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Maria Zajac-Kaye, Ph.D.

Maria Zajac-Kaye, Ph.DAssociate Professor

Office: CGRC 360
Email: mzajackaye@ufl.edu
Phone: (352) 273-9153
Fax: (352) 273-8299


Education and Training

Ph.D. – Department of Biochemical and Biophysical Sciences, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, MD (1982)
M.S. – Organic Chemistry, The Johns Hopkins University, Baltimore, MD (1975)
B.S. (Honors) – Chemistry, The City University of New York, New York, NY (1973)

Postdoctoral Training

Post Doctoral Fellow, Department of Experimental Cell Biology, Mt. Sinai School of Medicine, New York, NY (1983-1985)

Biotechnology Fellow, Medicine Branch, National Cancer Institute, NIH, Bethesda, MD (1985-1988)

Research Fellow, Medicine Branch, National Cancer Institute, NIH, Bethesda, MD (1988-1989)

Research Interests

My long-term research interests focus on understanding mechanisms of oncogenic transformation. We have recently studied the role of thymidylate synthase (TS) in tumorigenesis since TS plays a central role in DNA synthesis/repair and high levels of TS have correlated with a poor prognostic outcome in patients with lung, pancreas, colon, and rectal carcinomas. We demonstrated that ectopic expression of catalytically active human TS (hTS) was sufficient to induce a transformed phenotype in mammalian cells both in culture and in transgenic models confirming that it serves as a bona fide cancer therapeutic target. Our current work is focused on defining patterns of cooperation between TS and other cancer genes using a series of defined mouse models. Our goal is to use these transgenic animals to study the in vivo consequences of elevated TS on DNA stability, to test how this relates to tumorigenesis, and to improve the use of TS as a biomarker and therapeutic target.

Research Projects

Development of an animal model to study the effect of thymidylate synthase expression on the biology of exocrine pancreatic cancer

Cooperation of CDKN2A/p16 gene inactivation and thymidylate synthase overexpression in tumor development

Multiple endocrine neoplasia type 1 (MEN1) gene inactivation and thymidylate synthase overexpression in the development of islet cell carcinoma

Targeted drugs and siRNA delivery for pancreatic and lung cancer in an in vitro and in vivo animal models

References

Rony A. Francois(g), Kyungah Maeng(g), Akbar Nawab(p), Frederic J. Kaye(&), Steven N. Hochwald(&), and Maria Zajac-Kaye. 2015. Targeting Focal Adhesion Kinase and Resistance to mTOR Inhibition in Pancreatic Neuroendocrine Tumors. J Nat Cancer Inst. Published online May 2015. 107(8): 123-133. PMID: 25971297.

Cao C(p), Gao R(g), Zhang M(p), Amelio AL(p), Fallahi(&), M, Chen(&), Z, Gu Y(g), Hu C(p), Welsh EA(&), Engel BE(g), Haura EB(g), Cress WD(&), Wu L(&), Zajac-Kaye M, and Kaye FJ. 2015. Role of LKB1-CRTC1 on glycosylated COX-2 and response to COX-2 inhibition in lung cancer. J Natl Cancer Inst. Published on line Dec 2014 107(1): 358-368. | PubMed

Gao R(g), Cao C(p), Zhang M(p), Lopez MC(&), Yan Y(&), Chen Z(g), Mitani Y(&), Zhang L(&), Zajac-Kaye M, Liu B(&), Wu L(&), Renne R(&), Baker HV(&), El-Naggar A(&), and Kaye FJ. 2014. A unifying gene signature for adenoid cystic cancer identifies parallel MYB-dependent and MYB-independent therapeutic targets. Oncotarget. 5(24): 12528-42. | PubMed

Jianliang Zhang(&), Di-Hua He(&), Maria Zajac-Kaye, and Steven N. Hochwald. 2014. A small molecule FAK kinase inhibitor, GSK 2256098, inhibits growth and survival of pancreatic ductal adenocarcinoma cells. Cell Cycle. 13(19): 3143-9. | PubMed

Hui Yang(p), Tal H Salz(g), Daiqing Liao(&), Maria Zajac-Kaye, Suming Huang(&), and Yi Qiu. 2014. Overexpression of histone deacetylases in cancer cells is controlled by interplay of transcription factors and epigenetic modulators. FASEB J. 28(10): 4265-79. | PubMed

Antonio L. Amelio(p), Mohammad Fallahi(&), Frans X Schaub(&), Min Zhang(p), Mariam B. Lawani(&), Adam S. Alperstain(&), Mark R. Southern(&), Brandon M Young(&), Lizi Wu(&), Maria Zajac-Kaye, Frederic J Kaye(&), John L Cleveland(&), and Michael D. Cronkright. 2014. CRTC1/MAML2 Gain-of-Function Interactions with MYC Create a Gene Signature Predictive of Cancer with CREB-MYC Involvement. Proc Natl Acad Sci U S A. 111(32): E3260-8. | PubMed

Hye Seung Lee(p), Min Chen(&), Ji Hun Kim(&), Woo Ho Kim(&), Soyeon Ahn(&), Kyungah Maeng(g), Carmen J. Allegra(&), Frederic J. Kaye(&), Steven N. Hochwald(&), and Maria Zajac-Kaye. 2014. Analysis of 320 Gastroenteropancreatic Neuroendocrine Tumors Identifies TS Expression as Independent Biomarker for Survival. Int J Cancer. 135(1): 128-37. | PubMed

Deniz A. Ucar, Andrew T Magis, Nicholas Lawrence, Said Sebti, Elena Kurenova, Maria Zajac-Kaye, and Steven N. Hochwald. Inhibiting the interaction of cMET and IGF-1R with FAK effectively reduces growth ofpancreatic cancer cells in vitro and in vivo. Anticancer Agents in Medicinal Chemistry, Published on line Dec 14, 2012, v13, 595-602, 2013 | PubMed

Jianliang Zhang, Rony Francois, Renuka Iyer, Mukund Seshadri, Maria Zajac-Kaye and Steven Hochwald.- Current understanding of the molecular biology of pancreatic neuroendocrine tumors. J Natl Cancer Institute v105, 1005-1017, 2013 | PubMed

Ucar, DA, Kurenova, E, Garrett TJ, Cance WG, Nyberg C, Cox A, Massoll N, Ostrov DA, Lawrence N, Sebti SM, Zajac-Kaye M, Hochwald SN. Disruption of the protein interaction between FAK and IGF-1R inhibits melanoma tumor growth. Cell Cycle, 11, 3250-3259, 2012 PubMed

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