E-ISSN 2632-2498, Vol. 5, no SUPP1, p. I35-I48Article in journal (Refereed)
    Abstract [en]

    Meningiomas are the most common nonmalignant brain tumor in adults, with an increasing incidence of asymptomatic meningiomas diagnosed on more ubiquitous neuroimaging. A subset of meningioma patients bear 2 or more spatially separated synchronous or metachronous tumors termed "multiple meningiomas" (MM), reported to occur in only 1%-10% of patients, though recent data indicate higher incidence. MM constitute a distinct clinical entity, with unique etiologies including sporadic, familial and radiation-induced, and pose special management challenges. While the pathophysiology of MM is not established, theories include independent origin in disparate locations through unique genetic events, and the "monoclonal hypothesis" of a transformed neoplastic clone with subarachnoid seeding precipitating numerous distinct meningiomas. Patients with solitary meningiomas carry the risk of long-term neurological morbidity and mortality, as well as impaired health-related quality of life, despite being a generally benign and surgically curable tumor. For patients with MM, the situation is even less favorable. MM should be regarded as a chronic disease, and in many cases, the management goal is disease control, as cure is seldom possible. Multiple interventions and lifelong surveillance are sometimes necessary. We aim to review the MM literature and create a comprehensive overview, including an evidence-based management paradigm.

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  • 3.
    Guo, Min
    et al.
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden..
    van Vliet, Marjolein
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden..
    Zhao, Jian
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden..
    Díaz de Ståhl, Teresita
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden..
    Lindström, Mikael S.
    Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden..
    Cheng, Huaitao
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden..
    Heller, Susanne
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Disciplinary Domain of Medicine and Pharmacy, research centers etc., Uppsala Clinical Research Center (UCR).
    Nistér, Monica
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden..
    Hägerstrand, Daniel
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden..
    Identification of functionally distinct and interacting cancer cell subpopulations from glioblastoma with intratumoral genetic heterogeneity2020In: Neuro-Oncology Advances, E-ISSN 2632-2498, Vol. 2, no 1, article id vdaa061Article in journal (Refereed)
    Abstract [en]

    Background

    Glioblastomas display a high level of intratumoral heterogeneity with regard to both genetic and histological features. Within single tumors, subclones have been shown to communicate with each other to affect overall tumor growth. The aim of this study was to broaden the understanding of interclonal communication in glioblastoma.

    Methods

    We have used the U-343 model, consisting of U-343 MG, U-343 MGa, U-343 MGa 31L, and U-343 MGa Cl2:6, a set of distinct glioblastoma cell lines that have been derived from the same tumor. We characterized these with regard to temozolomide sensitivity, protein secretome, gene expression, DNA copy number, and cancer cell phenotypic traits. Furthermore, we performed coculture and conditioned media-based experiments to model cell-to-cell signaling in a setting of intratumoral heterogeneity.

    Results

    Temozolomide treatment of a coculture composed of all 4 U-343 cell lines presents a tumor relapse model where the least sensitive population, U-343 MGa 31L, outlives the others. Interestingly, the U-343 cell lines were shown to have distinct gene expression signatures and phenotypes although they were derived from a single tumor. The DNA copy number analysis revealed both common and unique alterations, indicating the evolutionary relationship between the cells. Moreover, these cells were found to communicate and affect each other’s proliferation, both via contact-dependent and -independent interactions, where NOTCH1, TGFBI, and ADAMTS1 signaling effects were involved, respectively.

    Conclusions

    These results provide insight into how complex the signaling events may prove to be in a setting of intratumoral heterogeneity in glioblastoma and provide a map for future studies.

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  • 4.
    Krynina, Olha
    et al.
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden..
    Díaz de Ståhl, Teresita
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden..
    Jylhä, Cecilia
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.;Karolinska Univ Hosp, Clin Genet & Genom, Stockholm, Sweden..
    Arthur, Cecilia
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.;Karolinska Univ Hosp, Clin Genet & Genom, Stockholm, Sweden..
    Giraud, Geraldine
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Neurooncology and neurodegeneration. Akademiska University Hospital, Uppsala, Sweden.
    Nyman, Per
    Linköping Univ Hosp, Crown Princess Victor Childrens Hosp, Dept Hlth, Linköping, Sweden.;Linköping Univ, Dept Med & Caring Sci, Linköping, Sweden.;Linköping Univ, Ctr Med Image Sci & Visualizat CMIV, Linköping, Sweden..
    Fritzberg, Anders
    Clin Pediat Falun Hosp, Daycare Unit Oncol & Hematol, Dalarna, Dalarna Region, Sweden..
    Sandgren, Johanna
    Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden.;Karolinska Univ Hosp, Clin Pathol & Canc Diagnost, Stockholm, Sweden..
    Tham, Emma
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.;Karolinska Univ Hosp, Clin Genet & Genom, Stockholm, Sweden..
    Sandvik, Ulrika
    Karolinska Inst, Dept Clin Neurosci, Div Neurosurg, Stockholm, Sweden..
    The potential of liquid biopsy for detection of the KIAA1549-BRAF fusion in circulating tumor DNA from children with pilocytic astrocytoma2024In: Neuro-Oncology Advances, E-ISSN 2632-2498, Vol. 6, no 1, article id vdae008Article in journal (Refereed)
    Abstract [en]

