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It is found that ULK3 contributes to autophagy and supports MM cell survival and calls for future development of more selective ULK3-directed therapies, calling for future development of more selective ULK3-directed therapies.
A mathematical model of tumor growth under fluctuating conditions with stochastic phenotypic epithelial-mesenchymal switch as the main mechanism of adaptation is developed, and non-trivial evolutionary outcomes are revealed, depending on the relative time scales of the underlying processes.
The immortalized non-tumorigenic breast epithelial cell line (MCF10A) develops neoplastic clones under fluctuating conditions in-vitro that mimic the harsh tumor microenvironment and is identified as a potential therapeutic target against epithelial-mesenchymal plasticity and metastatic spread in breast cancer.
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