Non-invasive diagnosis and surveillance of bladder cancer with driver and passenger DNAmethylation in a prospective cohort study
We studied DNA methylation markers in urine to enhance bladder cancer detection and classification. Our findings could transform non-invasive diagnosis and monitoring of this cancer and potentially other types as well, leading to major advances in cancer management with less invasive techniques.
Integrative single cell atlas revealed intratumoral heterogeneity generation from an adaptive epigenetic cell state in human bladder urothelial carcinoma
A subgroup of bladder cancer cells marked by TM4SF1 expression is a key source of tumor diversity (ITH). These cells, which show stem-cell features and foster various cell types within the tumor, are linked to more advanced cancer stages and poorer outcomes.
Unveiling the Mechanisms Behind Cancer Aggressiveness: How Epichaperomes Drive Cellular Plasticity
What makes cancer so aggressive and adaptable? Our latest research uncovers a hidden mechanism within cells—specialized protein networks called epichaperomes. These structures help cancer cells survive and thrive, reactivating developmental pathways and fueling unchecked growth.
A novel germline EGFR variant p.R831H causes predisposition to familial CDK12-mutant prostate cancer with tandem duplicator phenotype
This study is the first report identifying a pathogenic EGFR germline mutation in prostate cancer, suggesting venues for germline screening, non-invasive diagnosis and monitoring in clinical practice.
Deubiquitylase USP52 Promotes Bladder Cancer Progression by Modulating Ferroptosis through Stabilizing SLC7A11/xCT
We identified USP52 as a DUB that cleaves K48-linked ubiquitin at K4 and K12 of xCT. Loss of USP52 reduces cell proliferation by decreasing xCT and enhancing ferroptosis sensitivity. Combining USP52 depletion with IKE strongly inhibits BLCA progression, presenting a new potential therapy.
DNA polymerase POLD1 promotes proliferation and metastasis of bladder cancer by stabilizing MYC
Based on the bladder cancer (BLCA) pedigree containing germline mutation of POLD1 found in our last study, we further analyzed the molecular role of POLD1 driving tumorigenesis. We identified POLD1 as a promotor of BLCA via a MYC driven mechanism.
Pedigree analysis of a POLD1 germline mutation in urothelial carcinoma shows a close association between different mutation burdens and overall survival
We found a bladder cancer family in which germline mutations of POLD1 and somatic mutations of FGFR3 were prevalent. We studied the changes in the immune microenvironment in patients with this mutation in our cohort and a TCGA cohort and predicted the prognosis of patients with this subtype.
