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Uhrbom, Lene
Publications (10 of 57) Show all publications
Damhofer, H., Tatar, T., Southgate, B., Scarneo, S., Agger, K., Shlyueva, D., . . . Helin, K. (2024). TAK1 inhibition leads to RIPK1-dependent apoptosis in immune-activated cancers. Cell Death and Disease, 15, Article ID 273.
Open this publication in new window or tab >>TAK1 inhibition leads to RIPK1-dependent apoptosis in immune-activated cancers
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2024 (English)In: Cell Death and Disease, E-ISSN 2041-4889, Vol. 15, article id 273Article in journal (Refereed) Published
Abstract [en]

Poor survival and lack of treatment response in glioblastoma (GBM) is attributed to the persistence of glioma stem cells (GSCs). To identify novel therapeutic approaches, we performed CRISPR/Cas9 knockout screens and discovered TGFβ activated kinase (TAK1) as a selective survival factor in a significant fraction of GSCs. Loss of TAK1 kinase activity results in RIPK1-dependent apoptosis via Caspase-8/FADD complex activation, dependent on autocrine TNFα ligand production and constitutive TNFR signaling. We identify a transcriptional signature associated with immune activation and the mesenchymal GBM subtype to be a characteristic of cancer cells sensitive to TAK1 perturbation and employ this signature to accurately predict sensitivity to the TAK1 kinase inhibitor HS-276. In addition, exposure to pro-inflammatory cytokines IFN gamma and TNFα can sensitize resistant GSCs to TAK1 inhibition. Our findings reveal dependency on TAK1 kinase activity as a novel vulnerability in immune-activated cancers, including mesenchymal GBMs that can be exploited therapeutically.

Place, publisher, year, edition, pages
Springer Nature, 2024
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-527501 (URN)10.1038/s41419-024-06654-1 (DOI)001205160000003 ()38632238 (PubMedID)
Funder
EU, Horizon 2020, 749362
Available from: 2024-05-03 Created: 2024-05-03 Last updated: 2024-07-04Bibliographically approved
Babacic, H., Galardi, S., Umer, H. M., Hellström, M., Uhrbom, L., Maturi, N., . . . Pernemalm, M. (2023). Glioblastoma stem cells express non-canonical proteins and exclusive mesenchymal-like or non-mesenchymal-like protein signatures. Molecular Oncology, 17(2), 238-260
Open this publication in new window or tab >>Glioblastoma stem cells express non-canonical proteins and exclusive mesenchymal-like or non-mesenchymal-like protein signatures
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2023 (English)In: Molecular Oncology, ISSN 1574-7891, E-ISSN 1878-0261, Vol. 17, no 2, p. 238-260Article in journal (Refereed) Published
Abstract [en]

Glioblastoma (GBM) cancer stem cells (GSCs) contribute to GBM's origin, recurrence, and resistance to treatment. However, the understanding of how mRNA expression patterns of GBM subtypes are reflected at global proteome level in GSCs is limited. To characterize protein expression in GSCs, we performed in-depth proteogenomic analysis of patient-derived GSCs by RNA-sequencing and mass-spectrometry. We quantified > 10 000 proteins in two independent GSC panels and propose a GSC-associated proteomic signature characterizing two distinct phenotypic conditions; one defined by proteins upregulated in proneural and classical GSCs (GPC-like), and another by proteins upregulated in mesenchymal GSCs (GM-like). The GM-like protein set in GBM tissue was associated with necrosis, recurrence, and worse overall survival. Through proteogenomics, we discovered 252 non-canonical peptides in the GSCs, i.e., protein sequences that are variant or derive from genome regions previously considered non-protein-coding, including variants of the heterogeneous ribonucleoproteins implicated in RNA splicing. In summary, GSCs express two protein sets that have an inverse association with clinical outcomes in GBM. The discovery of non-canonical protein sequences questions existing gene models and pinpoints new protein targets for research in GBM.

