Adrianne Wallace-Povirk, PhD
Elucidating drivers of plasticity in subtypes of pancreatic cancer
Pancreatic cancer is not a uniform disease but is divided into two main subtypes, "classical" and "basal." Basal pancreatic cancer is more aggressive than classical, with poorer prognosis and worse response to therapy. These subtypes represent opportunities for personalized medicine if unique biological targets can be found between the two. Additionally the subtypes are not stationary but plastic — they can interconvert, which alters signalling in the tumor and the response to therapy. This project focuses on deciphering one of those plasticity factors, believed to be a critical driver of the subtypes: testing its influence on the ability of pancreatic cancer cells to achieve plasticity, on specific drug sensitivity, and its expression in donated patient tissue.
The work will establish the importance of this factor as a critical driver of the basal subtype, and as a potential biomarker of disease.
"I am passionate about solving the most difficult and puzzling diseases, and so my work has spanned from studying cisplatin-resistant ovarian cancer during graduate school to pancreatic cancer now, as a postdoctoral fellow. As a graduate student at Wayne State University my work focused on cancer metabolism and the role of one-carbon inhibitors on both tumor cells and tumor-associated macrophages. Now, as a postdoctoral fellow at the Henry Ford Pancreatic Cancer Center with Drs. Howard Crawford and Sita Kugel, I am studying the epigenetic factors which regulate the subtypes of pancreas cancer. My projects have focused on transcription factors and drug resistance as they influence plasticity between classical and basal pancreas cancer. The long-term goal is to decipher the differential biology between the subtypes in order to find actionable drug targets to move to clinical trials."
Seed grants start at $50,000 — awarded by scientists, reported on annually.
Donate →Adrianne Wallace-Povirk, PhD
Elucidating drivers of plasticity in subtypes of pancreatic cancer
Pancreatic cancer is not a uniform disease but is divided into two main subtypes, "classical" and "basal." Basal pancreatic cancer is more aggressive than classical, with poorer prognosis and worse response to therapy. These subtypes represent opportunities for personalized medicine if unique biological targets can be found between the two. Additionally the subtypes are not stationary but plastic — they can interconvert, which alters signalling in the tumor and the response to therapy. This project focuses on deciphering one of those plasticity factors, believed to be a critical driver of the subtypes: testing its influence on the ability of pancreatic cancer cells to achieve plasticity, on specific drug sensitivity, and its expression in donated patient tissue.
The work will establish the importance of this factor as a critical driver of the basal subtype, and as a potential biomarker of disease.
"I am passionate about solving the most difficult and puzzling diseases, and so my work has spanned from studying cisplatin-resistant ovarian cancer during graduate school to pancreatic cancer now, as a postdoctoral fellow. As a graduate student at Wayne State University my work focused on cancer metabolism and the role of one-carbon inhibitors on both tumor cells and tumor-associated macrophages. Now, as a postdoctoral fellow at the Henry Ford Pancreatic Cancer Center with Drs. Howard Crawford and Sita Kugel, I am studying the epigenetic factors which regulate the subtypes of pancreas cancer. My projects have focused on transcription factors and drug resistance as they influence plasticity between classical and basal pancreas cancer. The long-term goal is to decipher the differential biology between the subtypes in order to find actionable drug targets to move to clinical trials."
Seed grants start at $50,000 — awarded by scientists, reported on annually.
Donate →