A team of Weill Cornell Medicine investigators is working to cross-train the next generation of cancer researchers in cancer biology and the use of artificial intelligence tools for research.

Recently, a significant study conducted collaboratively by multiple hospitals in Shanghai was published in the prestigious journal SCIENCE CHINA Life Sciences. This work uncovers for the first time that ovarian cancer drives tumor growth and metastasis by secreting IL-1β-enriched extracellular vesicles (EVs), which activate the NF-κB signaling pathway in adipose-derived stem cells (ADSCs), thereby inducing adipose tissue senescence and associated metabolic disorders. The team has identified two targeted intervention strategies: the senolytic combination of dasatinib and quercetin, or the natural NF-κB inhibitor resveratrol. Both approaches markedly eliminate senescent ADSCs, ameliorate metabolic abnormalities, and suppress ovarian cancer progression. This study provides novel insights into treating ovarian cancer by modulating the tumor microenvironment (TME) and targeting senescent cells, and underscores the translational potential of natural compounds including quercetin and resveratrol in clinical applications.

Relevance exists between tumorigenesis and embryonic development. Distinct clinical and molecular features, as well as the relationship between the pattern of lymphoma invasion and germ layer development remain largely unknown. Researchers identified a germ layer-dependent specification of extranodal invasion (ENI) in diffuse large B-cell lymphoma. Upon R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) treatment, mesoderm-originating ENI (ENI-mesoderm) was significantly associated with inferior progression-free survival and overall survival, as compared to ectoderm-originating ENI (ENI-ectoderm) and endoderm-originating ENI (ENI-endoderm). Representative oncogenic mutations were MYD88, PIM1, and TBL1XR1 in ENI-ectoderm, TP53 and TET2 in ENI-endoderm, and MYD88, PIM1, TBL1XR1, and CD79B in ENI-mesoderm. Notably, organotrophic migration exhibited temporal disparities corresponding to germ layer development, occurring from ectoderm- to endoderm- and mesoderm-originating organs, with a similar trajectory to the germ layer process. Single-cell RNA sequencing revealed that malignant B cells follow a developmental trajectory mirroring the germ layer process, differentiating from a progenitor state enriched with NF-κB and T-cell activation signaling into two distinct branches by either upregulated B-cell receptor signaling (Path I) or sustained T-cell activation (Path II). Regarding immune checkpoints, ENI-ectoderm, ENI-endoderm, and ENI-mesoderm exhibited significant upregulation of LGALS9, PD-L1, and B7-H3, respectively. Their findings thus contributed to a better understanding of crosstalk between lymphoma progression and embryonic development, providing new insights into targeted approaches against germ layer-dependent invasion in cancer treatment.