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Viviane Muniz


viviane-muniz@uiowa.edu
Mentor: Dawn Quelle, Ph.D.
Lab Room: 2-369 BSB
Lab Phone: 319-335-7663

In vivo analyses of ARF signaling using a novel mouse model of pancreatic cancer and Parf cKO mice

The ARF tumor suppressor is inactivated in 40% of pancreatic ductal adenocarcinoma (PDAC), which is a highly aggressive, lethal cancer. We recently discovered a Partner of ARF (Parf) that is required for ARF function in cells lacking p53, which represents a majority of PDAC tumors. Parf is highly expressed in the normal pancreas and there is evidence that it is inactivated in human PDAC, supporting the idea that Parf is a tumor suppressor gene. Interestingly, Parf also has ARF-independent activities helps maintain chromosomal stability and inhibits the malignant progression of pancreatic cancer. This leads us to speculate Parf could be targeted for inactivation in both ARF-positive and ARF-negative PDAC tumors. The overall goal of this project is to determine if Parf normally suppresses PDAC development and/or metastasis in vivo. Our first aim is to determine if Parf overexpression or loss by RNAi in pancreatic cancer cells affects tumor formation and metastasis in mice. Our second aim is to cross gene-trapped Parf knockout mice with an established model of PDAC (conditional KrasG12D expression in the pancreas) to address if Parf inactivation cooperates with other mutations to accelerate PDAC progression.

Publications:

Muniz V, Barnes JM, Paliwal S, Zhang X, Tang X, Chen S, Zamba KD, Cullen JJ, Meyerholz DK, Meyers S, Davis N, Grossman SR, Henry MD, Quelle DE. The ARF tumor suppressor inhibits tumor cell colonization independent of p53 in a novel mouse model of pancreatic ductal adenocarcinoma metastasis. Mol Cancer Res. 2011 Jul;9(7):867-77. Epub 2011 Jun 2. PubMed PMID: 21636682; PubMed Central PMCID: PMC3140613.

di Tommaso A, Hagen J, Tompkins V, Muniz V, Dudakovic A, Kitzis A, Ladeveze V, Quelle DE. Residues in the alternative reading frame tumor suppressor that influence its stability and p53-independent activities. Exp Cell Res. 2009 Apr 15;315(7):1326-35. Epub 2009 Jan 27. PubMed PMID: 19331830; PubMed Central PMCID:PMC2665200.

Abstracts:

Muiz V, diTommaso A, Hagen J, Tompkins V, Kitzis A, Ladeveze V, Quelle DE. Residues in the ARF tumor suppressor that influence its stability and signaling activities. Mechanisms & models of Cancer. Cold Spring Harbor, NY. August 2008.

Muniz VP, Barnes JM, Zhang X, Tang X, Chen S, Zamba KD, Cullen JJ, Meyerholz DK, Meyers S, Davis JN, Henry MD, Quelle DE. The ARF tumor suppressor inhibits tumor cell colonization in a novel mouse model of pancreatic ductal adenocarcinoma metastasis. The Biology of Cancer: Microenvironment, Metastasis and Therapeutics. Cold Spring Harbor, NY. April 2011.



Honors and Awards

  • Vere D. Wenger Award, HCCC Cancer Genomics and Cell Growth Program, 2011
  • Tephly Student Travel Award, Department of Pharmacology, 2011
  • Biosciences Program Admissions Committee, 2008
  • MCB Admissions Committee, 2009
  • MCB Retreat Committee, 2011
  • Molecular & Cellular Biology Retreat Travel Award 2011