Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1097/00000478-199707000-00018 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Interaction of STIL with FOXM1 regulates SF3A3 transcription in the hepatocellular carcinoma development.
Cell Div
January 2025
Second Department of General Surgery, the First Hospital of Qiqihar, No. 700, Pukui avenue, Long sha District, Qiqihar, Heilongjiang, 161000, P. R. China.
Background: Dysregulation of SF3A3 has been related to the development of many cancers. Here, we investigated the functional role of SF3A3 in hepatocellular carcinoma (HCC).
Methods: SF3A3 expression in HCC tissues and cell lines was examined using RT-qPCR.
AN IMMUNOHISTOCHEMICAL AND MOLECULAR GENETIC STUDY OF 60 COLORECTAL CARCINOMA BRAIN METASTASES IN PURSUIT OF PREDICTIVE BIOMARKERS FOR CANCER THERAPY.
Hum Pathol
January 2025
Laboratory of Pathology, National Cancer Institute, Bethesda, Maryland.
Colorectal carcinoma brain metastases (n=60) were studied using next-generation sequencing and immunohistochemistry. RAS and BRAF mutations were detected in 58.2% and 7.
View Article and Find Full Text PDFNanosize Non-Viral Gene Therapy Reverses Senescence Reprograming Driven by PBRM1 Deficiency to Suppress iCCA Progression.
Adv Sci (Weinh)
January 2025
Department of Hepatic Surgery, Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Polybromo-1 (PBRM1) serves as a crucial regulator of gene transcription in various tumors, including intrahepatic cholangiocarcinoma (iCCA). However, the exact role of PBRM1 in iCCA and the mechanism by which it regulates downstream target genes remain unclear. This research has revealed that PBRM1 is significantly downregulated in iCCA tissues, and this reduced expression is linked to aggressive clinicopathological features and a poor prognosis.
View Article and Find Full Text PDFGa-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 PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!