Are nutrient addicts. Normal cells survive stress by becoming quiescent, but oncogenic mutations drive continuous growth making cancer cells vulnerable. 


Traditional cancer therapies are toxic. Newer, targeted therapies are limited by tumor heterogeneity and the development of resistance. 


that act as global regulators of nutrient uptake have inspired us to create small molecules with similar activities but superior drug properties. 

Welcome to the Edinger Lab

We use interdisciplinary, collaborative approaches to overcome challenging problems in the field of cancer metabolism. Rather than focusing on individual anabolic enzymes and metabolites, we target intracellular trafficking pathways to more globally disrupt nutrient acquisition. This holistic approach should limit the development of drug resistance and produce new therapies that are broadly active against cancers with many different driver mutations. By starting with endogenous molecules that have been optimized by evolution to balance growth suppression with toxicity, we can design compounds that are safe for normal cells despite their multi-faceted, anti-cancer actions. We embrace the pleiotropic actions of these compounds – their parallel effects allow them to function as single-agent combination therapies, generating complementary, anti-neoplastic actions without the pharmacologic complications associated with administering multiple drugs.


Develop innovative cancer therapies that are less toxic and more effective than currently available drugs both when used as single agents and in combination with existing therapies.


We target apical, regulatory nodes to disable multiple oncogenic pathways simultaneously. Using drug-like variants of natural molecules that control growth limits the toxicity of this approach.



By expanding our understanding of how cancer cells acquire and process nutrients, we hope to uncover new targets for cancer therapies and increase our knowledge of how cells respond to stress.

Aimee Edinger, VMD/PhD

Aimee Edinger is a professor of Developmental and Cell Biology in the UC Irvine School of Biological Sciences and a member of the NCI-designated Chao Family Comprehensive Cancer Center at UCI. She joined UCI in 2005 after completing a PhD in Virology, veterinary training (VMD), and a postdoctoral fellowship in Cancer Metabolism at the University of Pennsylvania in Philadelphia. Edinger lab research in leukemia, prostate, and breast cancer models has been funded by the National Cancer Institute, the National Institute of General Medical Sciences, the American Cancer Society, the Department of Defense’s Congressionally Directed Medical Research Program, the University of California Cancer Research Coordinating Committee, the Gabrielle’s Angel Foundation, the Ono Pharma Foundation, the William Lawrence and Blanche Hughes Foundation, the UCI Chao Family Comprehensive Cancer Center, the Anti-Cancer Challenge, and UCI Applied Innovation. Dr. Edinger is an inventor on six patents with others in process.

Professor Edinger has taught several of UCI’s undergraduate and graduate core courses and is actively engaged in the development of an Honors curriculum focused on critical analysis of primary research data and intellectual risk-taking. The Edinger lab includes a cohort of dedicated undergraduate researchers who make key contributions to our discovery efforts and publications. Dr. Edinger’s efforts to support UCI’s teaching mission have been recognized by a Chancellor’s Award for Excellence in Undergraduate Research and a Golden Apple teaching award from the School of Biological Sciences. Dr. Edinger has served as the Equity Advisor for the School since 2016. In this role, she works with School leadership to promote inclusive excellence and diversity among our faculty, staff, and students.

Current research in the Edinger Lab focuses on:


Sphingolipids have been called “tumor suppressor lipids” because they slow cell growth, induce differentiation, and trigger programmed cell death. Sphingolipids were named after the Sphinx due to their enigmatic actions. We dissect the complex molecular mechanisms underlying the ability of sphingolipids to restrict cancer initiation and growth with a focus on how these lipids control the endocytosis of cell-surface nutrient transporter proteins and the decision point where these proteins are either recycled back to the plasma membrane or sent to the lysosome for degradation. This work has revealed evolutionarily-conserved mechanisms for growth control that are disrupted in cancer cells.


Nutrient delivery to tumor cells is limited by abnormal, leaky blood vessels. When glucose, amino acids, and other building blocks are limited, cancer cells scavenge macromolecules from the tumor microenvironment and then degrade them into subunits that are used to fuel growth. Macropinocytosis is a non-specific, bulk uptake process through which macromolecules can be engulfed by membrane ruffles that close into large (0.2 – 5 μm) macropinosomes. Our work has shown that prostate and breast cancers rely on macropinocytosis to support their growth and survival. Inhibitors of macropinocytosis limit tumor growth in mice. We are dissecting the molecular signals that control macropinocytosis and exploring its role in tumor growth and progression with the goal of developing safe and effective inhibitors that can be used therapeutically.


In collaboration with chemist Stephen Hanessian, PhD, we have developed novel synthetic sphingolipids with anti-cancer properties. Like natural sphingolipids, our compounds slow cell growth, induce differentiation, and kill cancer cells. Unlike endogenous sphingolipids, our drug-like versions are resistant to metabolism, water-soluble, and orally bioavailable. We have demonstrated that these molecules are safe and effective in models of colon, prostate, and breast cancer. This work has led to the launch of a start-up biotech company that is moving these molecules to clinical trials in cancer patients. Through chemoproteomics conducted in collaboration with Pierre Thibault’s group at the University of Montreal, we are using our panel of analogs to dissect the protein targets responsible for the multifaceted effects of sphingolipids.


Antisense oligonucleotides (ASO) can, in principle, trigger the degradation of any cellular RNA. While many barriers to the widespread clinical use of ASO have been overcome by medicinal chemistry advances over the last three decades, the application of this powerful platform technology is limited by the inefficient entry of ASO into the cytosol of target cells. Our efforts to understand the signals that control endolysosomal trafficking have suggested several new ways to increase ASO uptake and release. Small molecules that potentiate ASO activity would have widespread clinical applications in patients with many diseases, not just cancer.