Place, publisher, year, edition, pages
John Wiley & Sons, 2023
Keywords
glioblastoma stem cells, mesenchymal, proneural, proteogenomics, proteomics, signature
National Category
Cancer and Oncology Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-502261 (URN)10.1002/1878-0261.13355 (DOI)000913628600001 ()36495079 (PubMedID)
Funder
EU, Horizon 2020, 76428Science for Life Laboratory, SciLifeLab
Available from: 2023-05-24 Created: 2023-05-24 Last updated: 2023-05-24Bibliographically approved
Ilkhanizadeh, S., Gracias, A., Aslund, A. K. O., Back, M., Simon, R., Kavanagh, E., . . . Nilsson, K. P. (2023). Live Detection of Neural Progenitors and Glioblastoma Cells by an Oligothiophene Derivative. ACS Applied Bio Materials, 6(9), 3790-3797
Open this publication in new window or tab >>Live Detection of Neural Progenitors and Glioblastoma Cells by an Oligothiophene Derivative
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2023 (English)In: ACS Applied Bio Materials, E-ISSN 2576-6422, Vol. 6, no 9, p. 3790-3797Article in journal (Refereed) Published
Abstract [en]

There is an urgent need for simple and non-invasive identification of live neural stem/progenitor cells (NSPCs) in the developing and adult brain as well as in disease, such as in brain tumors, due to the potential clinical importance in prognosis, diagnosis, and treatment of diseases of the nervous system. Here, we report a luminescent conjugated oligothiophene (LCO), named p-HTMI, for non-invasive and non-amplified real-time detection of live human patient-derived glioblastoma (GBM) stem cell-like cells and NSPCs. While p-HTMI stained only a small fraction of other cell types investigated, the mere addition of p-HTMI to the cell culture resulted in efficient detection of NSPCs or GBM cells from rodents and humans within minutes. p-HTMI is functionalized with a methylated imidazole moiety resembling the side chain of histidine/histamine, and non-methylated analogues were not functional. Cell sorting experiments of human GBM cells demonstrated that p-HTMI labeled the same cell population as CD271, a proposed marker for stem cell-like cells and rapidly migrating cells in glioblastoma. Our results suggest that the LCO p-HTMI is a versatile tool for immediate and selective detection of neural and glioma stem and progenitor cells.

Place, publisher, year, edition, pages
American Chemical Society (ACS), 2023
Keywords
bioelectronics, progenitor, brain tumor, methylation, p75NTR
National Category
Cancer and Oncology Neurosciences Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-519795 (URN)10.1021/acsabm.3c00447 (DOI)001064987700001 ()37647213 (PubMedID)
Funder
Swedish Cancer SocietyKnut and Alice Wallenberg FoundationSwedish Foundation for Strategic ResearchEU, European Research CouncilVinnovaSwedish Research Council
Available from: 2024-01-10 Created: 2024-01-10 Last updated: 2024-01-10Bibliographically approved
Weishaupt, H., Čančer, M., Rosén, G., Holmberg, K. O., Häggqvist, S., Bunikis, I., . . . Swartling, F. J. (2023). Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB-driven gliomas. Neuro-Oncology, 25(1), 97-107
Open this publication in new window or tab >>Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB-driven gliomas
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2023 (English)In: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 25, no 1, p. 97-107Article in journal (Refereed) Published
Abstract [en]

Background Malignant gliomas, the most common malignant brain tumors in adults, represent a heterogeneous group of diseases with poor prognosis. Retroviruses can cause permanent genetic alterations that modify genes close to the viral integration site. Methods Here we describe the use of a high-throughput pipeline coupled to the commonly used tissue-specific retroviral RCAS-TVA mouse tumor model system. Utilizing next-generation sequencing, we show that retroviral integration sites can be reproducibly detected in malignant stem cell lines generated from RCAS-PDGFB-driven glioma biopsies. Results A large fraction of common integration sites contained genes that have been dysregulated or misexpressed in glioma. Others overlapped with loci identified in previous glioma-related forward genetic screens, but several novel putative cancer-causing genes were also found. Integrating retroviral tagging and clinical data, Ppfibp1 was highlighted as a frequently tagged novel glioma-causing gene. Retroviral integrations into the locus resulted in Ppfibp1 upregulation, and Ppfibp1-tagged cells generated tumors with shorter latency on orthotopic transplantation. In human gliomas, increased PPFIBP1 expression was significantly linked to poor prognosis and PDGF treatment resistance. Conclusions Altogether, the current study has demonstrated a novel approach to tagging glioma genes via forward genetics, validating previous results, and identifying PPFIBP1 as a putative oncogene in gliomagenesis.

