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Associate Professor of Oncology
Associate Professor of Cell and Regenerative Biology
The goal of Dr. Weaver’s research is to determine the consequences of mitotic defects on tumor initiation, progression and response to chemotherapy. Defects during mitosis result in the production of daughter cells with an abnormal number of chromosomes, a condition known as aneuploidy. Aneuploidy is a hallmark of tumor cells, which has led to the hypothesis that aneuploidy promotes tumors. The Weaver laboratory has found in animal models and cell culture that aneuploidy can both promote and suppress tumors, depending on the rate of chromosome missegregation. Low rates of chromosome missegregation are weakly tumor promoting, while high rates of chromosome missegregation lead to cell death and tumor suppression due to the loss of one or more essential chromosomes. Recently, they have also shown that high rates of chromosome missegregation suppress tumor growth and progression, rather than tumor initiation. These results suggested the hypothesis that inducing high rates of chromosome missegregation could be a useful strategy for tumor therapy. Indeed, the Weaver laboratory has recently shown that paclitaxel (TaxolTM), a cornerstone of chemotherapy for the last 30 years, causes chromosome missegregation on multipolar spindles in breast cancers. Future experiments will utilize cell culture, mouse models and clinical studies to leverage our fundamental knowledge of mitosis to improve treatment outcomes for cancer patients.
Perform a PubMed Search for Dr. Beth A. Weaver’s Publications.