Investigating the family tree of a tumor to identify its cellular origins is a daunting task. Liu et al. (2011) now use an elegant lineage tracing technique (MADM) to visualize glioma from its earliest stages. They show that mutations originally induced in neural stem cells lie dormant and only trigger malignant transformation following differentiation into oligodendrocyte precursor cells.
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Ph.D. Human Genetics Program, Molecular Biology and Genomics Department, Human Genetics Institute "Dr. Enrique Corona-Rivera", University Center of Health Sciences, University of Guadalajara, Guadalajara, Mexico.
Background: Central nervous system tumors (CNSTs) represent a significant oncological challenge in pediatric populations, particularly in developing regions where access to diagnostic and therapeutic resources is limited.
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The resistance of cancer cells to apoptosis poses a significant challenge in cancer therapy, driving the exploration of alternative cell death pathways such as pyroptosis, known for its rapid and potent effects. While initial efforts focused on chemotherapy-induced pyroptosis, concerns about systemic inflammation highlight the need for precise activation strategies. Photothermal therapy emerges as a promising non-invasive technique, minimizing pyroptosis-related side effects by targeting tumors spatially and temporally.
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Magnetic resonance imaging (MRI) currently serves as the primary diagnostic method for glioma detection and monitoring. The integration of neurosurgery, radiation therapy, pathology, and radiology in a multi-disciplinary approach has significantly advanced its diagnosis and treatment. However, the prognosis remains unfavorable due to treatment resistance, inconsistent response rates, and high recurrence rates after surgery.
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Departamento de Biología Molecular y Bioquímica, Universidad de Málaga, 29071 Málaga, Spain.
Glutaminase controls the first step in glutaminolysis, impacting bioenergetics, biosynthesis and oxidative stress. Two isoenzymes exist in humans, GLS and GLS2. GLS is considered prooncogenic and overexpressed in many tumours, while GLS2 may act as prooncogenic or as a tumour suppressor.
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