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Glioblastoma a Malignant Form of Tumor: a Review on Its Cellular Target, Route, and Its Treatment

  • Neurogenic Niche (A Salmina, Section Editor)
  • Published:
Current Tissue Microenvironment Reports Aims and scope Submit manuscript

Abstract

Purpose of Review

The pathophysiology of glioblastoma is so complex; it affects a number of different cellular processes. The FDA has approved a number of treatments, including temozolomide and bevacizumab, yet the survival rate remains the same at 1 year or less. As a result of the failure of different chemotherapies and target pharmacological therapies, we must concentrate on the use of less toxic agents, such as natural compounds, which may have a greater prognostic value.

Recent Findings

This quick overview covers the following topics: Glioblastoma has a variety of various routes associated with it, including molecular and patrimonial indications. Treatments for glioblastoma are available. Certain natural compounds may have the ability to minimize toxicity while also improving prognostic value.

Summary

Glioblastoma multiforme is a grade 4 glioma brain tumor that develops from glial cells in the brain. The grade of a brain tumor indicates how probable it is to grow and spread. Grade 4 tumors are the most dangerous and aggressive. Despite the FDA’s approval of temozolomide with bevacizumab and several other drugs, the 1-year survival rate remains constant. We must focus on the use of less toxic agents, such as natural compounds, that may have a greater prognostic value and less toxicity, due to the failure of various chemotherapies, surgeries, radiation, and target pharmaceutical therapies.

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Abbreviations

ATRX:

Alpha-thalassemia\mental retardation syndrome X-linked

CDK4:

Cyclin-dependent kinase 4

CSF:

Cerebrospinal fluid

EGFR:

Epidermal growth factor receptor

FGFR:

Fibroblast growth factor receptor

FAK:

Focal adhesion kinase

GBM:

Glioblastoma

HIF-1:

Hypoxia-inducible factor-1

HGF:

Hepatocyte growth factor

IGF-1R:

Insulin-like growth factor 1 receptor

IHC:

Immunohistochemistry

IDH:

Isocitrate dehydrogenase

mTOR:

Mammalian target of rapamycin

MAPK:

Mitogen-activated protein kinase

MET:

Proto-oncogene mesenchymal epithelial transition

MGMT:

06-Methylguanine-DNA methyltransferase

PCR:

Polymerase chain reaction

PDGFR:

Platelet-derived growth factor receptor

PTEN:

Phosphatase and tensin homology

PXN:

Paxilline

TP53:

Tumor protein 53

TMZ:

Temozolomide

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Acknowledgements

The authors are grateful to the KS Vira College of Engineering and Management’s administration for providing all of the essential facilities to complete this work. The authors would also want to express their gratitude to all of the academic members of the Department of Biotechnology at the KS Vira College of Engineering and Management for their unwavering support throughout this research project. The authors would like to express their gratitude to Jing Yuan Fang and Bruce C. Richardson for allowing us to use a figure from their paper “The MAPK signalling pathways and colorectal cancer”.

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Iyman Amin: manuscript preparation, arrangement of data. PrashantSaxena: manuscript preparation, revisions in the manuscript, correspondence.

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Correspondence to Prashant Saxena.

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Highlights

Glioblastoma is one of the most violent types of brain tumor having the survival rate of maximum 12–15 months, although we have various treatments such as chemotherapy, TTF therapy, and target drug therapy.

Some of the molecular and genetic markers associated with glioblastoma are IDH, ATRX, TP53, 1p/19q co-deletion.

The pathways that lead to glioblastoma are RAS/MAPK/ERK and mTOR/P13K/AKT.

Natural compounds that have the capacity to suppress the activity of the tumor are quercetin found in Allium cepa, resveratrol found in Vitis vinifera, etc.

This article is part of the Topical Collection on Neurogenic Niche

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Amin, I., Prashant Saxena Glioblastoma a Malignant Form of Tumor: a Review on Its Cellular Target, Route, and Its Treatment. Curr. Tissue Microenviron. Rep. 3, 51–60 (2022). https://doi.org/10.1007/s43152-022-00037-4

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