Concentrated monoclonal antibodies MGMT
- Known as:
- Concentrated mab antibodies MGMT
- Catalog number:
- Mob423-05
- Product Quantity:
- 0.5ml
- Category:
- -
- Supplier:
- Diagnostic Biosystems
- Gene target:
- Concentrated monoclonal antibodies MGMT
Related genes to: Concentrated monoclonal antibodies MGMT
- Gene:
- MGMT NIH gene
- Name:
- O-6-methylguanine-DNA methyltransferase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 10q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-10-16
- Date modifiied:
- 2016-10-05
Related products to: Concentrated monoclonal antibodies MGMT
Related articles to: Concentrated monoclonal antibodies MGMT
- Glioblastoma multiforme (GBM) represents the most aggressive primary brain tumor in adults, characterized by significant heterogeneity, rapid progression, and resistance to existing therapies. Conventional therapies provide minimal survival advantages due to recurrence influenced by glioma stem-like cells (GSCs), adaptive signaling pathways, and a highly immunosuppressive tumor microenvironment (TME). Further, molecular profiling has revealed significant alterations, including EGFR amplification, IDH mutations, MGMT promoter methylation, and TERT promoter changes; however, challenges persist in the integration of genomic, epigenetic, metabolic, and transcriptomic data for the development of effective therapies. Thus, this review examines the limitations by integrating recent developments in molecular classification, dysregulated signaling pathways, metabolic reprogramming, and non-coding RNA-mediated regulation in GBM. Additionally, the manuscript emphasizes novel therapeutic strategies, such as nanomedicine, oncolytic virotherapy, immunotherapy, tumor-treating fields, and phytochemical-based interventions, as well as the increasing significance of artificial intelligence and machine learning in diagnosis and personalized treatment. Lastly, this review integrates mechanistic and translational insights to establish a framework addressing blood-brain barrier limitations, therapeutic resistance, and immune evasion, thereby facilitating the advancement of precision medicine approaches for enhanced GBM outcomes. - Source: PubMed
Publication date: 2026/06/08
Kumari SmitaMisra JyotsnaRavi KarthikeyanKumar NaveenJha Niraj KumarGupta Rohan - The clinical management of glioma is increasingly dependent on the tumor's molecular profile, particularly the mutation status of Isocitrate Dehydrogenase (IDH), the promoter methylation of O-6-Methylguanine-DNA Methyltransferase (MGMT), and the co-deletion of chromosomal arms 1p and 19q. Determining these markers requires invasive tissue sampling. This study aimed to develop and validate a multimodal artificial intelligence (AI) framework for the non-invasive and simultaneous prediction of these three key markers using routine preoperative CT and PET imaging. - Source: PubMed
Publication date: 2026/06/06
Abdallah AishaAltuwayjiri BasmahAlbloshi Abdullah M KAlthbiti AshrfMahbub Amani AAlawad Wedad MAlazzam Malik Bader - Glioblastoma is the most common malignant brain tumour in adults and carries a poor prognosis despite advances in molecular characterisation and therapy. The 2021 World Health Organisation classification redefined glioblastoma as an IDH-wildtype diffuse astrocytic tumour with aggressive histological or molecular features. Standard of care therapy has changed little over the last two decades, and outcomes remain suboptimal, with considerable heterogeneity in survival influenced by clinical, molecular, and treatment-related factors. - Source: PubMed
Publication date: 2026/06/05
Mustafa Yazan HKeogh Rachel JBarry Simon LDillon BryanMohammed WailLim ChrisJansen MichaelBermingham NiamhHiggins MartinO'Reilly SeamusGleeson Jack PBambury Richard M - H mutations and 1p19q co-deletion are the main biomarkers used in the nomenclature of glial tumors. Detection of 1p19q co-deletion directly diagnoses oligodendroglioma. The primary objective of this study was to evaluate the 1p19q co-deletion status in diffuse gliomas in accordance with the World Health Organization (WHO) integrated classification framework. In addition, we aimed to investigate the presence of 1p19q alterations in other, less frequently encountered glial-derived central nervous system tumors. - Source: PubMed
Publication date: 2026/05/04
Akar EzgiTure UgurSav Murat Aydin - Profiling the spatiotemporal dynamics of DNA demethylases is critical for deciphering the mechanisms of epigenetic regulation and genomic maintenance. However, existing fluorescent strategies often suffer from false-positive signals in living cells, primarily arising from non-specific nuclease degradation or instability of the complex amplification components. Herein, we present a generalisable "demethylation-activated" fluorescent light-up DNA aptamer (FLAP) strategy for high-contrast imaging of DNA alkylation repair in living cells. Our design relies on a precise "caging" strategy: site-specific methyl lesions (, O-meG) are engineered into the ligand-binding domain of the Bibb Lettuce aptamer, which disrupts its folding and suppresses fluorescence. Upon specific enzymatic repair, the aptamer structure is restored, triggering a robust fluorescence "turn-on" signal. This mechanism effectively minimises false-positive signals. The optimised probe detects MGMT activity with high sensitivity (LOD: 1.64 nM) and enables direct visualisation of active demethylation processes in MCF-7 cells, revealing distinct responses to inhibitors. Highlighting the modularity of the platform, we extended the design to detect AlkBH2 (LOD: 0.81 nM) simply by substituting the lesion with 1-methyladenine (1-meA). This work establishes a versatile and programmable framework for converting transient DNA repair events into quantifiable optical signals, providing a powerful tool for exploring epigenetic dynamics and cancer pharmacology. - Source: PubMed
Publication date: 2026/05/28
Luan XinyuZhang HanLi ZheMa MiaoZhang JunruiLiu FangZhai JunqiuLuan Tiangang