Thomas Graeber, Ph.D.

Professor, Molecular and Medical Pharmacology, Director, UCLA Metabolics Center

Dr. Graeber takes an interdisciplinary ‘systems biology’ approach that merges biology, chemistry, mathematics and computation/bioinformatics to understand how cancer cells communicate with their environments, process nutrients and evade therapies. Dr. Graeber gathers multiple types of large data sets from patient tumor samples and then applies computational approaches to find trends, such as how tumor cells metabolize nutrients differently from other cells. The ultimate goal of this work is to identify new ways to diagnose and treat cancer on a cellular, patient-specific level.

Dr. Graeber aims to make advances in understudied cancers with few or no available targeted therapies. Rather than focusing on how cancer affects one specific organ, such as the prostate or lungs, he looks for commonalities among different cancer types in order to identify vulnerabilities that can be targeted by new drugs or cellular therapies. He is currently collaborating with clinician scientists to identify the common genetic activities that enable aggressive, treatment-resistant cancers from different tissues to metastasize.

Another area of focus in Dr. Graeber’s lab is determining how cancer cells de-differentiate, or revert to an earlier stage of development. De-differentiation can also be linked to cancer stem cells, which are able to self-renew and give rise to all cell types found in a tumor. De-differentiated cells can evade common treatments such as chemotherapy and radiation and cause recurrence of the disease. He discovered that melanomas – cancers that arise from the cells that produce pigments – can be divided into four distinct subtypes according to their stages of differentiation or maturity. He then found that less-mature melanoma cells showed sensitivity to a self-inflicted cell death called ferroptosis. This led to the finding that certain subtypes of melanoma could be targeted by a combination of existing cancer therapies and ferroptosis-inducing drugs.

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