FGFR3 (Fibroblast growth factor receptor 3)

Our findings highlight key disease-associated phosphosites within the FGFRs and offer a foundation for advancing phosphosite-focused therapeutic research.

Collectively, these findings highlight Fgfr3+ endosteal stem cells as candidate cells of origin for osteosarcoma and underscore the dual role of SSC-derived lineages in both tumor initiation and progression. Targeting SSC-derived endosteal niches may provide new therapeutic opportunities for bone malignancies.

This cohort demonstrates both expected and distinct genomic features, including novel synonymous variants in oncogenic pathways. These findings suggest regional variation in NSCLC genomics and support further study of synonymous variants in disease progression.

Toripalimab demonstrated promising activity and manageable safety in pretreated mUTUC. High TMB was associated with numerically improved outcomes, suggesting its potential role as an exploratory biomarker for response to PD-1 blockade in this population.

The bindings of circFGFR3 to EIF4A3 and EIF4A3 to JAK2, STAT3, or STAT5 were analyzed. In conclusion, RBM15 promotes PD-L1-mediated immune escape and accelerates OC progression by upregulating circFGFR3 expression through m6A modification and activating the Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathway.

Our findings underscore the clinical significance of TROP2 expression in UTUC and suggest that IHC-based evaluation may contribute to prognostic risk stratification.

This has broadened the treatment landscape of the disease to include novel agents, such as antibody-drug conjugates (e.g., enfortumab vedotin) and targeted therapies, including the pan-fibroblast growth factor receptor (FGFR) inhibitor erdafitinib. Equally important is the standardization and timely implementation of FGFR3 testing in clinical practice to optimize treatment planning. This review addresses key considerations in FGFR3 testing in mUC and discusses how it can be routinely incorporated into clinical practice.

Our study establishes SDC1+ CAFs as a universal, metastasis-promoting CAF subset across multiple cancer types and uncovers a novel KLF6-CTGF-FGFR3 axis that drives EMT and tumour dissemination. These findings provide mechanistic insight into CAF-tumour cell crosstalk and highlight actionable stromal targets for anti-metastatic therapies across diverse malignancies.

This study provides the first comprehensive evaluation of FGFR1-4 expression in ccRCC and suggests that FGFR1 expression may contribute to the immunosuppressive tumor microenvironment by recruiting TAM. These findings indicate that FGFR1 could serve as a potential biomarker for therapeutic strategies and highlight the need for further research to explore FGFR-targeted therapies in ccRCC.

This study demonstrates that primary biallelic IGH translocations can lead to the coexistence of IGH::FGFR3 and IGH::CCND1, revealing a novel genetic mechanism driven by biallelic IGH translocations in the founding clone. Furthermore, it elucidates the clonal heterogeneity in biallelic IGH translocation events.

We detail limitations of programmed death-ligand 1 (PD-L1) expression, panel-based tumor mutational burden (TMB), clinic-ready toxicity pathways, immune-appropriate response criteria (iRECIST), pseudoprogression, hyperprogression, post-ICI sequencing (FGFR3 alterations, enfortumab vedotin-based therapy, chemotherapy, trials), and delivery models (navigation, electronic patient-reported outcomes, telemedicine, payment structures). Optimizing systemic frameworks for immunotherapy care requires careful evaluation of functional status, protocols for immune-related adverse events management, standardization for assessments of clinical responses, and ensuring equitable access to care. ctDNA and AI-assisted radiomics are promising adjuncts to clinical care, but still require multi-center prospective validation before adoption into routine practice.

Collectively, a TP53 abnormality at copy number (12/26, all cnLOH), sequence (55/60) and protein expression (46/48) level was detected in all 60 cases. In conclusion, integrated high-resolution copy number and histomolecular analysis expanded the spectrum of genetic changes associated with DHG-H3 G34, including the presence of universal TP53 abnormalities with frequent cnLOH-a copy number abnormality that has been largely unrecognized-for this new 2021 World Health Organization central nervous system tumor type.