    Background

    Low-grade gliomas (LGGs) represent children’s most prevalent central nervous system tumor, necessitating molecular profiling to diagnose and determine the most suitable treatment. Developing highly sensitive screening techniques for liquid biopsy samples is particularly beneficial, as it enables the early detection and molecular characterization of tumors with minimally invasive samples.

    Methods

    We examined CSF and plasma samples from patients with pilocytic astrocytoma (PA) using custom multiplexed droplet digital polymerase chain reaction (ddPCR) assays based on whole genome sequencing data. These assays included a screening test to analyze BRAF duplication and a targeted assay for the detection of patient-specific KIAA1549::BRAF fusion junction sequences or single nucleotide variants.

    Results

    Our findings revealed that 5 out of 13 individual cerebrospinal fluid (CSF) samples tested positive for circulating tumor DNA (ctDNA). Among these cases, 3 exhibited the KIAA1549::BRAF fusion, which was detected through copy number variation (CNV) analysis (n = 1) or a fusion-specific probe (n = 2), while 1 case each displayed the BRAF V600E mutation and the FGFR1 N577K mutation. Additionally, a quantitative analysis of cell-free DNA (cfDNA) concentrations in PA CSF samples showed that most cases had low cfDNA levels, below the limit of detection of our assay (<1.9 ng).

    Conclusions

    While CNV analysis of CSF samples from LGGs still has some limitations, it has the potential to serve as a valuable complementary tool. Furthermore, it can also be multiplexed with other aberrations, for example, to the BRAF V600 test, to provide important insights into the molecular characteristics of LGGs.

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  • 5. Werlenius, Katja
    et al.
    Stragliotto, Giuseppe
    Strandeus, Michael
    Blomstrand, Malin
    Carén, Helena
    Jakola, Asgeir S
    Rydenhag, Bertil
    Dyregaard, Dorte
    Dzhandzhugazyan, Karine N
    Kirkin, Alexei F
    Raida, Martin K
    Smits, Anja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurovetenskap. Institute of Neuroscience and Physiology, Department of Clinical Neuroscience, Sahlgrenska Academy, University of Gothenburg , Gothenburg , Sweden.
    Kinhult, Sara
    A randomized phase II trial of efficacy and safety of the immunotherapy ALECSAT as an adjunct to radiotherapy and temozolomide for newly diagnosed glioblastoma2021In: Neuro-Oncology Advances, E-ISSN 2632-2498, Vol. 3, no 1, article id vdab156Article in journal (Refereed)
    Abstract [en]

    Background: There is an urgent need for effective treatments against glioblastoma (GBM). In this trial, we investigated the efficacy and safety of an adoptive cell-based immunotherapy.

    Methods: Patients with newly diagnosed GBM were recruited at 4 study sites in Sweden. The patients were randomized 1:2 to receive either radiotherapy (RT), 60 Gy/30 fractions, with concomitant and adjuvant temozolomide (TMZ) only, or RT and TMZ with the addition of Autologous Lymphoid Effector Cells Specific Against Tumor (ALECSAT) in an open-label phase II trial. The primary endpoint was investigator-assessed progression-free survival (PFS). The secondary endpoints were survival and safety of ALECSAT.

    Results: Sixty-two patients were randomized to either standard of care (SOC) with RT and TMZ alone (n = 22) or SOC with ALECSAT (n = 40). Median age was 57 years (range 38-69), 95% of the patients were in good performance status (WHO 0-1). There was no significant difference between the study arms (SOC vs ALECSAT + SOC) in PFS (7.9 vs 7.8 months; hazard ratio [HR] 1.28; 95% confidence interval [CI] 0.70-2.36; P = .42) or in median overall survival (OS) (18.3 vs 19.2 months; HR 1.16, 95% CI 0.58-2.31; P = .67). The treatment groups were balanced in terms of serious adverse events (52.4% vs 52.5%), but adverse events ≥grade 3 were more common in the experimental arm (81.0% vs 92.5%).

    Conclusion: Addition of ALECSAT immunotherapy to standard treatment with radiochemotherapy was well tolerated but did not improve PFS or OS for patients with newly diagnosed GBM.

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