PTEN – A MOLECULAR MARKER FOR THE DIAGNOSIS OF GLIOMA BABUL REDDY TATIREDDY

Mapping Intimacies ◽

10.36106/gjra/1411304 ◽

2021 ◽

pp. 45-48

Author(s):

Babul Reddy Tatireddy

Keyword(s):

Brain Tumor ◽

Literature Search ◽

Recipient Cell ◽

Primary Brain Tumor ◽

The Novel ◽

Cellular Phenotype ◽

Therapeutic Approaches ◽

Downstream Signaling ◽

Novel Biomarkers ◽

Biomarker Research

Glioblastoma is an uncommon primary brain tumor accounts for upto 15.4% of all primary brain tumors. Although several modern therapies against glioma are discovered, management is still a critical concern. The existing therapies were relatively inconsistent; moreover, the procedures as well are difcult to treat. These ineffective therapeutic approaches led researchers to identify the novel biomarkers that can be implemented with the existing therapies for better management. In this view, along with biomarker research, a literature search for exosomal PTEN detection in glioblastoma was conducted and the recent studies observed that exosomes can transport tumor-suppressive proteins (PTEN) and oncogenic mRNAs, microRNAs to a recipient cell, which subsequently activates the downstream signaling pathways and inuences the cellular phenotype. These exosomes facilitate the transfer of PTEN released from tumor cells to receipt cells that leads to tumor progression. Similarly, glioma was also associated with a reduction or loss of PTEN expression. Hence, our present review aimed to provide a holistic picture of glioblastoma, its pathogenesis and novel biomarkers with an emphasis on PTEN detection in exosomes for the early identication of glioblastoma

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Wnt/β-catenin Antagonists: Exploring New Avenues to Trigger Old Drugs in Alleviating Glioblastoma Multiforme

Current Molecular Pharmacology ◽

10.2174/1874467214666210420115431 ◽

2021 ◽

Vol 14 ◽

Author(s):

Daisy S. Precilla ◽

Shreyas S. Kuduvalli ◽

Mugilarasi Purushothaman ◽

Parthiban Marimuthu ◽

Muralidharan A. Ramachandran ◽

...

Keyword(s):

Glioblastoma Multiforme ◽

Epigallocatechin Gallate ◽

Drug Repurposing ◽

Primary Brain Tumor ◽

The Novel ◽

Therapeutic Approaches ◽

Computational Tools ◽

Effective Combination ◽

Effective Treatment Modality ◽

Old Drugs

Background: Glioblastoma multiforme is one of the most heterogenous primary brain tumor with high mortality. Nevertheless, of the current therapeutic approaches, survival rate remains poor with 12 to 15 months following preliminary diagnosis, this warrants the need for effective treatment modality. Wnt/β-catenin pathway is presumably the most noteworthy pathway up-regulated in almost 80% GBM cases contributing to tumor-initiation, progression and survival. Therefore, therapeutic strategies targeting key components of Wnt/β-catenin cascade using established genotoxic agents like temozolomide and pharmacological inhibitors would be an effective approach to modulate Wnt/β-catenin pathway. Recently, drug repurposing by means of effective combination therapy has gained importance in various solid tumors including GBM, by targeting two or more proteins in a single pathway, thereby possessing the ability to overcome the hurdle implicated by chemo-resistance in GBM. Objective: In this context, by employing computational tools, an attempt has been carried out to speculate the novel combinations against Wnt/β-catenin signaling pathway. Methods: We have explored the binding interactions of three conventional drugs namely temozolomide, metformin, chloroquine along with three natural compounds viz., epigallocatechin gallate, naringenin and phloroglucinol on the major receptors of Wnt/β-catenin signaling. Results: It was noted that all the experimental compounds possessed profound interaction with the two major receptors of Wnt/β-catenin pathway. Conclusion: To the best of our knowledge, this study is the first of its kind to characterize the combined interactions of the afore-mentioned drugs on Wnt/β-catenin signaling in silico and this will putatively open up new avenues for combination therapies in GBM treatment.

