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Enhanced oncogenic signalling as a driver of metastasis Instead of co-opting entire developmental, regenerative or homoeostatic programmes, another possible mechanism by which cancer clones can acquire metastatic traits is through optimising or fine-tuning the phenotypic output of already activated oncogenic signalling pathways at the transcriptional level

Cancer stem cells from human breast tumors are involved in spontaneous metastases in orthotopic mouse models

Organelles, metabolism, sex differences, and the epigenome are critical gateways to future discoveries in neuroscience, while clinical investigations require a deep understanding of the biology underlying spatial pathology

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