Tumors are heterogeneous ecosystems in which cancer cells coexist within a complex tumor immune microenvironment (TIME). The malignant, stromal, and immune cell compartments establish a plethora of bidirectional cell-cell communication crosstalks that influence tumor growth and metastatic dissemination, which we are only beginning to understand. Cancer cells either co-opt or promote the formation of new blood and lymphatic vessels to cope with their need for nutrients and oxygen.
View Article and Find Full Text PDFp57 is a cyclin/CDK inhibitor and a negative regulator of cell proliferation. Here, we report that p57 regulates intestinal stem cell (ISC) fate and proliferation in a CDK-independent manner during intestinal development. In the absence of p57, intestinal crypts exhibit an increased proliferation and an amplification of transit-amplifying cells and of Hopx ISCs, which are no longer quiescent, while Lgr5 ISCs are unaffected.
View Article and Find Full Text PDFAlthough melanoma is notorious for its high degree of heterogeneity and plasticity, the origin and magnitude of cell-state diversity remains poorly understood. Equally, it is unclear whether growth and metastatic dissemination are supported by overlapping or distinct melanoma subpopulations. Here, by combining mouse genetics, single-cell and spatial transcriptomics, lineage tracing and quantitative modelling, we provide evidence of a hierarchical model of tumour growth that mirrors the cellular and molecular logic underlying the cell-fate specification and differentiation of the embryonic neural crest.
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