Scientific Reports volume 16, Article number: 1,279 (2026) Cite this article.
Scientific Reports volume 16, Article number: 1,279 (2026) Cite this article.
Ferroptosis: a promising therapeutic strategy in glioblastomađ
â Glioblastoma multiforme (GBM) is an aggressive brain tumor characterized by rapid growth and resistance to conventional therapies. Recent research highlights ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, as a novel and promising approach for GBM treatment.
â One key mechanism underlying ferroptosis in GBM is glutathione depletion. Inhibition of the cystine/glutamate antiporter system (xCT) limits cystine uptake, leading to reduced glutathione synthesis. As a consequence, the antioxidant enzyme GPX4 becomes inactivated, impairing the cellâs ability to detoxify lipid peroxides.
â Lipid peroxidation is a central event in ferroptosis. Polyunsaturated fatty acids (PUFAs) incorporated into membrane phospholipids are highly susceptible to oxidative damage. Their conversion into peroxidized phospholipids (PL-PUFA-PE) disrupts membrane integrity and drives lethal oxidative stress.
â Iron metabolism further amplifies ferroptotic signaling in GBM cells. Elevated intracellular iron, particularly the FeÂČâș pool, catalyzes redox reactions that generate reactive oxygen species (ROS). This iron-driven ROS production accelerates lipid peroxidation and pushes tumor cells toward ferroptotic death.
â Collectively, glutathione depletion, GPX4 inactivation, uncontrolled lipid peroxidation, and dysregulated iron metabolism converge to induce ferroptosis. Targeting these interconnected pathways offers a potential strategy to overcome therapy resistance and selectively eliminate GBM cells.
Pentose phosphate pathway in axonal regeneration.
Various signaling pathways play an important role in neuronal homeostasis and regeneration.
The researchers in this study determine that the pentose phosphate pathway (PPP) plays a dual role in enabling homeostatic and regenerative adaptations to environmental stimuli and injuries.
They show that sciatic nerve axoplasms are enriched PPP and maintains redox balance via NADPH production but following sciatic nerve injury, the PPP is required for regeneration by fueling ribonucleotide synthesis through ribose-5-phosphate.
However, after spinal cord injury (SCI), PPP remain inactive and neuronal transketolase overexpression or oral ribose supplementation, promotes metabolic reprogramming, restores sensory and motor axonal growth. sciencenewshighlights ScienceMission https://sciencemission.com/pentose-phosphate-pathway-is-a-metabolic-checkpoint
The pentose phosphate pathway plays a dual role in enabling homeostatic and regenerative adaptations to environmental stimuli and injuries and can be leveraged to promote regeneration and recovery after spinal cord injury.
As for decay accelerating factor (DAF); also known as CD55, it is a type I cell surface protein that forms a single chain anchored to the membrane by glycosylphosphatidylinositol (GPI). It binds C3b and C4b inhibiting thereby the formation of C3 convertase and decreasing its half-life, thus providing a protective barrier threshold for plasma membranes of normal autologous cells against complement deposition and activation9,10.
The role of the complement system in cancer is complicated and has been debated for long. Malignant transformation is generally accompanied by genetic and epigenetic modifications which drastically alter patterns of glycosylation, cell-surface proteins and phospholipids11. These alterations can be identified by innate and adaptive immune mechanisms that guard the host against cancer development12. This is the known basis of the immune surveillance hypothesis. There is no direct evidence to support the argument that complement is able to eradicate emerging tumors. Nevertheless, taking into consideration that complement is intended for the recognition of non-self-elements, it is assumed that alterations in the tumor cell membranesâ composition render these cells as targets for complement recognition13. However, the relationship between inflammation and cancer is complicated and subject to contradictory forces14. Therefore, while acute responses are considered a vital part of the defense against cancerous cells, continuous inflammation in the tumor microenvironment increases the threat of neoplastic transformation and has several tumor-promoting effects15.
The current study aims at investigating the expression levels of mCRPs; CD46 and CD55 in the acute lymphocytic leukemia and acute myelogenous leukemia and to further elucidate its role in Egyptian cancer patients. To the best of our knowledge this study is one of very few studies tackling the complicated role of the complement system in acute leukemia.
Appleâs blockbuster holiday quarter was impressive â but it shouldnât give cover to avoid an AI reckoning. Also: A new MacBook Pro is planned for the macOS 26.3 release cycle; the company explores a clamshell follow-up to its upcoming foldable phone; and an updated AirTag finally rolls out.
Last week in Power On: Inside Appleâs AI shake-up and its plans for two new versions of Siri powered by Gemini.
On stage at Imagination In Actionâs AI Summit in Davos with John Werner, founder and CEO of Imagination In Action, Yann LeCun discusses the inevitable shift from current large language models to a new paradigm of âphysical AIâ based on world models. LeCun opens up about the importance of maintaining open-source research to mitigate the geopolitical risks of concentrated AI power.
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A study of 86,000 adults across Europe links multilingualism to slower biological aging. Researchers found that people who speak multiple languages tend to maintain better cognitive function and physical health than their monolingual peers.
Among adults with treatment-refractory, HER2-positive BiliaryTractCancer, zanidatamab produced sustained, meaningful clinical responses and extended survival compared to prior standards.
In patients with immunohistochemistry (IHC) 3+ tumors, response rates and overall survival were notably higher than those with IHC 2+ tumors, substantiating the use of reflex IHC testing to identify candidates for HER2-targeted therapy.
Safety remained consistent over 33 months of follow-up, and the ongoing HERIZON-BTC-302 phase 3 trial is assessing zanidatamab alongside first-line standard care in this setting.
This follow-up analysis of the phase 2 HERIZON-BTC-01 trial evaluates the efficacy, patient-reported outcomes, and safety profile of zanidatamab in patients with ERBB2-amplified biliary tract cancer with a HER2 immunohistochemistry score of 3+ or 2+ after 33 months of follow-up.