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Vrushank G. Dave, MS, PhD

Where You Are:
Vrushank G. Dave, MS, PhD

Office  (813) 974-0930

Education And Training
  • Postdoctoral Fellow, University of Cincinnati College of Medicine, 1996 - Cell and Molecular Biology
  • PhD, Jawaharlal Nehru University, 1994 - Biotechnology (Cell & Microbiology)
  • MSc, MS University, 1987 - Biotechnology (Cell & Microbiology)

As a molecular biologist with a keen interest in developing mouse models of solid cancers, my lab, over the last 5 years has generated lung-specific doxycycline inducible & conditional (Cre/loxP) mouse models to elucidate molecular mechanisms of aberrant transcription regulation & cell signaling events lung cancer. We are using systems biology approach mainly focusing to mechanistic understanding of initiation of lung cancer and Epithelail-Mesencymal Transitions (EMT) during the process of metastasis.

The PTEN and the LKB1 lung-specific conditional-deficiency models are also utilized to identify gene signatures of epithelial cell polarity (AJRCB 2008) & Epithelial-Mesenchymal Transition (EMT) regulated by miRNA and master transcription factors Snail, Slug, Twist ZEB1, ZEB2 etc.

We have also developed conditional mouse models for pVHL/HIFs & lung-specific CDC42-Flox mice to identify, enrich and study cancer and normal Stem cell properties

Other interests include Transcriptional regulatory networks in the lung mediated by Calcinurin/NFAT signaling (JBC 2004, JCI 2006) & Structure-function studies on Transcription factor-DNA & protein-protein interaction in specific gene regulation. (MCB 2000, MCB 2000, Biochemistry 2005 & JMB 2006)

  • Malaney P, Nicosia SV, Davé V. One mouse, one patient paradigm: New avatars of personalized cancer therapy. Cancer Lett. 2014 Mar;344(1):1-12. Pubmedid: 24157811.
  • Malaney P, Uversky VN, Davé V. The PTEN Long N-tail is intrinsically disordered: increased viability for PTEN therapy. Mol Biosyst. 2013 Oct;9(11):2877-2888. Pubmedid: 24056727.
  • Pathak RR, Grover A, Malaney P, Quarni W, Pandit A, Allen-Gipson D, Dave V. Loss of Phosphatase and Tensin Homolog (PTEN) Induces Leptin-mediated Leptin Gene Expression: FEED-FORWARD LOOP OPERATING IN THE LUNG. J Biol Chem. 2013 Oct;288(41):29821-29835. Pubmedid: 23963458. Pmcid: PMC3795281.
  • Davé V, Wert SE, Tanner T, Thitoff AR, Loudy DE, Whitsett JA. Conditional deletion of Pten causes bronchiolar hyperplasia. Am J Respir Cell Mol Biol. 2008 Mar;38(3):337-345. Pubmedid: 17921358. Pmcid: PMC2258453.
  • Chaney BA, Clark-Baldwin K, Dave V, Ma J, Rance M. Solution structure of the K50 class homeodomain PITX2 bound to DNA and implications for mutations that cause Rieger syndrome. Biochemistry-Us. 2005 May;44(20):7497-7511. Pubmedid: 15895993.
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