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PACAP and VIP induce expression of the novel neurotrophin-1/B-cell stimulating factor-3 (Cardiotrophin-like cytokine) in pituitary folliculostellate TtT/GF cells: downstream signaling events involve PKA, PKC and ERK1/2

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/s-2004-819305 ◽

2004 ◽

Vol 112 (S 1) ◽

Author(s):

G Vlotides ◽

K Zitzmann ◽

D Engelhardt ◽

G Spoettl ◽

J Meinecke ◽

...

Keyword(s):

B Cell ◽

The Novel ◽

Downstream Signaling ◽

Signaling Events ◽

Stimulating Factor

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Disease Mechanisms and Therapeutic Approaches in C9orf72 ALS-FTD

Biomedicines ◽

10.3390/biomedicines9060601 ◽

2021 ◽

Vol 9 (6) ◽

pp. 601

Author(s):

Keith Mayl ◽

Christopher E. Shaw ◽

Youn-Bok Lee

Keyword(s):

The Body ◽

The Novel ◽

Therapeutic Approaches ◽

Gain Of Function ◽

Pathogenic Mechanisms ◽

Hexanucleotide Repeat ◽

Primary Driver ◽

Hexanucleotide Repeat Expansion ◽

Expansion Mutation ◽

Lateral Sclerosis

A hexanucleotide repeat expansion mutation in the first intron of C9orf72 is the most common known genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Since the discovery in 2011, numerous pathogenic mechanisms, including both loss and gain of function, have been proposed. The body of work overall suggests that toxic gain of function arising from bidirectionally transcribed repeat RNA is likely to be the primary driver of disease. In this review, we outline the key pathogenic mechanisms that have been proposed to date and discuss some of the novel therapeutic approaches currently in development.

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Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis

Cells ◽

10.3390/cells10061411 ◽

2021 ◽

Vol 10 (6) ◽

pp. 1411

Author(s):

Don Carlo Ramos Batara ◽

Moon-Chang Choi ◽

Hyeon-Uk Shin ◽

Hyunggee Kim ◽

Sung-Hak Kim

Keyword(s):

Brain Tumor ◽

Glioblastoma Multiforme ◽

Cancer Biology ◽

Molecular Mechanisms ◽

Primary Brain Tumor ◽

Molecular Target ◽

Therapeutic Strategies ◽

Homeostatic Mechanism ◽

Cellular Context ◽

Cellular Components

Glioblastoma multiforme (GBM) is the most common and aggressive type of primary brain tumor in adults, with a poor median survival of approximately 15 months after diagnosis. Despite several decades of intensive research on its cancer biology, treatment for GBM remains a challenge. Autophagy, a fundamental homeostatic mechanism, is responsible for degrading and recycling damaged or defective cellular components. It plays a paradoxical role in GBM by either promoting or suppressing tumor growth depending on the cellular context. A thorough understanding of autophagy’s pleiotropic roles is needed to develop potential therapeutic strategies for GBM. In this paper, we discussed molecular mechanisms and biphasic functions of autophagy in gliomagenesis. We also provided a summary of treatments for GBM, emphasizing the importance of autophagy as a promising molecular target for treating GBM.

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Molecular Mechanisms of Drug Resistance in Glioblastoma

International Journal of Molecular Sciences ◽

10.3390/ijms22126385 ◽

2021 ◽

Vol 22 (12) ◽

pp. 6385

Author(s):

Maya A. Dymova ◽

Elena V. Kuligina ◽

Vladimir A. Richter

Keyword(s):

Drug Resistance ◽

Brain Tumor ◽

Molecular Mechanisms ◽

Primary Brain Tumor ◽

Therapeutic Resistance ◽

Molecular Characteristics ◽

Blood Brain ◽

Conventional Radiation ◽

The Brain ◽

Made In

Glioblastoma multiforme (GBM) is the most common and fatal primary brain tumor, is highly resistant to conventional radiation and chemotherapy, and is not amenable to effective surgical resection. The present review summarizes recent advances in our understanding of the molecular mechanisms of therapeutic resistance of GBM to already known drugs, the molecular characteristics of glioblastoma cells, and the barriers in the brain that underlie drug resistance. We also discuss the progress that has been made in the development of new targeted drugs for glioblastoma, as well as advances in drug delivery across the blood–brain barrier (BBB) and blood–brain tumor barrier (BBTB).

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