Deciphering the roles of micro-environmental stress types in cancer initiation and progression
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What drives a cancer’s evolution, including its initiation? This has been the focus of many published studies in the past century. Among the various proposals, the predominating theory in the past four decades has been that cancer is the result of genomic mutations. However, the mutation-centric view of cancer drivers have been challenged by a number of recent studies, partially inspired by the fact that only a very few common mutations have been observed across different tissues of the same cancer type or even different cells in the same tissue. In this dissertation, I have listed four research topics in my explorative research of the roles of micro-environmental stresses in cancer initiation and progression in the past five years. The topics include: (1) Cancer may be a pathway to cell survival under persistent hypoxia and elevated ROS: A model for solid-cancer initiation and early development; (2) Population Dynamics inside Cancer Biomass Driven by Repeated Hypoxia-Reoxygenation Cycles; (3) Elucidation of Drivers of High-Level Production of Lactates throughout a Cancer Development; and (4) A bi-clustering based approach to comprehensively predict the functional gain or loss of somatic mutations. Through these projects, I have raised one functional model of the role of hypoxia and oxidative stress in cancer initiation, one mechanistical model of the detailed mechanisms that how inflammation induce cancer, identified several possible dyregulations of stromal cells and their association with cancer imitation and progression, and a series of method to model cancer transcriptomics and genomics data.