Place, publisher, year, edition, pages
Oxford University Press, 2023
Keywords
forward genetics screen, glioblastoma, liprin-beta-1, PDGFB, RCAS
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-496938 (URN)10.1093/neuonc/noac158 (DOI)000834326400001 ()35738865 (PubMedID)
Funder
EU, Horizon 2020, 640275Swedish Cancer SocietySwedish Research CouncilRagnar Söderbergs stiftelseSwedish Childhood Cancer Foundation
Available from: 2023-02-22 Created: 2023-02-22 Last updated: 2023-02-22Bibliographically approved
Ramachandran, M., Vaccaro, A., van de Walle, T., Georganaki, M., Lugano, R., Vemuri, K., . . . Dimberg, A. (2023). Tailoring vascular phenotype through AAV therapy promotes anti-tumor immunity in glioma. Cancer Cell, 41(6), 1134-1151
Open this publication in new window or tab >>Tailoring vascular phenotype through AAV therapy promotes anti-tumor immunity in glioma
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2023 (English)In: Cancer Cell, ISSN 1535-6108, E-ISSN 1878-3686, Vol. 41, no 6, p. 1134-1151Article in journal (Refereed) Published
Abstract [en]

Glioblastomas are aggressive brain tumors that are largely immunotherapy resistant. This is associated with immunosuppression and a dysfunctional tumor vasculature, which hinder T cell infiltration. LIGHT/TNFSF14 can induce high endothelial venules (HEVs) and tertiary lymphoid structures (TLS), suggesting that its therapeutic expression could promote T cell recruitment. Here, we use a brain endothelial cell-targeted ad-eno-associated viral (AAV) vector to express LIGHT in the glioma vasculature (AAV-LIGHT). We found that systemic AAV-LIGHT treatment induces tumor-associated HEVs and T cell-rich TLS, prolonging survival in aPD-1-resistant murine glioma. AAV-LIGHT treatment reduces T cell exhaustion and promotes TCF1+CD8+ stem-like T cells, which reside in TLS and intratumoral antigen-presenting niches. Tumor regres-sion upon AAV-LIGHT therapy correlates with tumor-specific cytotoxic/memory T cell responses. Our work reveals that altering vascular phenotype through vessel-targeted expression of LIGHT promotes efficient anti-tumor T cell responses and prolongs survival in glioma. These findings have broader implications for treatment of other immunotherapy-resistant cancers.

Place, publisher, year, edition, pages
Elsevier BV, 2023
Keywords
glioblastoma, TNFSF14, LIGHT, lymphotoxin αβ, tertiary lymphoid structures, stem-like T cells, high endothelial venules, antigen-presenting niches
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-508441 (URN)10.1016/j.ccell.2023.04.010 (DOI)001025445800001 ()37172581 (PubMedID)
Funder
Swedish Cancer Society, CAN 2017/502Swedish Cancer Society, 20 1008 PjFSwedish Cancer Society, 201010 UsFSwedish Cancer Society, 190184PjSwedish Research Council, 2016-02495Swedish Research Council, 2020-02563Swedish Research Council, 2019-01326Knut and Alice Wallenberg Foundation, KAW 2019.0088Swedish Childhood Cancer Foundation, TJ 2019-0014Swedish Cancer Society, CAN 2015/1216
Available from: 2023-08-02 Created: 2023-08-02 Last updated: 2024-02-28Bibliographically approved
Xie, Y., He, L., Zhang, Y., Huang, H., Yang, F., Chao, M., . . . Zhang, L. (2023). Wnt signaling regulates MFSD2A-dependent drug delivery through endothelial transcytosis in glioma. Neuro-Oncology, 25(6), 1073-1084
Open this publication in new window or tab >>Wnt signaling regulates MFSD2A-dependent drug delivery through endothelial transcytosis in glioma
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2023 (English)In: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 25, no 6, p. 1073-1084Article in journal (Refereed) Published
Abstract [en]

Background: Systemic delivery of anti-tumor therapeutic agents to brain tumors is thwarted by the blood-brain barrier (BBB), an organotypic specialization of brain endothelial cells (ECs). A failure of pharmacological compounds to cross BBB is one culprit for the dismal prognosis of glioblastoma (GBM) patients. Identification of novel vascular targets to overcome the challenges posed by the BBB in tumors for GBM treatment is urgently needed.

