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Historically, tumors have been traditionally viewed as collections of cells, each with their own distinct properties, and therefore independently responsible for many of the observed cellular and molecular alterations. However, in the era of single-cell technologies, tumors have increasingly been recognized as communities of cancer cells that are organized and communicate with each other by niche-forming factors.
We have used the PILGRM pipeline for the retrospective analysis of a large public database of TCGA HCC tumors (n=325) to extract the information of the mutational status of the tumors in three metastasis driver pathways, namely NOTCH, WNT and EGFR. Based on this analysis, and our previous work on liver cancer, we hypothesized that NOTCH signaling may contribute to the development of metastatic HCC. Therefore, we created a NOTCH high-risk model and showed that this epigenetically induced NOTCH high-risk model develops more liver and lung metastases, when compared to a NOTCH low-risk model. NOTCH inhibition by Dibenzazepine (DBZ) inhibits the progression of this in vivo high-risk model. Further, inhibition of NOTCH signaling by DBZ also inhibits the development of liver and lung metastases in nude mice carrying NOTCH high-risk subcutaneous tumor xenografts. Overall, this study establishes that NOTCH signaling plays a critical role in the development of metastases from NOTCH high-risk HCC tumors.
Recent technology and advances in the field of cancer research has demonstrated a large role of the tumor microenvironment in mediating the effects of therapies. Immune cell infiltrates show significant heterogeneity in many types of cancer, having been shown to play an important role in tumor progression, controlling metastasis and treatment resistance. The question is how these infiltrates are modulated in response to therapeutic interventions? While solid tumors are seldom characterized by specific immune infiltrates, specific immune cell types are associated with improved survival in gastrointestinal cancers, acute myeloid leukemia, chronic lymphocytic leukemia and Hodgkin lymphoma. In this study we looked at the effect of a platinum-based drug, cisplatin, and immune checkpoint blockade on the gut tumor microenvironment. d2c66b5586