University of Wisconsin Molecular and Cellular Pharmacology Graduate Program

 

Beth A. Weaver , Ph.D.

Assistant Professor
Department of Pharmacology

baweaver@wisc.edu

Trainer in the Following Programs:

  • Molecular and Cellular Pharmacology Program
  • Cellular and Molecular Biology Program

Awards and Honors:

  • 2006-2008 Postdoctoral Fellowship, Philip Morris Foundation
  • 2006 Brigid G. Leventhal Scholar in Cancer Research Award
  • 1999-2002 National Cancer Institute Training Grant Recipient
  • 1999 Teaching Assistant, University of California, San Diego

Research interests: 
1) chromosome segregation during mitosis
2) effects of chromosome missegregation on tumors

Research Description:



Chromosome segregation during mitosis is a highly regulated process designed to create two genetically identical daughter cells.  Errors in chromosome segregation lead to aneuploidy, an abnormal chromosome number.  Aneuploidy has been recognized as a common characteristic of tumor cells for over 100 years.  However, whether aneuploidy is a cause or a consequence of cancerous transformation has been difficult to determine.  This is because most methods of inducing aneuploidy cause additional defects that can promote tumorigenesis, such as DNA damage.  To circumvent this problem, we use cells and animals that develop aneuploidy without other defects due to reduction of the mitosis-specific protein CENP-E.  We have found that aneuploidy in the absence of other defects can indeed promote tumorigenesis.  However, we also made the unexpected discovery that, under certain conditions, aneuploidy can be detrimental to tumor growth, and this finding may have therapeutic implications. 

Future research in the lab will focus on 1) genes required for accurate chromosome segregation; 2) the types of chromosome segregation errors that drive tumor promotion versus tumor suppression; and 3) the context-dependent factors that influence the effects of aneuploidy on normal cells and on tumors.

Selected Publications: Articles on PubMed

  • Weaver BAA and Cleveland DW. (2007). Aneuploidy: instigator and inhibitor of tumorigenesis. Cancer Res. 67:10103-5.

  • Weaver BAA and Cleveland DW. (2007). Comment on A centrosome-independent role for gamma-TuRC proteins in the spindle assembly checkpoint. Science. 18:982.

  • Weaver BAA, Silk AD, Montagna C, Verdier-Pinard P, and Cleveland DW. (2007). Aneuploidy acts both oncogenically and as a tumor suppressor. Cancer Cell. 11:25-36.

  • Weaver BAA and Cleveland DW. (2006). Does aneuploidy cause cancer? Curr Opin Cell Biol. 18:658-67.

  • Weaver BAA, Silk AD, and Cleveland DW. (2006). Nondisjunction, aneuploidy and tetraploidy. Nature. 442:9-10.

  • Weaver BAA and Cleveland DW. (2005). Decoding the links between mitosis, cancer, and chemotherapy: The mitotic checkpoint, adaptation, and cell death. Cancer Cell. 8:7-12.

  • Kops GJPL, Weaver BAA, and Cleveland DW. (2005). On the road to cancer: aneuploidy and the mitotic checkpoint. Nat Rev Cancer. 5:773-85.

  • Kops GJPL, Kim Y, Weaver BA, Mao Y, McLeod I, Yates JR, Tagaya M, and Cleveland DW. (2005). ZW10 links mitotic checkpoint signaling to the structural kinetochore. J Cell Biol. 169:49-60.

  • Weaver BA, Bonday ZQ, Putkey FR, Kops GJPL, Silk AD, and Cleveland DW. (2003). Centromere-associated protein-E is essential for the mammalian mitotic checkpoint to prevent aneuploidy due to single chromosome loss. J Cell Biol. 162:551-63.

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