Methods: Temozolomide (TMZ) delivery was investigated in CT2A and PDGFB-driven RCAS/tv-a orthotopic glioma models. Transcriptome analysis was performed on ECs from murine gliomas. Mfsd2a deficient, Cav1 deficient, and Mfsd2a EC-specific inducible mice were developed to study the underlying molecular mechanisms.

Results: We demonstrated that inhibiting Wnt signaling by LGK974 could increase TMZ delivery and sensitize glioma to chemotherapy in both murine glioma models. Transcriptome analysis of ECs from murine gliomas revealed that Wnt signaling inhibition enhanced vascular transcytosis as indicated by the upregulation of PLVAP and downregulation of MFSD2A. Mfsd2a deficiency in mice enhances TMZ delivery in tumors, whereas constitutive expression of Mfsd2a in ECs suppresses the enhanced TMZ delivery induced by Wnt pathway inhibition in murine glioma. In addition, Wnt signaling inhibition enhanced caveolin-1 (Cav1)-positive caveolae-mediated transcytosis in tumor ECs. Moreover, Wnt signaling inhibitor or Mfsd2a deficiency fails to enhance TMZ penetration in tumors from Cav1-deficient mice.

Conclusions: These results demonstrated that Wnt signaling regulates MFSD2A-dependent TMZ delivery through a caveolae-mediated EC transcytosis pathway. Our findings identify Wnt signaling as a promising therapeutic target to improve drug delivery for GBM treatment.

Place, publisher, year, edition, pages
Oxford University Press, 2023
Keywords
blood-brain barrier, drug delivery, endothelial cell, glioblastoma, Wnt signaling
National Category
Cell and Molecular Biology Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-512762 (URN)10.1093/neuonc/noac288 (DOI)000921976900001 ()36591963 (PubMedID)
Available from: 2023-09-28 Created: 2023-09-28 Last updated: 2023-09-28Bibliographically approved
Lu, X., Maturi, N. P., Jarvius, M., Yildirim, I., Dang, Y., Zhao, L., . . . Chen, X. (2022). Cell-lineage controlled epigenetic regulation in glioblastoma stem cells determines functionally distinct subgroups and predicts patient survival. Nature Communications, 13, Article ID 2236.
Open this publication in new window or tab >>Cell-lineage controlled epigenetic regulation in glioblastoma stem cells determines functionally distinct subgroups and predicts patient survival
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2022 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 13, article id 2236Article in journal (Refereed) Published
Abstract [en]

The epigenetic regulation of glioblastoma stem cell (GSC) function remains poorly understood. Here, the authors compare the chromatin accessibility landscape of GSC cultures from mice and patients and suggest that the epigenome of GSCs is cell lineage-regulated and could predict patient survival. There is ample support for developmental regulation of glioblastoma stem cells. To examine how cell lineage controls glioblastoma stem cell function, we present a cross-species epigenome analysis of mouse and human glioblastoma stem cells. We analyze and compare the chromatin-accessibility landscape of nine mouse glioblastoma stem cell cultures of three defined origins and 60 patient-derived glioblastoma stem cell cultures by assay for transposase-accessible chromatin using sequencing. This separates the mouse cultures according to cell of origin and identifies three human glioblastoma stem cell clusters that show overlapping characteristics with each of the mouse groups, and a distribution along an axis of proneural to mesenchymal phenotypes. The epigenetic-based human glioblastoma stem cell clusters display distinct functional properties and can separate patient survival. Cross-species analyses reveals conserved epigenetic regulation of mouse and human glioblastoma stem cells. We conclude that epigenetic control of glioblastoma stem cells primarily is dictated by developmental origin which impacts clinically relevant glioblastoma stem cell properties and patient survival.

