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“Weak Links” in Cancer Proteostasis Networks as New Therapeutic Targets

“Weak Links” in Cancer Proteostasis Networks as New Therapeutic Targets


Martin Kampmann, PhD
Assistant Professor, Department of Biochemistry and Biophysics
University of California, San Francisco
San Francisco, California


All cells must balance the amount of protein that they produce with the amount of protein that they discard. To achieve this balance, cells use robust systems to maintain protein homeostasis, a process that is termed proteostasis. Cancer cells are rapidly dividing and tend to accumulate genetic changes that result in mutated proteins. It is thought that this higher burden of mutated proteins makes cancer cells unusually dependent on the cellular systems that maintain proteostasis. Drugs that partially disrupt proteostasis have transformed patient care in some types of cancer, such as multiple myeloma. However, less than 1 percent of the factors within proteostasis pathways have been explored as possible targets for cancer therapeutics providing many possible opportunities to develop new cancer drugs targeted at these pathways. This study proposes to use cutting-edge genomics methods, coupled with dedicated drug discovery methods, to identify and validate the next generation of drug targets in the proteostasis network in multiple myeloma, castration-resistant prostate cancer, and aggressive forms of these diseases. Dr. Kampmann has pioneered a new genomics approach to rapidly identify the “weak points” in cancer cell proteostasis. The ultimate goal of this study is to create a genetic map of alterations in the dynamic proteostasis network, and to develop drugs that target those pathways as new cancer therapeutics.

Updated: May 2016