Page 47 - The Hormel Institute 2024 Annual Report

Our research focuses on uncovering key mechanisms for preventing and treating chronic diseases, especially cancer. A
major goal is to understand the complex interac- tions between tumor cells and the tumor micro- environment, which influence cancer progres- sion, metastasis, and resistance to therapies.
Currently, we are focusing on skin cancer. Solar ultraviolet (UV) light, a well-known envi- ronmental carcinogen, triggers inflammation and contributes to the rise of non-melanoma skin cancer (NMSC) cases each year. Reducing the occurrence of cutaneous squamous cell carcinoma (cSCC) is vital to lowering the high treatment costs and severe outcomes linked to this disease.
UV-induced DNA damage plays a critical role
in skin damage, immune system modulation, and cancer development in NMSC. UV radiation causes direct DNA mutations, leading to genetic instability, which in turn sparks inflammation and weakens the immune system, creating favorable conditions for tumor formation. Pro- longed UV exposure damages the skin, disrupts immune defenses, and promotes cancer growth.
Understanding these processes is key to devel- oping better prevention and treatment strate- gies. Our current work is focused on identifying key molecular targets that connect UV exposure, DNA damage, immune response, and skin can- cer development. This will help us improve the timing and methods for targeted immunopre- vention, potentially reducing the rise of non-mel- anoma skin cancer and improving prevention strategies for other epithelial cancers.
In addition to our work on non-melanoma skin cancer, we are also studying melanoma, one of the deadliest cancers. Despite significant prog- ress in melanoma treatments, including target- ed and immune therapies that have improved patient outcomes, many still die due to drug resistance, metastasis, and limited responses
to immune treatments. In this project, we are analyzing data from the The Cancer Genome Atlas and GEO databases, along with our RNA- seq results, to identify new therapeutic targets. We then use pre-clinical models to explore how these targets impact drug resistance, metastasis, and immune therapy responses in melanoma.
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