Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
The transcription factor MYC is a well-described oncogene with an important role in lymphomagenesis, but its significance for clinical outcome in mantle cell lymphoma (MCL) remains to be determined. We performed an investigation of the expression of MYC protein in a cohort of 251 MCL patients complemented by analyses of structural aberrations and mRNA, in a sub-cohort of patients. Fourteen percent (n=35) of patients showed high MYC protein expression with >20% positive cells (MYChigh), among whom only one translocation was identified, and 86% (n=216) of patients showed low MYC protein expression. Low copy number gains of MYC were detected in ten patients, but with no correlation to MYC protein levels. However, MYC mRNA levels correlated significantly to MYC protein levels with a R2 value of 0.76. Patients with a MYChigh tumor had both an independent inferior overall survival and an inferior progression-free survival (hazard ratio [HR]=2.03, 95% confidence interval [95% CI]: 1.2-3.4 and HR=2.2, 95% CI: 1.04-4.6, respectively) when adjusted for additional high-risk features. Patients with MYChigh tumors also tended to have additional high-risk features and to be older at diagnosis. A subgroup of 13 patients had concomitant MYChigh expression and TP53/p53 alterations and a substantially increased risk of progression (HR=16.9, 95% CI: 7.4-38.3) and death (HR=7.8, 95% CI: 4.4-14.1) with an average overall survival of only 0.9 years. In summary, we found that at diagnosis a subset of MCL patients (14%) overexpressed MYC protein, and had a poor prognosis but that MYC rearrangements were rare. Tumors with concurrent MYC overexpression and TP53/p53 alterations pinpointed MCL patients with a dismal prognosis with a median overall survival of less than 3 years. We propose that MYC needs to be assessed beyond the current high-risk factors in MCL in order to identify cases in need of alternative treatment.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10985440 | PMC |
| http://dx.doi.org/10.3324/haematol.2023.283352 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
New Experimental Mouse Models to Evaluate the Role of Transforming Growth Factor-Beta in Liver Tumorigenesis.
Liver Int
October 2025
TGF-Beta and Cancer Group - Oncobell Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.
Background And Aims: Hepatocellular carcinoma (HCC) has a poor prognosis and limited treatment options. TGF-β is a promising therapeutic target, but its dual role, as both a tumour suppressor and promoter, complicates its clinical application. While its effects on tumour cells are increasingly understood, its impact on the tumour stroma remains unclear.
View Article and Find Full Text PDFIntegrative network toxicology and molecular docking reveal 4-Nonylphenol's multifaceted mechanisms in breast cancer pathogenesis.
PLoS One
September 2025
Department of Hepatobiliary Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Objective: This study employs integrated network toxicology and molecular docking to investigate the molecular basis underlying 4-nonylphenol (4-NP)-mediated enhancement of breast cancer susceptibility.
Methods: We integrated data from multiple databases, including ChEMBL, STITCH, Swiss Target Prediction, GeneCards, OMIM and TTD. Core compound-disease-associated target genes were identified through Protein-Protein Interaction (PPI) network analysis.
An inhibitor of UHM splicing factors exerts anti-leukemic activity by altering cell cycle progression and reducing lysosome acidification.
Cell Signal
September 2025
Departments of Pharmaceutical Sciences, College of Pharmacy, University of Tennessee Health Science Center, Memphis, TN 38163, USA. Electronic address:
Mature mRNAs are generated by spliceosomes that recruit factors to aid RNA splicing in which introns are removed and exons joined. Among the splicing factors, a family of proteins contain a homologous U2 Auxiliary Factor (U2AF) Homology Motif (UHM) to bind with factors containing U2AF ligand motifs (ULM) and recruit them to regulate 3' splice site selection. Mutations and overexpression of UHM splicing factors are frequently found in cancers.
View Article and Find Full Text PDFTRIM31 acts as an intermediate molecule in the process by which Snai2 impairs the proliferation of cervical cancer cells.
Front Oncol
August 2025
Department of Reproductive Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Snai2 is a transcription factor that inhibits the proliferation of cervical cancer cells and tumor growth. The expression of Snai2 inhibited the expression of β-catenin and impaired Wnt/β-catenin signaling pathway activity. The results of the RNA sequence in Snai2-overexpressing cervical cancer cells implied a strong correlation between Snai2 and TRIM31 with ubiquitin ligase activity.
View Article and Find Full Text PDFMED10 as a Novel Oncogenic Driver in HCC: Promoting Cell Cycle Progression and Proliferation Through RAF1 Activation.
Front Biosci (Landmark Ed)
August 2025
Department of Hepatobiliary Surgery, General Hospital of Ningxia Medical University, 750004 Yinchuan, Ningxia Hui Autonomous Region, China.
Background: Mediator complex subunit 10 (MED10) serves as a critical regulator of eukaryotic gene expression by facilitating RNA polymerase II activity. Our investigation aims to characterize MED10's functional contributions and underlying molecular pathways in hepatocellular carcinoma (HCC) development.
Methods: MED10 expression patterns in HCC and their correlation with clinicopathological parameters and patient outcomes were examined using bioinformatics databases and immunohistochemistry.