Comprehensive study of FOXA1-chromatin-modulating prostate cancer risk variants
Thesis event information
Date and time of the thesis defence
Place of the thesis defence
Auditorium K101 of the Faculty of Biochemistry and Molecular Medicine (Aapistie 7), Oulu University.
Topic of the dissertation
Comprehensive study of FOXA1-chromatin-modulating prostate cancer risk variants
Doctoral candidate
Master of clinical medicine Binjie Luo
Faculty and unit
University of Oulu Graduate School, Faculty of Biochemistry and Molecular Medicine, Disease Networks research unit
Subject of study
Biochemistry and molecular medicine
Opponent
Ph.D. / Asocciate professor Jian Yan, City University of Hong Kong
Custos
Ph.D / Professor Gonghong Wei, Faculty of Biochemistry and Molecular Medicine(FBMM), Oulu University
A detailed study of how changes in a gene called FOXA1 affect prostate cancer risk by influencing DNA activity
Prostate cancer is one of the most common cancers in men worldwide, with genetics playing a key role in its development. My research focused on understanding how specific genetic variations, particularly in non-coding regions of DNA, influence prostate cancer risk. These variations can affect how genes are regulated without altering the actual genetic code.
I studied a gene called FOXA1, which acts as a "pioneer" factor, opening up tightly packed DNA to allow other important proteins to interact with it. FOXA1 is crucial in prostate cancer because it helps regulate many other genes that control cell growth and survival.
Through advanced techniques, I discovered specific genetic changes, known as single nucleotide polymorphisms (SNPs), in regions where FOXA1 binds to DNA. These changes influence how strongly FOXA1 can interact with the DNA, which in turn affects the activity of nearby genes. Among these, I identified key genes, like TLE4, USP39, and CPNE1, that play roles in the development and progression of prostate cancer.
One exciting finding was that these genes are involved in processes like blood vessel formation (angiogenesis), which is critical for tumor growth. Clinically, patients with high levels of FOXA1 and its related genes tended to have worse outcomes, suggesting these pathways could be targeted for new treatments. For example, therapies that block blood vessel growth could be promising for these patients.
Overall, my study sheds light on the genetic and biological mechanisms underlying prostate cancer, offering insights that may lead to better diagnostic tools and treatments in the future.
I studied a gene called FOXA1, which acts as a "pioneer" factor, opening up tightly packed DNA to allow other important proteins to interact with it. FOXA1 is crucial in prostate cancer because it helps regulate many other genes that control cell growth and survival.
Through advanced techniques, I discovered specific genetic changes, known as single nucleotide polymorphisms (SNPs), in regions where FOXA1 binds to DNA. These changes influence how strongly FOXA1 can interact with the DNA, which in turn affects the activity of nearby genes. Among these, I identified key genes, like TLE4, USP39, and CPNE1, that play roles in the development and progression of prostate cancer.
One exciting finding was that these genes are involved in processes like blood vessel formation (angiogenesis), which is critical for tumor growth. Clinically, patients with high levels of FOXA1 and its related genes tended to have worse outcomes, suggesting these pathways could be targeted for new treatments. For example, therapies that block blood vessel growth could be promising for these patients.
Overall, my study sheds light on the genetic and biological mechanisms underlying prostate cancer, offering insights that may lead to better diagnostic tools and treatments in the future.
Last updated: 25.11.2024