Joshua Saldivar, PhD
Portland, Oregon
Assistant Professor of the Division of Oncological Sciences and CEDAR
Knight Cancer Institute, School of Medicine
Oregon Health and Science University
Portland, Oregon
American Association for Cancer Research
Understanding how cancer stem cells form and promote recurrence and metastasis.
Breast cancer causes over 40,000 deaths every year in the U.S. In many instances, cancer malignancy is due to a population of cells in the tumor, known as cancer stem cells. Cancer stem cells promote tumor recurrence following treatment and drive metastasis, both determinants of patient survival. How cancer stem cells form is poorly understood. For his American Association for Cancer Research project supported by BCRF, Dr. Saldivar is working to understand how cancer stem cells emerge in breast cancer to ultimately target these cells with new treatments and improve survival.
Dr. Saldivar is studying an enzyme that responds to DNA damage, called ATR, that promotes the emergence of breast cancer stem-like cells in response to high levels of a protein that regulates cell proliferation, called MYC. In the first year of the project, Dr. Saldivar and his team have focused on developing a laboratory model in which to study how ATR and MYC work together to transforms normal cells into stem cells.
Using this system, Dr. Saldivar will study the activity of ATR and MYC to understand how cancer stem cells emerge and whether drugs targeting ATR, currently being tested in the clinic, could effectively target cancer stem cells in patients.
Joshua Saldivar, PhD is an Assistant Professor of the Division of Oncological Sciences and CEDAR at the Knight Cancer Institute, Oregon Health and Science University. Dr. Saldivar earned his PhD at The Ohio State University in biomedical sciences with an emphasis in genetics and his MS and BS at the University of Arkansas, Fayetteville in food science and biochemistry, respectively.
His research focuses on understanding the mechanisms that coordinate DNA replication and transcription and how deregulation of these two fundamental processes is linked to epigenetic reprograming in cancer, with a particular focus on breast cancer. His previous work as a PhD student in the lab of Dr. Kay Huebner centered on understanding the cellular events that initiate replication stress-induced genome instability in precancerous cells. There, he discovered a novel mechanism for the origin of genome instability and the initiation of the preneoplastic process.
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