Background: Mortality rate is dramatically high in high grade brain tumors. The presence of multiple drug resistance transporters in glioblastoma multiforme, has contributed largely to the poor efficacy of targeted therapy against cancer in the central nervous system.

Aim: To analyze the percentage of survival and mortality of patients with glioblastoma multiforme in a cohort of patients in Chile and to co-rrelate the chemo-resistance of these cells with the expression level of multiple drug resistance transporters.

Materials And Methods: Eighteen biopsies of glioblastoma multiforme were obtained from patients at the Institute of Neurosurgery Dr. Asenjo (INCA). The tumor cells were obtained from primary cultures and the expression and activity of multiple drug resistance transporters was assessed by RT-PCR and immunohistochemistry. Population-based study was performed using the databases of the Department of Neurosurgery of INCA.

Results: The number of patients with glioblastoma multiforme increased between 2007 and 2009, from 3.5% to 7.9% of total brain tumors. Mortality of these tumors is 90 % at three years. A high expression and activity of the multiple drugs resistance associated protein 1 (Mrp1) transporter was observed in primary cultures of biopsies.

Conclusions: We propose that Mrp1 activity is responsible for the chemo-resistance of the glioblastoma multiforme and inhibition of this transporter could represent a plausible strategy for the treatment.

Download full-text PDF

Source

Publication Analysis

Top Keywords

glioblastoma multiforme
20
multiple drug
12
drug resistance
12
biopsies glioblastoma
8
brain tumors
8
resistance transporters
8
patients glioblastoma
8
primary cultures
8
expression activity
8
activity multiple
8

Similar Publications

We aimed to build a robust classifier for the MGMT methylation status of glioblastoma in multiparametric MRI. We focused on multi-habitat deep image descriptors as our basic focus. A subset of the BRATS 2021 MGMT methylation dataset containing both MGMT class labels and segmentation masks was used.

View Article and Find Full Text PDF

IDO1 inhibits ferroptosis by regulating FTO-mediated m6A methylation and SLC7A11 mRNA stability during glioblastoma progression.

Cell Death Discov

January 2025

State Key Laboratory of Functions and Applications of Medicinal Plants, School of Basic Medical Sciences, Guizhou Provincial Engineering Technology Research Center for Chemical Drug R&D, Guizhou Medical University, Guiyang, China.

Indoleamine 2, 3-dioxygenase 1 (IDO1) has been recognized as an enzyme involved in tryptophan catabolism with immunosuppressive ability. This study determined to investigate the impact of IDO1 on glioblastoma multiforme (GBM) cells. Here, we showed that the expression of IDO1 was markedly increased in patients with glioma and associated with GBM progression.

View Article and Find Full Text PDF

Stereotactic injection of murine brain tumor cells for neuro-oncology studies.

Methods Cell Biol

January 2025

Department of Radiation Oncology, Weill Cornell Medicine, New York, NY, United States. Electronic address:

Glioblastomas (GBMs) are the most common and aggressive brain tumors, with a poor prognosis. Effective preclinical models are crucial to investigate GBM biology and develop novel treatments. Syngeneic models, which consist in injecting murine GBM cells into mice with a similar genetic background, offer reproducibility, cost-effectiveness, and an intact immune system, making them ideal for immunotherapy research.

View Article and Find Full Text PDF

Background: B7 homolog 3 (B7-H3), an overexpressed antigen across multiple solid cancers, represents a promising target for CAR T cell therapy. This study investigated the expression of B7-H3 across various solid tumors and developed novel monoclonal antibodies (mAbs) targeting B7-H3 for CAR T cell therapy.

Methods: Expression of B7-H3 across various solid tumors was evaluated using RNA-seq data from TCGA, TARGET, and GTEx datasets and by flow cytometry staining.

View Article and Find Full Text PDF

The natural product micheliolide promotes the nuclear translocation of GAPDH via binding to Cys247 and induces glioblastoma cell death in combination with temozolomide.

Biochem Pharmacol

January 2025

College of Chemistry and Frontiers Science Center for New Organic Matter, Haihe Laboratory of Sustainable Chemical Transformations, Nankai University, Tianjin 300071, China. Electronic address:

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is significantly upregulated in glioblastoma (GBM) and plays a crucial role in cell apoptosis and drug resistance. Micheliolide (MCL) is a natural product with a variety of antitumour activities, and the fumarate salt form of dimethylamino MCL (DMAMCL; commercial name ACT001) has been tested in clinical trials for recurrent GBM; this compound suppresses the proliferation of GBM cells by rewiring aerobic glycolysis. Herein, we demonstrated that MCL directly targets GAPDH through covalent binding to the cysteine 247 (Cys247) residue.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!