Place, publisher, year, edition, pages
Springer NatureSpringer Nature, 2022
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-474702 (URN)10.1038/s41467-022-29912-2 (DOI)000787388900011 ()35469026 (PubMedID)
Funder
Swedish Research Council, 2016-06794Swedish Research Council, 2017-02074Swedish Research Council, 2018-02906Knut and Alice Wallenberg FoundationSwedish Cancer Society, 15 0877Swedish Cancer Society, 18 0763Swedish Cancer Society, 21 1518Swedish Cancer Society, 21 1449Swedish Cancer Society, 22 0491 JIAHedlund foundationScience for Life Laboratory, SciLifeLabKjell and Marta Beijer FoundationHarald and Greta Jeansson FoundationGöran Gustafsson Foundation for promotion of scientific research at Uppala University and Royal Institute of TechnologyÅke Wiberg Foundation
Note

De två första författarna delar förstaförfattarskapet.

De två sista författarna delar sistaförfattarskapet.

Available from: 2022-05-25 Created: 2022-05-25 Last updated: 2024-01-15Bibliographically approved
Zhao, L., Xing, P., Polavarapu, V. K., Zhao, M., Valero-Martínez, B., Dang, Y., . . . Chen, X. (2021). FACT-seq: profiling histone modifications in formalin-fixed paraffin-embedded samples with low cell numbers. Nucleic Acids Research, 49(21), Article ID e125.
Open this publication in new window or tab >>FACT-seq: profiling histone modifications in formalin-fixed paraffin-embedded samples with low cell numbers
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2021 (English)In: Nucleic Acids Research, ISSN 0305-1048, E-ISSN 1362-4962, Vol. 49, no 21, article id e125Article in journal (Refereed) Published
Abstract [en]

The majority of biopsies in both basic research and translational cancer studies are preserved in the format of archived formalin-fixed paraffin-embedded (FFPE) samples. Profiling histone modifications in archived FFPE tissues is critically important to understand gene regulation in human disease. The required input for current genome-wide histone modification profiling studies from FFPE samples is either 10-20 tissue sections or whole tissue blocks, which prevents better resolved analyses. But it is desirable to consume a minimal amount of FFPE tissue sections in the analysis as clinical tissues of interest are limited. Here, we present FFPE tissue with antibody-guided chromatin tagmentation with sequencing (FACT-seq), the first highly sensitive method to efficiently profile histone modifications in FFPE tissues by combining a novel fusion protein of hyperactive Tn5 transposase and protein A (T7-pA-Tn5) transposition and T7 in vitro transcription. FACT-seq generates high-quality chromatin profiles from different histone modifications with low number of FFPE nuclei. We proved a very small piece of FFPE tissue section containing similar to 4000 nuclei is sufficient to decode H3K27ac modifications with FACT-seq. H3K27ac FACT-seq revealed disease-specific super enhancers in the archived FFPE human colorectal and human glioblastoma cancer tissue. In summary, FACT-seq allows decoding the histone modifications in archival FFPE tissues with high sensitivity and help researchers to better understand epigenetic regulation in cancer and human disease.

Place, publisher, year, edition, pages
Oxford University PressOxford University Press (OUP), 2021
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-463617 (URN)10.1093/nar/gkab813 (DOI)000733312000005 ()34534335 (PubMedID)
Funder
Swedish Research Council, VR-2016-06794Swedish Research Council, VR-2017-02074Swedish Cancer Society, CAN 2018/772Åke Wiberg Foundation, M20-0007Kjell and Marta Beijer FoundationHarald and Greta Jeansson FoundationGöran Gustafsson Foundation for promotion of scientific research at Uppala University and Royal Institute of TechnologyLinnaeus scholarship foundation
Available from: 2022-01-10 Created: 2022-01-10 Last updated: 2024-01-15Bibliographically approved
Xie, Y., He, L., Lugano, R., Zhang, Y., Cao, H., He, Q., . . . Zhang, L. (2021). Key molecular alterations in endothelial cells in human glioblastoma uncovered through single-cell RNA sequencing. JCI Insight, 6(15), Article ID e150861.
Open this publication in new window or tab >>Key molecular alterations in endothelial cells in human glioblastoma uncovered through single-cell RNA sequencing
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2021 (English)In: JCI Insight, ISSN 2379-3708, Vol. 6, no 15, article id e150861Article in journal (Refereed) Published
Abstract [en]

