Results 151 to 160 of about 81,769 (261)

Histone H3K18 Lactylation Promotes the Malignant Progression of Wilms Tumor via a PSRC1/AKT/HIF‐1α Positive Feedback Loop

open access: yesAdvanced Science, EarlyView.
In nephroblastoma, aberrant glycolysis drives lactate accumulation, which elevates histone H3K18 lactylation via p300. Lactylation of the PSRC1 promoter activates its transcription. PSRC1 competitively binds AKT, relieving PTEN‐mediated inhibition and triggering AKT/mTOR/HIF‐1α signaling.
Yanping Wang   +6 more
wiley   +1 more source

Estudo dos efeitos da cisplatina sobre o sistema trocador cistina-glutamato em células de glioblastoma humano a172 [PDF]

open access: yes, 2011
TCC(graduação) - Universidade Federal de Santa Catarina. Centro de Ciências Biológicas. Biologia.Gliomas malignos correspondem a um grupo heterogêneo de tumores do sistema nervoso central (SNC).
Bittencourt, Lucas Felipe Fernandes
core  

ZBTB11 Promotes Breast Cancer Progression by Activating FBXO28‐Mediated MST1 Degradation and Suppressing Hippo Signaling

open access: yesAdvanced Science, EarlyView.
ZBTB11 is identified as an oncogenic transcription factor that activates FBXO28 in breast cancer. FBXO28 promotes K48‐linked ubiquitination and degradation of MST1, suppressing Hippo signaling and enhancing epithelial–mesenchymal transition and metastasis. This transcription‐to‐ubiquitination cascade defines a prognostic biomarker axis and highlights a
An Xu   +10 more
wiley   +1 more source

Reversing Temozolomide Resistance in Glioblastoma Based on Cuproptosis‐Mediated Positive Feedback Loop

open access: yesAdvanced Science, EarlyView.
To effectively reverse TMZ resistance, this work proposes a cuproptosis‐mediated positive feedback loop that integrates mitochondrial dysfunction, ATP depletion, AMPK‐p53 signaling, and glycolytic inhibition, ultimately amplifying cell death. This cuproptosis‐mediated feedback loop simultaneously disrupts multiple resistance pathways in GBM, including ...
Wenjie Feng   +9 more
wiley   +1 more source

Identifying a Csmd3+ Microglial Subpopulation that Drives Cold‐to‐Hot Transition and Immune‐Cure in Glioblastoma

open access: yesAdvanced Science, EarlyView.
The study establishes an immune‐cure (ICu) mouse model based on a TMEMed G422TN‐GBM system that faithfully recapitulates human TMEMed GBM. scRNA‐seq analysis reveals a Csmd3+ microglial subset with innate immune memory (IIM) potential that potently suppresses GBM growth, drives a TME cold‐to‐hot transition, and induces 100% ICu in long‐term survival ...
Hai‐Feng Jiang   +12 more
wiley   +1 more source

VERIFICATION OF THE EXPERIMENTAL SYSTEM FOR THE APPLICATION OF THE QMR SIGNAL FOR THE TREATMENT OF GLIOBLASTOMA

open access: yes
reservedIl glioblastoma è tra i tumori umani quello più aggressivo e con il più alto tasso di recidiva; i pazienti cui viene diagnosticato hanno un’aspettativa di vita di 14-15 mesi nonostante l’intervento chirurgico di rimozione e le cure radio ...
PAVIN, ENRICO
core  

The role of mitochondrial DNA in the tumor biology of glioblastoma multiforme and multiple myeloma [PDF]

open access: yes
Cancer cells preferentially metabolise glucose via aerobic glycolysis (the Warburg effect), which is less energy efficient in teens of ATP production compared to oxidative phosphorylation (OXPHOS).
Yeung, Ka Yu
core  

Genetic Ablation and Multi‐Omics Profiling Reveal CEP55 as a Key Driver of Tumorigenesis in Diverse Cancer Models

open access: yesAdvanced Science, EarlyView.
Genetic ablation of Cep55 in Pten‐deficient mouse models delays tumorigenesis. Integrated multi‐omics analyses (proteomics, phosphoproteomics, and spatial transcriptomics) reveal that CEP55 regulates oncogenic signaling (RAS/ERK, PI3K/AKT), integrin/FAK‐mediated adhesion, extracellular matrix (ECM) remodeling, and endocytosis.
Behnam Rashidieh   +22 more
wiley   +1 more source

ENHANCING GLIOBLASTOMA THERAPY: COMBINING DEEP LEARNING SEGMENTATION WITH ROBOTIC HISTOTRIPSY

open access: yes
Glioblastoma multiforme (GBM) is the most aggressive and prevalent adult brain cancer, with a median survival of 14 months due to its rapid growth, invasiveness, and resistance to conventional treatments.
Dorosti, Shadi
core  

Crosstalk Between CTSB+ Glioblastoma Cells and S100A10+ Macrophages: A Self‐Reinforcing Circuit Promotes Immune Evasion and Limits Response to Immunotherapy

open access: yesAdvanced Science, EarlyView.
In glioblastoma, M2‐polarized macrophages secrete IL‐6, which activates STAT3 signaling in tumor cells to upregulate CTSB. Tumor‐derived CTSB binds the C‐terminus of macrophage S100A10, reinforcing M2 polarization and further IL‐6 secretion, thereby establishing a feedforward IL‐6/STAT3/CTSB/S100A10 loop. This cascade drives tumor growth, invasion, and
Hao Zhang   +11 more
wiley   +1 more source

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