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Ga-NOTA-RM26 PET/CT in the evaluation of glioma: a pilot prospective study.
EJNMMI Res
January 2025
Department of Neurosurgery, Center for Malignant Brain Tumors, National Glioma MDT Alliance, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.
Background: Gliomas are the most common malignant primary tumors of the central nervous system. There is an urgent need for new convenient, targeted and specific imaging agents for gliomas. This study aimed to firstly evaluate the feasibility of Ga-NOTA-RM26 PET/CT imaging in glioma and analyze the relationship between the imaging characteristics and glioma grade, classification and molecular alterations.
View Article and Find Full Text PDFConcurrent RB1 and P53 pathway disruption predisposes to the development of a primitive neuronal component in high-grade gliomas depending on MYC-driven EBF3 transcription.
Acta Neuropathol
January 2025
Pathology Unit, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
The foremost feature of glioblastoma (GBM), the most frequent malignant brain tumours in adults, is a remarkable degree of intra- and inter-tumour heterogeneity reflecting the coexistence within the tumour bulk of different cell populations displaying distinctive genetic and transcriptomic profiles. GBM with primitive neuronal component (PNC), recently identified by DNA methylation-based classification as a peculiar GBM subtype (GBM-PNC), is a poorly recognized and aggressive GBM variant characterised by nodules containing cells with primitive neuronal differentiation along with conventional GBM areas. In addition, the presence of a PNC component has been also reported in IDH-mutant high-grade gliomas (HGGs), and to a lesser extent to other HGGs, suggesting that regardless from being IDH-mutant or IDH-wildtype, peculiar genetic and/or epigenetic events may contribute to the phenotypic skewing with the emergence of the PNC phenotype.
View Article and Find Full Text PDFComplex p53 dynamics regulated by miR-125b in cellular responses to reactive oxidative stress and DNA damage.
Brief Bioinform
November 2024
Department of Translational Research, Dasman Diabetes Institute, Dasman 15462, Kuwait City, Kuwait.
In response to distinct cellular stresses, the p53 exhibits distinct dynamics. These p53 dynamics subsequently control cell fate. However, different stresses can generate the same p53 dynamics with different cell fate outcomes, suggesting that the integration of dynamic information from other pathways is important for cell fate regulation.
View Article and Find Full Text PDFPrognostic value of CTF1 in glioma and its role in the tumor microenvironment.
Transl Cancer Res
December 2024
Department of Radiation Oncology, The Second Hospital of Lanzhou University, Lanzhou, China.
Background: Within the realm of primary brain tumors, specifically glioblastoma (GBM), presents a notable obstacle due to their unfavorable prognosis and differing median survival rates contingent upon tumor grade and subtype. Despite a plethora of research connecting cardiotrophin-1 (CTF1) modifications to a range of illnesses, its correlation with glioma remains uncertain. This study investigated the clinical value of CTF1 in glioma and its potential as a biomarker of the disease.
View Article and Find Full Text PDFOncoproteins E6/E7 of the human papillomavirus types 16 & 18 synergize in modulating oncogenes and tumor suppressor proteins in colorectal cancer.
Expert Rev Proteomics
January 2025
College of Medicine, QU Health, Qatar University, Doha, Qatar.
Objective: Our study presents a novel analysis of the oncogenes and tumor suppressor proteins directly modulated by E6/E7 of high-risk HPV types 16 and 18, in colorectal cancer (CRC).
Methods: HCT 116 (KRAS mutant) & HT-29 (TP53 mutant) cell models of CRC were transduced with E6/E7 of HPV16 and HPV18, individually and in combination. Further, we utilized a liquid chromatography mass spectrometry (LC-MS/MS) approach to analyze and compare the proteomes of both CRC cell models.
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