FGFR2 fusion

In patients with cholangiocarcinoma previously treated with immune checkpoint inhibitors (n = 20), the combination regimen achieved an ORR of 20.0% and a disease control rate of 75.0%. These findings support further development of tinengotinib, both as monotherapy and in combination with immunotherapy.

In summary, our study establishes the comprehensive molecular atlas and a targeted therapeutic subtyping framework, revealing therapeutic vulnerabilities and providing novel insights for advancing precision oncology in OCCC management.

Integrated genomic and transcriptomic profiling refines prognostic stratification in cholangiocarcinoma independent of therapeutic actionability. KRAS-TP53 co-mutation and the Mesenchymal transcriptomic subtype represent independent high-risk markers detectable on routine FFPE tissue. These features complement actionable alterations and may inform patient selection and clinical trial design.

Pemigatinib plus paclitaxel demonstrated antitumor activity with an acceptable safety profile in FGFR2-amplified gastric cancer. Further investigation is warranted to elucidate resistance mechanisms and validate these findings in larger cohorts.

The most common baseline regimen was gemcitabine + cisplatin (34.4%). Treatment patterns, adherence, OS, HCRU, and costs demonstrated consistent trends across racial subgroups. Real-world pemigatinib treatment patterns and survival outcomes were consistent with findings from clinical trials and support continued use of pemigatinib across diverse patient groups as a key second-line treatment for CCA.

One oncocytic case showed HRAS and AKT1 activating mutations; the other basaloid case had a FGFR2::SORB3 fusion. Spatial transcriptomics revealed divergent intra- and inter-tumoral signatures emphasizing the transcriptomic heterogeneity within biphasic components.

Systemic chemotherapy with gemcitabine plus cisplatin has remained the standard first-line treatment for more than a decade because most patients are diagnosed at an advanced or unresectable stage, but the associated survival benefit is limited. Accordingly, optimizing patient selection by integrating molecular and immunologic characteristics has become a critical objective for improving clinical outcomes. This review provides an overview of the recent progress in immunotherapy and targeted therapy for BTC, focusing on pivotal clinical trials, therapeutic efficacy, current limitations, and future perspectives for personalized treatment strategies.

In each molecular category, secondary alterations can occur; most notably TERT promoter and TP53 mutations occur with increasing frequency in high-grade differentiated, poorly differentiated, and anaplastic thyroid carcinomas. This article will review the diagnostic, prognostic, and therapeutic significance of molecular alterations across the spectrum of follicular cell derived thyroid tumors and discuss strategies for investigating unusual molecular alterations encountered in clinical practice.

Unlike HCC, roughly 45% of iCCA harbor alterations amenable to precision oncology approaches, including fibroblast growth factor receptor 2 (FGFR2) fusions, isocitrate dehydrogenase 1 (IDH1) mutations, ERBB2 alterations, and BRAF mutations. In this review, we explore how this framework has reshaped liver cancer care and discuss the resulting breakthroughs in management and emerging directions that may further improve therapeutic strategies.

Framing the FGF-FGFR network as an integrated rheostat offers a unifying mechanistic paradigm that links epithelial damage, metabolic dysregulation, and cancer development. It underscores the need for context-selective therapeutic interventions that reconcile tissue repair with long-term oncogenic risk.

P3, N=480, Recruiting, J-Pharma Co., Ltd. | Initiation date: Jan 2026 --> Apr 2026

P2, N=30, Recruiting, Elevar Therapeutics | Not yet recruiting --> Recruiting