Chronic stress is increasingly being recognized as a major risk factor for cancer. Living with cancer impacts brain’s cognitive processing of stress. However, the true relationship between chronic stress and cancer is unknown, because it is difficult to measure the perception of chronic stress in cancer patients. I have exploited the Drosophila model and developed a novel framework to study the perception and central processing of social isolation, a highly relevant etiological stress factor for chronic diseases, such as cancer, diabetes, and depression. Perception of social isolation is known to promote tumor progression in Drosophila. The goal of this proposal is to combine this framework ...

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Chronic stress is increasingly being recognized as a major risk factor for cancer. Living with cancer impacts brain’s cognitive processing of stress. However, the true relationship between chronic stress and cancer is unknown, because it is difficult to measure the perception of chronic stress in cancer patients. I have exploited the Drosophila model and developed a novel framework to study the perception and central processing of social isolation, a highly relevant etiological stress factor for chronic diseases, such as cancer, diabetes, and depression. Perception of social isolation is known to promote tumor progression in Drosophila. The goal of this proposal is to combine this framework with tumorigenesis models to study the reciprocal relationship between chronic stress and cancer on mechanistic levels. Specifically, to elucidate how chronic stress impacts cancer progression, I will use neural, genetic, behavioral, and environmental manipulation strategies to block or accelerate the perception of social isolation and apply profiling methods in tumor tissues to identify molecular mechanisms that mediate this “mind-to-body” conversation underlying chronic stress-mediated cancer progression. On the reciprocal side, to delineate the “body-to-mind” pathway, I hypothesized that change in stress-sensitive health behaviors, particularly sleep, can serve as the body’s own early diagnostic alarm to signal tumor onset. I will systematically document health behavior phenotypes in a suite of drug-induced, age-induced, and transgene-induced tumorigenesis fly models. Lastly, I will establish a transgenic high throughput platform to study “oncohistones,” driver mutations in aggressive pediatric cancers, and investigate how histone mutations initiate tumorigenesis, as well as impact sleep behaviors. Investigating the mechanisms by which chronic stress and cancer interact will ultimately lead to treatments to alleviate the suffering caused by chronic stress and cancer.

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