Pancreatic Ductal Adenocarcinoma

The correspondence rate between primary PDAC and the matched metastatic sites was: 70.0% for PDAC/LNM, 93.3% for PDAC/PM, and 100.0% for PDAC/LIVM. This study shows a high rate of correspondence of CLDN18-positivity between primary PDAC and different metastatic sites, providing a strong rationale for further exploring and testing anti-CLDN18.2 therapeutic strategies in this lethal malignancy.

This validation study demonstrates statistically significant improvements in PancreaSeq GC for mucinous cysts and advanced neoplasia, establishing it as a clinically valuable tool for the preoperative evaluation of pancreatic cysts.

Collectively, these results underscore the potential of PRP as a therapeutic candidate for disrupting the intricate interactions within the PDAC TME. Further research and clinical investigations are necessary to validate the translational potential of PRP as an adjunct therapy for PDAC.

P3, N=501, Active, not recruiting, Revolution Medicines, Inc. | Recruiting --> Active, not recruiting

Molecular testing is feasible and may even be more successful in cytologic smears than in biopsies or resections. High diagnostic yield and rapid processing favor their integration into routine molecular workflows. The superior performance of smears may relate to reduced stromal content and minimal processing delays. Cytologic specimens showed 100% DNA QC success, even when RNA QC failed, supporting their reliability. Although RNA analysis had a modest failure rate, its overall success suggests it can be incorporated into routine testing, particularly as fusion-driven targets gain clinical relevance.

We implement an extended neoadjuvant regimen-typically a minimum of eight cycles of FOLFIRINOX-aiming for normalization of CA19-9 levels...IMV, inferior mesenteric vein; LGV, left gastric vein; SMA, superior mesenteric artery artery; SV, splenic vein; SMV, superior mesenteric vein; RHA, right hepatic artery Prioritizing tumor biology, meticulous preoperative planning, and attention to key vascular technical details to ensure radical resection represent our three core oncologic landmarks. Further international, multicenter studies are needed to validate and promote the standardization of surgery for BR-PC and LAPC.

The prognostic model EFFscore exhibits remarkable predictive performance, accurately reflecting the malignant potential of PDAC. P2RY6 serves as a key oncogenic factor driver in PDAC, its targeted inhibition significantly suppresses tumor progression, highlighting its dual potential as a diagnostic biomarker and therapeutic target.

This study provides a spatially resolved molecular map of IPMN progression, delineating key transcriptomic and immune signatures. These findings advance the understanding of IPMN biology and highlight potential biomarkers for risk stratification and therapeutic strategies.

Our data further demonstrated that pharmacological or genetic inhibition of c-Myc effectively reversed the resistance phenotype mediated by HDAC5 loss, suggesting a therapeutic strategy centered on "KRAS-MYC dual-node blockade." Furthermore, the expression levels of HDAC5 and the acetylation status of c-Myc may serve as potential biomarkers for predicting the therapeutic response to MRTX1133. These findings provide insights into overcoming resistance to KRASG12D inhibitors and offer potential biomarkers and combinatorial therapeutic strategies for precision treatment of PDAC.

Additionally, fostamatinib inhibited PDAC cell proliferation even in the absence of viral infection, while ruxolitinib did not. Our data suggest that fostamatinib may be repurposed as an effective drug that enhances OV therapy in PDAC by promoting OV replication and suppressing tumor growth.

The effector Th and Tc are the dominant prognostic T cell subsets in PDAC, whereas Treg abundance alone is an incomplete surrogate of immunosuppression. These findings describe the immunobiological landscape of PDAC.

Currently, selpercatinib, larotrectinib, and repotrectinib are approved by the FDA for the treatment of certain solid tumors harboring specific gene fusions. Recent studies on zenocutuzumab resulted in the FDA-accelerated approval for NGR1 fusion-positive NSCLC and PDAC. Germline mutations may specifically increase responsiveness to poly(ADP-ribose) polymerase (PARP) inhibitors or platinum-based treatments. Comprehensive genomic profiling, incorporating fusion detection and germline testing, is essential to identify patients who may benefit from precision-based approaches.