FGFR2 fusion

Our findings provided preliminary evidence that novel FGFR2 fusions might act as primary oncogenic drivers in a rare subset of KIT/PDGFRA wild-type GISTs. These cases highlight the importance for comprehensive genomic profiling and suggest that fibroblast growth factor receptor-targeted inhibitors could be a potential therapeutic strategy for advanced or imatinib-resistant diseases, warranting further investigation in larger cohorts.

Cross-cancer analyses underscore the necessity of PDAC-specific strategies despite shared genomic drivers. Collectively, these insights support routine germline and somatic testing, enrollment in biomarker-matched trials, and rational combination strategies, establishing molecular profiling as central to advancing precision treatment in pancreatic cancer.

Immunotherapy in PSC-associated BTCs appeared safe, with a potential signal of effectiveness. Given the sample size and retrospective design, these results are hypothesis-generating. Together, these results demonstrate the unique biology underlying PSC-associated BTCs, highlighting the need for prospective trials and the development of specialized treatment strategies.

HER2 amplification was associated with worse OS; dMMR and BRCA mutations showed a trend toward improved OS.ConclusionReal world first-line chemoimmunotherapy for advanced BTC achieved outcomes comparable to those in pivotal trials. The ECOG performance status, serum albumin level, and HER2 status were prognostic for OS, supporting the importance of baseline patient selection and molecular profiling in treatment planning.

Of the 85 cases, disease control was achieved in 49 cases, 44 cases of which were biliary tract cancer. FGFR2 might be a promising therapeutic target not only for cholangiocarcinoma with fusion but also for esophagus/stomach cancer and breast cancer with FGFR2 alterations.

BTCs have been traditionally managed with gemcitabine and cisplatin (GC), but this standard of care has shown limited efficacy due to early recurrence, high resistance rates, and molecular heterogeneity...Additionally, novel regimens including nanoliposomal irinotecan and dual ICI combinations represent viable second-line options...Personalized treatment guided by molecular characteristics is now central to improving outcomes. Future efforts must prioritize the identification of biomarkers, clarification of resistance mechanisms, and optimization of multimodal treatment strategies to maximize patient benefit.

The possibility of molecular glioblastoma should be considered for these tumors. It is thus recommended to perform genetic testing on diffuse gliomas with PLNTY features in order to facilitate integrated diagnosis and provide molecular evidence for accurate evaluation of prognoses.

For adjuvant treatment, capecitabine (based on the BILCAP trial) and S-1 (from the ASCOT trial) have become standard regimens. Neoadjuvant therapy using gemcitabine-platinum combinations and locoregional strategies such as hepatic artery infusion chemotherapy (HAIC) and yttrium-90 radioembolization (Y-90 TARE) have improved resectability and survival outcomes...FGFR2 fusions, IDH1 mutations, and BRAF V600E mutations can be targeted with inhibitors such as pemigatinib, ivosidenib, and dabrafenib-trametinib, respectively, showing promising response rates in clinical trials...Combination strategies involving PD-1 inhibitors with radiotherapy or anti-angiogenic agents are further expanding the potential for treatment. Future efforts should focus on standardizing resectability criteria, expanding access to molecular profiling, and accelerating Phase III trials.

Introduction: Gastrointestinal stromal tumors (GISTs) are primarily driven by mutations in KIT (KIT proto-oncogene receptor tyrosine kinase) or PDGFRA (platelet-derived growth factor receptor alpha), but resistance to tyrosine kinase inhibitors (TKIs) such as imatinib remains a major clinical challenge. Although direct evidence remains limited, particularly regarding DNA repair and polymorphisms, FGFR2-targeted therapies (e.g., erdafitinib, pemigatinib) show potential, especially in combination with TKIs or DNA-damaging agents. Future research should prioritize GIST-specific clinical trials, the development of FGFR2-driven models, and standardized molecular diagnostics to validate FGFR2 as a therapeutic target.

The Hannover CLIP technique effectively combines controlled, recirculated HOPE with vvECMO. This approach minimizes ischemic injury to the liver, kidneys, and intestines and facilitates safe resection of highly complex central liver tumors under TVE.

Targeted therapies based on genomic information are limited in the treatment of advanced gastric cancer. Thus, this case suggests that pemigatinib may represent a promising targeted therapy option for patients with advanced gastric cancer harbouring FGFR2 alterations.

Evidence from recently completed and ongoing clinical trials evaluating these therapies, both as monotherapy and in combination with chemotherapy and/or immunotherapy, supports this shift. Continued research aimed at refining treatment selection and advancing personalized therapeutic strategies is essential, with the goal of achieving longer survival and improved quality of life for patients undergoing second-line therapy for CCA.