Bernice Goldblatt Scholar
Tell us a little about yourself:
I was born and raised in semi-arid northern Mexico, and migrated to the United States while a teenager. As an undergraduate I majored in Pre-Medicine, with academic minors in Chemistry, Physiology, and Biotechnology. I then pursued training in Molecular, Cellular and Developmental Biology, during this experience my interests and appreciation for basic science, and its application to disease matured.
What motivates you to pursue a PhD in cancer biology?
There are several motivations to this, but two of them being pure curiosity and this excitement that arises from exploring the obscure. Cancer is a devastating disease, and is also its devastating nature and complexity that drives me into the lab.
My interests in molecules and cancer biology grew gradually as academic and scientific opportunities became more attainable — it was a realization of science as a passion, but also a vivid awareness on the inequities surrounding access to scientific training and literacy. As a result, one of my central goals with pursuing advanced cancer training is to also contribute bridging accessibility of the academic cancer research enterprise to marginalized communities— from access to cancer research training to clinical trials.
What are you working on now?
My current work in Dr. Shannon Elf’s and Dr. Scott Oakes’ labs focuses on understanding how “cellular stress” in the form of improperly folded proteins alters cancer cell reprograming.
Cancer cells often encounter extrinsic (e.g., hypoxia, nutrient depravation) and intrinsic stress (e.g., somatic mutations, oncogene activation) that compromise protein folding capacity in an organelle known as the endoplasmic reticulum (ER). In response to these stress forms, the ER activates signaling pathways that are involved in dealing with the misfolded protein load and promote adaptation.
One of my projects currently focuses on understanding the role of these ER-stress adaptive signaling pathways in blood cancers, particularly, myeloproliferative neoplasms (MPN) and acute myeloid leukemia (AML), with the ultimate goal of defining whether these ER-stress adaptive signaling pathways represent a therapeutic gain in preclinical models of these malignancies.