About me
What are the mechanisms which promote the generation and maintenance of cancer cell heterogeneity in human tumors?
I am an NIH F31 fellow pursuing a Ph.D. in Biomedical Engineering at The University of Texas at Austin under the mentorship of Dr. Amy Brock. My work is specifically focused on creating and applying novel tools in systems biology to reveal the impact of intercellular interactions and cell-cell fusion in cancer progression.
Research philosophy
Cancer is a horrific disease, yet a cure for cancer stands miles away until our understanding of the fundamental mechanisms that promote tumor formation and evolution catch up.
Drawn to cancer research in both fascination and horror, I am unafraid to collect tools and perspectives across disciplines to generate and test hypotheses. I currently take an eco-evolutionary perspective and use experimentation, bioinformatics, and mathematical modeling to better understand the nature of cancer. My lifetime goal is to see the results my work have a transformative impact on the life of just one cancer patient and hopefully many, many more.
Key skills
Flow Cytometry and FACS
Live-cell imaging
Karyotyping
Ecological modeling
ClonMapper DNA barcoding
NGS preparation and analysis
Single-cell analysis
Research themes
Tumor heterogeneity
Cell-cell fusion
Polyploidy
Aneuploidy
Tumor ecology
Chemoresistance
Current Projects
The role of gross ploidy alterations in chemotherapeutic response
Ploidy altering mechanisms such as cell-cell fusion and whole genome doubling (WGD) can drive intratumoral heterogeneity and may play a prominent role in chemotherapeutic response. This project seeks to quantify the prevalence and consequences of large scale ploidy alterations during chemotherapeutic treatment at single cell resolution. We expect to reveal targetable drivers of whole genome instability with radical implications for the treatment and prognosis of many cancer types.
Characterizing subpopulations within isogenic cancer cell populations
Subpopulations can arise and persist within isogenic populations of cancer cells. This project seeks to understand the mechanisms which promote co-existence of multiple phenotypic subpopulations over time and uncover the conditions which provide asymmetric selection to steer the evolution of the bulk population. We expect to reveal targetable interaction modalities which may inform treatment strategies for heterogeneous tumors.
andrealgardner@utexas.edu