Pancreatic Cancer

B1.23.2 treatment of the human KLM-1 pancreatic cancer model in humanized (NSG-IL15) mice provides evidence of suppression of tumor growth. Such anti-MHC-I mAb that block inhibitory KIR/HLA interactions may prove useful for tumor immunotherapy.

These interactions suggest that MRW constituents' function as non-nucleoside DNMT-1 inhibitors and ROS-immune modulators that disrupt oncogenic feedback loops and re-activate apoptotic pathways. Collectively, these findings identify MRW as a multi-target phytomedicine integrating ROS-mediated oxidative stress, epigenetic remodeling, and immune-apoptotic signaling, supporting its translational potential as a low-toxicity adjunct strategy to conventional pancreatic cancer therapies.

Combinatorial nanobody-based CAR-M and CAR-NK therapy reprograms the TME and establishes a CXCL9-driven feed-forward loop between macrophages and NK cells, leading to synergistic innate immune activation and potent tumor control. This strategy provides a mechanistically grounded and translationally feasible framework for next-generation CAR-based immunotherapies targeting MSLN-expressing solid tumors.

P1, N=46, Recruiting, AstraZeneca | N=162 --> 46 | Trial completion date: Aug 2039 --> Jul 2029

IL-12 expression also augmented the direct oncolytic effect of oHSV-2 in immunodeficient hosts. This synergistic approach achieves durable potent tumor clearance with reduced CAR-T doses, offering a transformative strategy against pancreatic cancer and other challenging solid malignancies.

Interestingly, several prostate cancer-associated genes were also associated with breast, cervical, and lung cancers. These findings suggest potential biological mechanisms linking immune cells to cancer development and progression, highlighting the complex role of the immune system in cancer.

Collectively, these findings establish estrogen as a key modulator of CAF heterogeneity and highlight a novel mechanism of tumor-stroma cross-talk with potential therapeutic implications for stroma-directed interventions in pancreatic cancer. See related article by Manoukian et al., p. 571.

18F-NOTA-R49 demonstrates high affinity and specificity and excellent tumor-targeting properties. It shows better diagnostic efficacy than 18F-FDG in various malignant tumors, indicating a significant clinical translation potential.

Specifically, we identified the GTP‒Gly/Asp/Val12Ras‒Gln61Ras‒Tyr64Ras‒Ile36Ras‒Ile803RBD pathway that exhibits divergent behavior in wild-type versus mutant systems. The interaction dynamics represented here may serve as a good reference point for studies aiming to develop mutant-specific targeting against tumors harboring Ral overactivity.

It is the first pancreatic carcinoma type in which a basal molecular phenotype can be indicated clinically by both imaging and histopathology, with major potential management implications (as it is also enriched in actionable targets like ARID1A). Recognition of this category is critical for cancer research, as it offers an invaluable group to study plasticity, stroma versatility, necrosis mechanisms, and the basal type in pancreatic cancer.

These results suggest that cardiac surgery with CPB increases the plasma levels of several growth factors, thus potentially promoting pancreatic cancer cell proliferation, as seen in the in vitro study using serum from non-cancer patients.