Raquel Santana da Cruz

I am a qualified postdoctoral from Georgetown University, Washington, DC with a plethora of experience and expertise with cell culture and animal models to study metabolism and cancer development. I earned my bachelor?s degree in Biology at Centro Universitário São Camilo, Sao Paulo, Brazil. Throughout these four years, I have taken over two internships with cancer research, where I was involved in a joint research project on the effect of an adequate nutritional therapy could attenuate inflammatory mediators after surgical trauma, which is a critical step for avoiding post-operative immune dysfunction and multiple organ failure. I obtained a Bachelor of Education becoming a qualified high school teacher (intermediate/ superior levels) in Brazil. In 2016, I earned my Ph.D. in the field of Food Science, at the Faculty of Pharmaceutical Sciences, University of Sao Paulo. During this course, I have furthered my research strategies, targeting breast cancer programming in early-life, specifically whether zinc supplementation or deficiency in pregnancy period changes the susceptibility of female offspring to chemically induced mammary carcinogenesis in mouse models. Currently, I?m doing my postdoctoral at Georgetown University, where I have put these tactics and expertise the directly develop the project which seeks to understand how paternal experience may affect offspring breast cancer risk. For that we have been analyzing transcriptomic data to determine altered pathways involved in the inherited breast cancer and pancreatic cancer risk and if epigenetics markers those alterations. My extraordinary ability has already translated into two first-author manuscripts, which was recently published in Breast Cancer Research and Endocrine-Related Cancer. The first published manuscript describes our findings on how ancestral malnutrition leads to metabolic rewiring in female offspring?s mammary tissues and tumors through the LKB1/AMPK pathway in a mouse model. My findings could help explain how different breast cancer metabolic phenotypes arise and may be relevant to health disparities in breast cancer. The other manuscript in which I?m also the first author describes that parental obesity in pre-conception (fathers) or pregnancy (mothers) is associated with the accelerated development of pancreatic cancer in the next generation. My findings give to support the epidemiologic study suggesting that childhood and early life overweight/obesity and metabolic dysfunction are more strongly associated with pancreatic cancer than obesity that develops later in life. Interventions to reduce adiposity and metabolic dysfunction in early life may be an effective way to prevent pancreatic cancer and likely other malignancies. The postdoctoral position has allowed me to gain new expertise and knowledge to become an independent researcher in cancer and metabolism. (Source: Lattes Curriculum)