FGFR3 mutation

Tumor tissue and serial plasma samples were collected from 15 patients with aUC treated with dose-dense methotrexate, vinblastine, doxorubicin, and cisplatin (ddMVAC). While the NOIR-SS-based assay proved sensitive and informative, limitations include the cost and time required for sequencing, potential temporal discordance between tissue and plasma sampling, and the absence of correction for clonal hematopoiesis of indeterminate potential. Overall, ctDNA profiling using this targeted panel and NOIR-SS suggested the feasibility of sensitive, non-invasive molecular monitoring in aUC, and may have future clinical applicability if validated prospectively in larger cohorts.

The expression of SF3A3 in LIHC tumors is correlated with adverse pathological features and poor prognosis and potential biological mechanisms underlying the role of SF3A3 in LIHC were elucidated. This study highlights SF3A3 as a promising biomarker for prognosis and disease severity in LIHC. Keywords SF3A3, TCGA, GTEx, LIHC, tumor, prognosis, biomarker.

The consistent association of these variant patterns with S249C or Y373C mutations suggests that hotspot FGFR3 alterations can persist across morphologic contexts in noninvasive and invasive disease. Recognition of these variant histologies may therefore support consideration of targeted FGFR testing.

Stage-tailored strategies are emerging, including risk assessment in NMIBC, refining adjuvant decisions in MIBC, and treatment monitoring in mUC. Integration of ctDNA-guided approaches should proceed alongside prospective validation to ensure safe and effective adoption.

Using a large-scale Japanese genomic panel dataset, we characterized the molecular alterations associated with S/DD. S/DD frequently exhibits low Nectin-4 expression and basal-like molecular features, which may have implications for treatment selection and inform future therapeutic strategies.

In contrast, tumors that do not respond to chemotherapy harbor different genetic changes that help them survive and grow. These findings may help physicians choose more effective and personalized treatments in the future.

This study confirms that, despite its name, PLNTY is not limited to pediatric patients. Findings underscore the highly epileptogenic nature of PLNTY and its recognizable electroclinical features, potentially related to its distinctive neuropathology. Most PLNTYs show mitogen-activated protein kinase (MAPK) pathway activating alterations, demonstrated by BRAFV600E mutation and FGFR3 fusion.

Our study demonstrates that CT-derived radiomics features can capture biologically and clinically relevant information in muscle-invasive bladder cancer. These findings support the potential utility of radiomics as a noninvasive, scalable adjunct to genomic profiling in MIBC.

P1/2, N=75, Completed, Tyra Biosciences Inc. | Suspended --> Completed

dUM provides robust, reproducible prognostic information and significantly improves molecular risk stratification in NMIBC. These findings support its potential integration into risk-adapted surveillance strategies, pending validation in larger populations.

Using transcriptomic profiles, a single-sample classifier was developed to categorize tumors into integrated molecular clusters. This study provides an integrated classification system to understand the heterogeneity of NMIBC and establish a preclinical framework for clinical management, therapeutic targets, and monitoring of clinical trials.

FGFR3 mutation was not detected in any of the cases. Urothelial carcinomas occurring in children and young adults exhibit a distinct molecular profile compared with those in older patients, characterized by a higher frequency of HRAS mutations and a significantly lower prevalence of TERT promoter and FGFR3 alterations.