Heather Giza

Heather Giza

Graduate Student


I did my undergraduate work at Binghamton University, State University of New York, just a few hours from where I grew up. There I obtained a B.S in biochemistry and a B.A in Studio Art -- along the way I was able to tutor and T.A for students in biochemistry/organic chemistry courses. Through undergrad I conducted research in the Ming An/Lan Yao lab studying a pH low insertion peptide (pHLIP), looking at it's insertion dynamics for my honor's thesis in research. In the summers I worked internships at Regeneron pharmaceuticals in NY. All of these experiences let me explore biomedical research and have brought me to graduate school today where I now work with Costas Lyssiotis to study cystine metabolism in pancreatic cancer.

Outside of my scientific endeavors, I'm a yogi and consider myself an active artist on a few formats, whether that be traditionally with oil paints or with making scientific illustrations. I am also a huge fan of camp fashion- I love embroidering my own clothes and sewing old fabrics together to make weird outfits. And I also make soundcloud beats in my down time-- musically i'm trying to coin the name "PhG" (because my initials are HG :) ) but we'll see where that goes, currently I'm running out of fake emails to give FL studio for their free demo software!

Research Interests

In Costas lab I will exploring the metabolic vulnerabilities of pancreatic cancer through cystine metabolism. The purpose of the project is to see if modulating the cystine metabolism of cancer/supporting cells can be used beneficially to potentiate immunotherapy. To give some context-- a more recent form of non-apoptotic cell death called ferroptosis involves iron and peroxided lipids. Typically, these lipids are quenched by enzymes like GPX4. Blocking of GPX4 with an inhibitor is one way to achieve ferroptosis, but these chemicals aren't available for in vivo use. However, GPX4 uses GSH as a cofactor- GSH being a cheap antioxidant of the cell. To make GSH and keep GPX4 running, cells will import cystine through a system xCT transporter, and from there it can be used to make GSH.

Our lab has seen that pancreatic cancer cells can be sensitized to ferroptosis by knocking out the system xCT transporter or treating with cysteinase, and it's even been seen that these cells show classic markers of immunogenic cell death. Because of these findings we're interested in seeing just how sensitive these cells are to ferroptosis in vivo, but there are still many mysteries I'll be looking into. For example, knocking out system xCT sensitizes tumors to ferroptosis and impairs tumor growth, but relapse is also observed meaning that ferroptosis alone isn't sufficient to take down these tumors. Given that the complex tumor microenvironment in pancreatic cancer supports tumor growth, I will be looking at to what extent T-cells, myeloid cells, and fibroblast play a role in ferroptosis. I'll see if depleting these tumors of myeloid cells causes a CTL infiltration, and finally I'll be looking to see if combinatorial targeting the immune system and cysteine metabolism can synergistically promote ferroptosis to get tumor regression.


cell culture, genetic mouse models, confocal microscopy imaging, histoimmunochemistry, flow cytometry, metabalomics


"Biophysical studies of pHLIP", Giza H., An M., Yao L., Klees L., at Binghamton University Undergraduate Conference in Chemistry

"An Alternative Method of Titer Determination" Giza H., Junaid Z., at Regeneron Pharmaceuticals Intern Expo


2017 Binghamton University Summer Scholars Award 2017
2015-2019 New York State STEM Scholarship 2015-2019
2015-2019 New York State Merit Scholarship award 2015-2019
2018 Best poster/prettiest postern Regeneron Pharmaceuticals Intern expo
2018-2019 David P Mancini Fine Arts Scholarship
2018-2019 Sharon S Brehm Scholarship
2019 ACS Division of Organic Chemistry Outstanding Senior Student Award