Passage of systemically delivered pharmacological agents into the brain is largely blocked by the blood-brain-barrier (BBB), an organotypic specialization of brain endothelial cells (ECs). Tumor vessels in glioblastoma (GBM), the most common malignant brain tumor in humans, are abnormally permeable, but this phenotype is heterogeneous and may differ between the tumor's center and invasive front. Here, through single-cell RNA sequencing (scRNA-seq) of freshly isolated ECs from human glioblastoma and paired tumor peripheral tissues, we have constructed a molecular atlas of human brain ECs providing unprecedented molecular insight into the heterogeneity of the human BBB and its molecular alteration in glioblastoma. We identified 5 distinct EC phenotypes representing different states of EC activation and BBB impairment, and associated with different anatomical locations within and around the tumor. This unique data resource provides key information for designing rational therapeutic regimens and optimizing drug delivery.

Place, publisher, year, edition, pages
American Society For Clinical InvestigationAmerican Society for Clinical Investigation, 2021
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-452129 (URN)10.1172/jci.insight.150861 (DOI)000684579600029 ()34228647 (PubMedID)
Funder
Swedish Cancer Society, 20 1008 PjFSwedish Cancer Society, 20 1010 UsFSwedish Research Council, 2020-02563Knut and Alice Wallenberg Foundation, KAW 2019.0088
Available from: 2021-09-10 Created: 2021-09-10 Last updated: 2024-01-15Bibliographically approved
Maturi, N. P., Tan, E.-J., Xie, Y., Sundström, A., Bergström, T., Jiang, Y. & Uhrbom, L. (2020). A molecularly distinct subset of glioblastoma requires serum-containing media to establish sustainable bona fide glioblastoma stem cell cultures. Glia, 68(6), 1228-1240
Open this publication in new window or tab >>A molecularly distinct subset of glioblastoma requires serum-containing media to establish sustainable bona fide glioblastoma stem cell cultures
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2020 (English)In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 68, no 6, p. 1228-1240Article in journal (Refereed) Published
Abstract [en]

Glioblastoma (GBM) is the most frequent and deadly primary malignant brain tumor. Hallmarks are extensive intra-tumor and inter-tumor heterogeneity and highly invasive growth, which provide great challenges for treatment. Efficient therapy is lacking and the majority of patients survive less than 1 year from diagnosis. GBM progression and recurrence is caused by treatment-resistant glioblastoma stem cells (GSCs). GSC cultures are considered important models in target identification and drug screening studies. The current state-of-the-art method, to isolate and maintain GSC cultures that faithfully mimic the primary tumor, is to use serum-free (SF) media conditions developed for neural stem cells (NSCs). Here we have investigated the outcome of explanting 218 consecutively collected GBM patient samples under both SF and standard, serum-containing media conditions. The frequency of maintainable SF cultures (SFCs) was most successful, but for a subgroup of GBM specimens, a viable culture could only be established in serum-containing media, called exclusive serum culture (ESC). ESCs expressed nestin and SOX2, and displayed all functional characteristics of a GSC, that is, extended proliferation, sustained self-renewal and orthotopic tumor initiation. Once adapted to the in vitro milieu they were also sustainable in SF media. Molecular analyses showed that ESCs formed a discrete group that was most related to the mesenchymal GBM subtype. This distinct subgroup of GBM that would have evaded modeling in SF conditions only provide unique cell models of GBM inter-tumor heterogeneity.

Place, publisher, year, edition, pages
Wiley, 2020
Keywords
exclusive serum culture, glioblastoma stem cell, inter-tumor heterogeneity, microenvironment, self-renewal, tumor cell plasticity, tumor initiation
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy) Neurosciences Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-423507 (URN)10.1002/glia.23773 (DOI)000503902300001 ()31868967 (PubMedID)
Funder
Swedish Cancer Society, 2012/488Swedish Cancer Society, 2015/656Swedish Cancer Society, 2018/777Swedish Research Council, 2012-02591Swedish Research Council, 2018-02906
Available from: 2020-10-27 Created: 2020-10-27 Last updated: 2022-10-08Bibliographically approved
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