Cancer stem cells in brain tumors: From origin to clinical implications

Lin, Shuyun; Li, Kaishu; Qi, Ling

doi:10.1002/mco2.341

Cited by 7 publications

(3 citation statements)

References 267 publications

(547 reference statements)

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“…Malignant brain tumors are a heterogeneous group of histologically diverse tumors with poor prognosis and high morbidity and mortality rates [171,172]. Patient-derived iPSCs and brain organoids have been employed in cancer research as well as in the field of brain tumors, including glioblastoma, medulloblastoma and meningioma.…”

Section: Organoids Models For Brain Tumorsmentioning

confidence: 99%

Advanced Cellular Models for Rare Disease Study: Exploring Neural, Muscle and Skeletal Organoids

Bombieri,

Corsi,

Trabetti

et al. 2024

IJMS

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Organoids are self-organized, three-dimensional structures derived from stem cells that can mimic the structure and physiology of human organs. Patient-specific induced pluripotent stem cells (iPSCs) and 3D organoid model systems allow cells to be analyzed in a controlled environment to simulate the characteristics of a given disease by modeling the underlying pathophysiology. The recent development of 3D cell models has offered the scientific community an exceptionally valuable tool in the study of rare diseases, overcoming the limited availability of biological samples and the limitations of animal models. This review provides an overview of iPSC models and genetic engineering techniques used to develop organoids. In particular, some of the models applied to the study of rare neuronal, muscular and skeletal diseases are described. Furthermore, the limitations and potential of developing new therapeutic approaches are discussed.

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Section: Organoids Models For Brain Tumorsmentioning

confidence: 99%

Advanced Cellular Models for Rare Disease Study: Exploring Neural, Muscle and Skeletal Organoids

Bombieri,

Corsi,

Trabetti

et al. 2024

IJMS

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“…Similarly, CSCs in solid tumors or DTCs with stem-like characteristics utilize oxidative phosphorylation [133], together with fermentative glycolysis [134]. The expression of glycerol-3-phosphate dehydrogenase 1 (GPD1) and the B-cell lymphoma 2 gene (BCL-2) is frequently observed in leukemia [135] and brain tumor cells [136][137][138] that are in a dormant state. These genes are involved in an effective oxidative phosphorylation program.…”

Section: Hypoxia and Metabolic Dynamicsmentioning

confidence: 99%

Tumor Dormancy and Reactivation: The Role of Heat Shock Proteins

Amissah,

Combs,

Shevtsov

2024

Cells

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Tumors are a heterogeneous group of cell masses originating in various organs or tissues. The cellular composition of the tumor cell mass interacts in an intricate manner, influenced by humoral, genetic, molecular, and tumor microenvironment cues that dictate tumor growth or suppression. As a result, tumors undergo a period of a dormant state before their clinically discernible stage, which surpasses the clinical dormancy threshold. Moreover, as a genetically imprinted strategy, early-seeder cells, a distinct population of tumor cells, break off to dock nearby or extravasate into blood vessels to secondary tissues, where they form disseminated solitary dormant tumor cells with reversible capacity. Among the various mechanisms underlying the dormant tumor mass and dormant tumor cell formation, heat shock proteins (HSPs) might play one of the most important roles in how the dormancy program plays out. It is known that numerous aberrant cellular processes, such as malignant transformation, cancer cell stemness, tumor invasion, metastasis, angiogenesis, and signaling pathway maintenance, are influenced by the HSPs. An accumulating body of knowledge suggests that HSPs may be involved in the angiogenic switch, immune editing, and extracellular matrix (ECM) remodeling cascades, crucial genetically imprinted strategies important to the tumor dormancy initiation and dormancy maintenance program. In this review, we highlight the biological events that orchestrate the dormancy state and the body of work that has been conducted on the dynamics of HSPs in a tumor mass, as well as tumor cell dormancy and reactivation. Additionally, we propose a conceptual framework that could possibly underlie dormant tumor reactivation in metastatic relapse.

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“…Gliomas have two cell types: glioma stem cells (GSCs) and differentiated tumor cells [4]. Notably, some commonalities can be observed in GSCs within GBM, such as self-renewal, nondifferentiation, tumor invasion, and drug resistance, as well as differences in marker expression and differentiation potential [5].…”

Section: Introductionmentioning

confidence: 99%