Lukas Kenner

This study shows nanoplastics induce DNA mutations in Salmonella by disrupting DNA structure and altering mutational patterns through surface chemistry and DNA topology.

This study establishes a murine tumoroid biobank to identify oncogenic pathways and drug vulnerabilities in prostate cancer, finding that PTEN loss drives cancer pathways and that specific compounds inhibit tumor growth.

This study uses single-cell transcriptomics to analyze T cell lymphomas, identifies developmental origins, and discovers SYK and TIM3 as potential therapeutic targets.

This study identifies castration-tolerant Club-like cells in prostate cancer and shows that targeting FOSL1/AP-1 and PIM kinases reduces their progenitor properties and tumor growth.

This study identifies TRβ as a driver of prostate cancer growth and shows that NH-3 inhibits PCa cell proliferation and tumor growth, particularly in castration-resistant models.

This study demonstrates the use of O-PTIR spectroscopy for label-free detection of micro- and nanoparticles in tissues, showing superior resolution and signal quality compared to FTIR.

This study shows that polystyrene nanoparticles (PS-NPs) cause DNA damage, oxidative stress, migration, and mitogenic pathways in non-malignant lung cells but not in cancer cells.

This study evaluates IQDMA, a multi-kinase inhibitor, as a targeted therapy for cutaneous T-cell lymphoma, showing significant tumor volume reduction and STAT3/5 pathway inhibition compared to PUVA.

The paper shows that IGF-1 reprograms bone mesenchymal stem cells in EWS::FLI1-mutant mice, leading to tumor formation, with Yap1 playing a central role, and suggests combined IGF-1R and YAP/TEAD inhibition as a potential treatment.

This study evaluates small molecule STAT3/5 inhibitors for treating AML and NKCL, showing growth arrest and synergy with existing therapies in vitro and in vivo.

This study shows that activating GP130 in prostate epithelial cells suppresses tumor growth through senescence and immune activation, suggesting a new therapeutic approach.

This study identifies FGFR2 as a driver of resistance to lorlatinib in ALK-expressing neuroblastoma and shows that FGFR inhibition synergizes with lorlatinib to improve outcomes.

This study shows conventional therapy in CRC induces immunoediting and changes immune contexture, with AI identifying mucin deposits as a potential surrogate marker.

This study shows JUN suppresses prostate cancer progression by inducing senescence and immune cell recruitment, with JUN depletion accelerating tumor growth.