gemcitabine

P3, N=0, Withdrawn, University Hospital, Rouen | N=10 --> 0 | Not yet recruiting --> Withdrawn

We report the case of a 26-year-old man with a primary mediastinal yolk sac tumor who progressed despite multimodal therapy, including etoposide, ifosfamide, and cisplatin chemotherapy, high-dose carboplatin and etoposide with autologous stem cell transplantation, gemcitabine and paclitaxel, surgical debulking, and radiation therapy. No further disease-directed therapies were available, and he ultimately died from progressive metastatic disease. This case highlights the aggressive biology of platinum-resistant primary mediastinal yolk sac tumors, illustrates primary resistance to programmed death-1 inhibition, and underscores the urgent need for more effective salvage strategies in this high-risk population.

A 40-year-old woman with FIGO stage IVB, BRCA-wildtype HGSOC developed rapid multi-drug resistance following neoadjuvant chemotherapy, optimal cytoreduction, and progression on maintenance olaparib/bevacizumab, gemcitabine, and a USP1 inhibitor. By utilizing topoisomerase I inhibitors, agents like YL205 bypass microtubule-stabilization resistance induced by prior taxane exposure, while "bystander effects" address intratumoral heterogeneity. Longitudinal, biomarker-matched strategies and proactive toxicity management are essential to achieving deep tissue clearance in heavily pretreated HGSOC.

P2, N=33, Not yet recruiting, University of Washington | Initiation date: Jun 2026 --> Sep 2026

P1/2, N=6, Not yet recruiting, Shanghai 6th People's Hospital

P1, N=12, Suspended, City of Hope Medical Center | Recruiting --> Suspended

Analyzed variables included demographics, tumor characteristics (location, stage), NAC regimens (FOLFIRINOX, GEMCAP, gemcitabine monotherapy), response to therapy (RECIST criteria), surgical outcomes (resection rate, R0 resection), CA19-9 levels, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and survival outcomes (overall survival (OS) and progression-free survival (PFS))...Elevated pre-treatment CA19-9, NLR, and PLR may identify patients less likely to benefit from NAC. Biomarker-driven trials are warranted to optimize patient selection and personalize treatment strategies, especially in resource-constrained settings.

This study broadens our understanding of SCARB2 in ovarian cancer. SCARB2 overexpression induces extensive lysosomal reprogramming in A2780 ovarian cancer cells and modulates chemotherapy response.

P2, N=49, Active, not recruiting, The Lymphoma Academic Research Organisation | Recruiting --> Active, not recruiting

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.

An analysis of paired serum samples from pancreatic cancer patients revealed that gemcitabine-based first-line therapy elicits a marked increase in circulating FTH1 protein, underscoring its potential as a real-time indicator of therapeutic efficacy. Collectively, FTH1 orchestrates iron rewiring and redox homeostasis under nutrient stress within the tumor microenvironment, driving PDAC progression and offering dual clinical value as both a target and a therapeutic-response indicator.

The patient did not respond to gemcitabine and cisplatin-based systemic chemotherapy. Selpercatinib, a selective inhibitor of receptor tyrosine kinase RET, blocks RET kinase activity by binding to its adenosine triphosphate-binding site, thus preventing the kinase from phosphorylating substrates and halting oncogenic signaling. The patient was treated with selpercatinib, which produced a durable response lasting over 15 months in this chemotherapy-refractory patient, highlighting the efficacy of selpercatinib in HOOK3-RET fusion-positive pancreatic cancer.