Correction: Glioblastoma Formation from Cell Population Depleted of Prominin1-Expressing Cells

Nishide, Kenji; Nakatani, Yuka; Kanazawa, Hiroshi; Kondo, Toru

doi:10.1371/annotation/d1e654f7-c02d-458c-8dc7-da7ae96aa594

Cited by 6 publications

(3 citation statements)

References 30 publications

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“…We performed a thorough literature review concerning all the possible positive prognostic factors not included in our study, finding as possibly critical the role played by cancer stem cells (CSCs, CD33+). These cells constitute a small fraction of the tumor population and present "migration" tendencies (which helps to explain the infiltrative nature of GBM); CSCs are able to give rise to CD33differentiated clones, demonstrating a higher potential growth rate thus contributing to the genesis of the "tumor-bulk" [31][32][33].…”

Section: Discussionmentioning

confidence: 99%

Long Term Survival in Patients Suffering from Glio-blastoma Multiforme: A Single-Center Observational Cohort Study

et al. 2019

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Background: Glioblastomas (GBM) are generally burdened, to date, by a dismal prognosis, although long term survivors have a relatively significant incidence. Our specific aim was to determine the exact impact of many surgery-, patient-and tumor-related variables on survival parameters. Methods: The surgical, radiological and clinical outcomes of patients have been retrospectively reviewed for the present study. All the patients have been operated on in our institution and classified according their overall survival in long term survivors (LTS) and short term survivors (STS). A thorough review of our surgical series was conducted to compare the oncologic results of the patients in regard to: (1) surgical-(2) molecular and (3) treatment-related features. Results: A total of 177 patients were included in the final cohort. Extensive statistical analysis by means of univariate, multivariate and survival analyses disclosed a survival advantage for patients presenting a younger age, a smaller lesion and a better functional status at presentation. From the histochemical point of view, Ki67 (%) was the strongest predictor of better oncologic outcomes. A stepwise analysis of variance outlines the existence of eight prognostic subgroups according to the molecular patterns of Ki67 overexpression and epidermal growth factor receptor (EGFR), p53 and isocitrate dehydrogenase (IDH) mutations. Conclusions: On the grounds of our statistical analyses we can affirm that the following factors were significant predictors of survival advantage: Karnofsky performance status (KPS), age, volume of the lesion, motor disorder at presentation and/or a Ki67 overexpression. In our experience, LTS is associated with a gross total resection (GTR) of tumor correlated with EGFR and p53 mutations with regardless of localization, and poorly correlated to dimension. We suppose that performing a standard molecular analysis (IDH, EGFR, p53 and Ki67) is not sufficient to predict the behavior of a GBM in regards to overall survival (OS), nor to provide a deeper understanding of the meaning of the different genetic alterations in the DNA of cancer cells. A fine molecular profiling is feasible to precisely stratify the prognosis of GBM patients.

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Section: Discussionmentioning

confidence: 99%

Long Term Survival in Patients Suffering from Glio-blastoma Multiforme: A Single-Center Observational Cohort Study

et al. 2019

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“…CTRL-NSCL61 and gp53-NSCL61s were suspended in culture medium and injected into the brains of 5-8-week-old female mice, as previously described [14,19]. Mice were maintained until manifestation of neurological signs or for 30 days post-transplantation.…”

Section: Intracranial Cell Transplantation Into Nod-scid Mice Brains ...mentioning

confidence: 99%

Induction of tumor-initiating cells and glioma-initiating cells from fetal neural stem cells through p53 genome editing

Ohtsu

2022

Preprint

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The elucidation of the properties of malignant glioma and development of therapeutic methods require model cells with characteristics such as invasiveness, multinuclearity, and ability for mitosis. A previous study has shown that overexpression of active HRas (HRasL61) in neural stem/progenitor cells isolated from fetal telencephalic neuroepithelial cells with homozygous deletion of the p53 locus forms glioma-initiating cells (GICs). The orthotopically transplantation of 10 cells into the forebrain of immunodeficient mice, resulted in the development of glioblastoma multiforme-like malignant brain tumors. In this study, GICs were induced from wild-type fetal neural stem/progenitor cells. Through forced expression of CRISPR-associated protein 9 together with a guide RNA that recognizes the p53 gene, neural stem/progenitor cells containing p53 knockout cells were obtained. Furthermore, HRasL61 was forced-expressed and transplanted into the immunodeficient mice. These cells were tumor-initiating cells (TICs) with tumorigenicity in the brain. However, no invasiveness to the brain was observed. The p53 homozygous-deleted cells obtained through single-cell cloning from TICs were GICs, forming glioblastoma multiforme-like tumors. The induced GICs strongly expressed the GIC marker. These results indicate that GICs can be induced through genetic recombination using genome editing. This study suggests that the use of genome editing may lead to the elucidation of the oncogenic mechanisms of human cells that cannot delete genes.

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“…According to the following findings, there has been confirmation and refutation of CD133’s significance as a GSC marker. Numerous samples, and even the same tumor types with CD133+ GSCs, showed tumorigenic CD133- cells [ 27 , 28 , 29 , 30 ]. A lack of technical consensus can only partially explain these controversial observations.…”

Section: Introductionmentioning

confidence: 99%

Progress in Glioma Stem Cell Research

Ramar,

Guo,

Hudson

et al. 2023

Cancers

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Glioblastoma multiforme (GBM) represents a diverse spectrum of primary tumors notorious for their resistance to established therapeutic modalities. Despite aggressive interventions like surgery, radiation, and chemotherapy, these tumors, due to factors such as the blood–brain barrier, tumor heterogeneity, glioma stem cells (GSCs), drug efflux pumps, and DNA damage repair mechanisms, persist beyond complete isolation, resulting in dismal outcomes for glioma patients. Presently, the standard initial approach comprises surgical excision followed by concurrent chemotherapy, where temozolomide (TMZ) serves as the foremost option in managing GBM patients. Subsequent adjuvant chemotherapy follows this regimen. Emerging therapeutic approaches encompass immunotherapy, including checkpoint inhibitors, and targeted treatments, such as bevacizumab, aiming to exploit vulnerabilities within GBM cells. Nevertheless, there exists a pressing imperative to devise innovative strategies for both diagnosing and treating GBM. This review emphasizes the current knowledge of GSC biology, molecular mechanisms, and associations with various signals and/or pathways, such as the epidermal growth factor receptor, PI3K/AKT/mTOR, HGFR/c-MET, NF-κB, Wnt, Notch, and STAT3 pathways. Metabolic reprogramming in GSCs has also been reported with the prominent activation of the glycolytic pathway, comprising aldehyde dehydrogenase family genes. We also discuss potential therapeutic approaches to GSC targets and currently used inhibitors, as well as their mode of action on GSC targets.

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Correction: Glioblastoma Formation from Cell Population Depleted of Prominin1-Expressing Cells

Cited by 6 publications

References 30 publications

Long Term Survival in Patients Suffering from Glio-blastoma Multiforme: A Single-Center Observational Cohort Study

Long Term Survival in Patients Suffering from Glio-blastoma Multiforme: A Single-Center Observational Cohort Study

Induction of tumor-initiating cells and glioma-initiating cells from fetal neural stem cells through p53 genome editing

Progress in Glioma Stem Cell Research

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