Exploitation of adaptive evolution in glioma treatment

Cordner, Ryan; Black, Keith L.; Wheeler, Christopher J.

doi:10.2217/cns.12.46

Cited by 7 publications

(8 citation statements)

References 50 publications

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“…Brain glioma is the most common malignant tumor of the primary tumors in the central nervous system and the main cause of death of the patients with intracranial tumor (1,2). So far, the clinical approaches to treat brain glioma include surgery, radiotherapy, and chemotherapy (3)(4)(5)(6), but the overall curative effect is far from satisfactory.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of the Kank1 gene-induced brain glioma apoptosis and blockade of the cell cycle in G0/G1 phase

Guo

Fan

Bian

et al. 2014

International Journal of Oncology

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The Kank1 gene is one of the important members of the Kank gene family. As an important adaptor protein, Kank1 plays a significant role in the genesis and development of many malignant tumors. It was recently discovered that the Kank1 gene is a new cancer suppressor, and its expression is significantly downregulated or it is not expressed in kidney cancer, bladder cancer, prostate cancer, lung cancer and breast cancer. However, no report on the role of Kank1 in the genesis of brain glioma is available to date. In this study, we found significantly lower expression of the Kank1 gene in human brain glioma cells compared to the other cells evaluated. We used RNA interference techniques to silence Kank1 gene expression and found acceleration of tumor cell proliferation. However, when the Kank1 gene was upregulated, cell apoptosis occurred and the cell cycle was blocked in the G0/G1 phase. Also, we found that upregulating the Kank1 gene may result in the change of mitochondrial membrane potential, and the regulation of Bax and Bcl-2 may promote the mitochondria to release cytochrome C so as to activate Caspase-9 and -3. Thus, the human brain glioma apoptosis induced by upregulation of the Kank1 gene is closely relevant to the mitochondrial pathway.

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Section: Introductionmentioning

confidence: 99%

Upregulation of the Kank1 gene-induced brain glioma apoptosis and blockade of the cell cycle in G0/G1 phase

Guo

Fan

Bian

et al. 2014

International Journal of Oncology

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“…While various additional mechanisms of glioma resistance to chemo- and radiotherapy have been observed and studied for years ( 28 – 30 ), the impact of surgical lesioning on the microenvironment at the resection border and its effect on local tumor recurrence has received little attention in the past. Preclinical research has implicated both normal and tumor cells in a repair mechanism that triggers tumor progression.…”

Section: Discussionmentioning

confidence: 99%

Progression Patterns in Non-Contrast-Enhancing Gliomas Support Brain Tumor Responsiveness to Surgical Lesions

Brenner¹,

Hartzendorf²,

Vogt³

et al. 2022

Pathol. Oncol. Res.

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Purpose: The overall benefit of surgical treatments for patients with glioma is undisputed. We have shown preclinically that brain tumor cells form a network that is capable of detecting damage to the tumor, and repair itself. The aim of this study was to determine whether a similar mechanism might contribute to local recurrence in the clinical setting.Methods: We evaluated tumor progression patterns of 24 initially non-contrast-enhancing gliomas that were partially resected or biopsied. We measured the distance between the new contrast enhancement developing over time, and prior surgical lesioning, and evaluated tumor network changes in response to sequential resections by quantifying tumor cells and tumor networks with specific stainings against IDH1-R132H.Results: We found that new contrast enhancement appeared within the residual, non-enhancing tumor mass in 21/24 patients (87.5%). The location of new contrast enhancement within the residual tumor region was non-random; it occurred adjacent to the wall of the resection cavity in 12/21 patients (57.1%). Interestingly, the density of the glioma cell network increased in all patient tumors between initial resection or biopsy and recurrence. In line with the histological and radiological malignization, Ki67 expression increased from initial to final resections in 14/17 cases.Conclusion: The non-random distribution of glioma malignization in patients and unidirectional increase of anatomical tumor networks after surgical procedures provides evidence that surgical lesions, in the presence of residual tumor cells, can stimulate local tumor progression and tumor cell network formation. This argues for the development of intraoperative treatments increasing the benefits from surgical resection by specifically disrupting the mechanisms of local recurrence, particularly tumor cell network functionality.

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“…While GSCs comprise as few as 1% of cells in any given GBM tumor, they are responsible for a majority of tumor recurrences due to their ability to regenerate tumor heterogeneity which allows for the development of resistance to both standard chemotherapeutic agents as well as targeted therapies [ 37 ] . For this reason, many of the molecular mechanisms uncovered in the recent studies discussed here have been determined in the context of GSC populations.…”

Section: The Role Of Glioma Stem Cells In Resistancementioning

confidence: 99%

Mechanisms of temozolomide resistance in glioblastoma - a comprehensive review

Singh¹,

Miner²,

Hennis³

et al. 2020

CDR

180

194

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Glioblastoma (GBM) is the most common primary malignant brain tumor in adults and has an exceedingly low median overall survival of only 15 months. Current standard-of-care for GBM consists of gross total surgical resection followed by radiation with concurrent and adjuvant chemotherapy. Temozolomide (TMZ) is the firstchoice chemotherapeutic agent in GBM; however, the development of resistance to TMZ often becomes the limiting factor in effective treatment. While O6-methylguanine-DNA methyltransferase repair activity and uniquely resistant populations of glioma stem cells are the most well-known contributors to TMZ resistance, many other molecular mechanisms have come to light in recent years. Key emerging mechanisms include the involvement of other DNA repair systems, aberrant signaling pathways, autophagy, epigenetic modifications, microRNAs, and extracellular vesicle production. This review aims to provide a comprehensive overview of the clinically relevant molecular mechanisms and their extensive interconnections to better inform efforts to combat TMZ resistance.

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Exploitation of adaptive evolution in glioma treatment

Cited by 7 publications

References 50 publications

Upregulation of the Kank1 gene-induced brain glioma apoptosis and blockade of the cell cycle in G0/G1 phase

Upregulation of the Kank1 gene-induced brain glioma apoptosis and blockade of the cell cycle in G0/G1 phase

Progression Patterns in Non-Contrast-Enhancing Gliomas Support Brain Tumor Responsiveness to Surgical Lesions

Mechanisms of temozolomide resistance in glioblastoma - a comprehensive review

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