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Search Results to Kay Macleod

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keywords Metastasis
overview The deadliest aspect of the majority of human cancers is metastasis, the multi-step process by which cancer cells escape the confines of the primary site (such as breast, pancreas or other organs) and travel in the circulation to distant sites (such as brain, liver or lungs) where they can lodge, invade and grow out as secondary tumors or metastases. Many factors play into cancer metastasis including how disseminating tumor cells respond to stresses such as nutrient deprivation and altered cellular attachments. These stresses are known to activate a process known as autophagy and research in the Macleod Lab seeks to understand and clarify the role of autophagy in tumor growth and progression to metastasis. We are particularly interested in understanding how defects in the turnover of mitochondria (the energy factory of the cell) by mitophagy, leads to tumor invasion and metastasis. Our research addresses how mitophagy is induced and how mitophagy contributes to cellular homeostasis. This includes examining how physiological stresses, such as hypoxia and nutrient deprivation remodel the mitochondrial reticulum, how mitochondrial stress is sensed in the cell and how mitophagy is coordinated with other mitochondrial quality control pathways to promote cellular function. These mechanisms are frequently deregulated in cancers and research in the Macleod Lab also examines how defective mitophagy and mitochondrial dysfunction contributes to tumor progression and metastasis. Mitochondria are highly dynamic organelles and while their function in metabolism and control of apoptosis is well known, work in the Macleod Lab also examines how mitochondria modulate cell fate more broadly, including stemness and in metaplasia, and how they modulate cell motility and invasiveness. This is performed using novel mouse models, engineered cell lines and primary human tumor samples with a focus on breast, pancreas and liver cancers.

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  • Neoplasm Metastasis