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Patek Lab

   

 

Paul Q. Patek

Professor, Department of Microbiology

University of Hawaii

 

    Postdoctoral Fellow and Assistant Research Professor
    The Salk Institute, La Jolla, California

 

    Ph.D., University of Texas, Graduate School of Biomedical Sciences
    Houston,  Texas

 

    B.S., Biology, University of Southern California

               

Contact:
   University of Hawaii
   Department of Microbiology
   Snyder Hall 207, 2538 The Mall
   Honolulu, HI 96822


   Tel: 808 956-7025
   Fax: 808 956-5339
   email: patek@hawaii.edu

   
     

 

Our Research

 

Cancer develops from normal cells through a number of cellular changes. We have developed cell lines that have some of the changes associated with cancer.  By studying the cells that are intermediate between normal and cancer, we hope to better understand cancer development.

Important steps on the pathway from normal to cancer include acquisition of resistance to normal growth regulatory mechanisms.  Some of these mechanisms involve cell death.  That is, usually, cells with abnormal behavior can be triggered by internal or external stimuli to die.  Many cancer cellsí failure to properly undergo programmed cell death is key in their survival and their ability to grow continuously.

Our studies are aimed at understanding the role of certain genes and proteins associated with programmed cell death and evaluating whether these genes and proteins are functioning properly in cancer cells.

Our current work is focused on determining how expression of cancer-associated genes c-myc and p53 affects sensitivity to TNF and FasL induced programmed cell death in cell lines representing various stages on the pathway to cancer.  We are also using our cell lineages to determine whether activation of caspase-2 plays a role in the differential sensitivity of cells to TNF- and FasL-mediated cytotoxicity. 

       In addition, studies are underway to  characterize TNF- and FasL-induced changes in mitochondrial membranes.   This involves monitor the appearance of mitochondrial-associated proteins involved programmed cell death such as caspase-2, caspase-9, cytochrome c, and apoptosis Inducing factor.

In addition to the above studies, we are involved in development of electronic biosensors to detect environmental toxins or microorganisms.  These sensors use antibodies or nucleic acids as highly specific receptors for binding material in the environment.  The binding produces a signal in an electronic device developed by Dr. James Holm-Kennedy (University of Hawaii Department of Electrical Engineering).

 

   Some Publications

Patek, P.Q., Lin, Y. and Collins, J.L.  Natural Cytotoxic Cells and Tumor Necrosis Factor Activate the Same Lytic Mechanism. J. Immunol. 138:1641-1646 (1987).

Collins, J.L. Kao, M-S, and Patek, P.Q. Humans Express Natural Cytotoxic (NC) Cell Activity That Is Similar To Murine NC Activity. J. Immunol. 138:4180-4184 (1987).

Lin, Y., Case, P.G., and Patek, P.Q.  Inhibition of Tumor Necrosis Factor and Natural Cytotoxic Cell Lytic Activity By A Spleen Cell-Elaborated Factor. Immunol. 63:663 (1988)

Patek, P.Q. and Collins, J.L.  Tumor Surveillance Revisited: Natural Cytotoxic Cells Deter Tumorigenesis. Cell Immunol. 116:240-249 (1988).

Lin, Y., Collins, J.L., Case, P.G. and Patek P.Q.  The Effect of Mycoplasma on Natural Cytotoxic Activity and the Release of Tumor Necrosis Factor-Alpha By Spleen Cells.  Infect. and Immun. 56:3072-3075 (1988).

Patek, P.Q., Lin, Y. and Case, P.G.  Cell Lines Cultured at High Density Are Resistant to Lysis By Tumor Necrosis Factor and Natural Cytotoxic Cells. Proc. Soc. Exp. Biol. Med. 190:234-239 (1989).

Patek,  P.Q.  and Lin, Y.  Natural Cytotoxic Activity Is Not Necessarily Mediated By The Release of  Tumor Necrosis Factor. Immunol. 67:509-513 (1989).

Patek, P.Q. and Collins, J.L. Natural Cytotoxic Cells Activity. In: Natural Immunity, Ed., D. Nelson. pp 147‑171. Academic Press,  San Diego (1989).

Patek, P.Q. and Lin, Y.  The In Vitro Selection of a Cell Line For Resistance to Lysis by Tumor Necrosis Factor Selects For Reduced Tumorigenicity.  J. Immunol. 146:3457-3461 (1991).

Sasaki, C. and Patek, P.Q.  Inhibition of Tumour Necrosis Factor Mediated Lysis by Spleen Cell Conditioned Medium. Int. J. Immunopharmac, 16:301-309 (1993).

Matsui, N. and Patek, P.Q.  Transformed B Cell lines Express Cell‑Associated Tumor Necrosis Factor and Mediated Natural Cytotoxic Activity. Cellular Immunol., 154:358-368  (1994)

Sasaki, C. and Patek, P.Q.  The involvement of protein tyrosine kinase activity in a tumor necrosis factor resistance mechanism, Proc. Soc. Exp. Biol. Med. 210:25-32 (1995).

Park, D.J.and Patek, P.Q.  Park, D.J. and Patek, P.Q.  Detergent and enzyme treatment of apoptotic cells for the observation of DNA fragmentation.  BioTechniques, 24:558-560 (1998).

Sasaki, C, and Patek, P.Q.  Transformation is associated with an increase in sensitivity to TNF-mediated lysis as a result of an increase in TNF-induced protein tyrosine phosphatase activity. Int. J Cancer. 81:141-147, (1999).

Park, D.J. Chang, W-C. and Patek, P.Q.  Protein kinase C mediates TNF-induced internucleaosomal DNA fragmentation. Biochem. Pharm., submitted.

 

Grant support:

Hawaii Community Foundation  1-04 to 2-06.  Programmed cell death and cancer progression. P.I. Paul Patek

COBRE subproject. 1-04 to 12-05.  Biosensors.   P.I James Holm-Kennedy, co-P.I Paul Patek et al.

U.S. Dept. of Agriculture, 9/1/02 to 8/30/06. New Methodologies for detection and identification of invasive bacterial pathogens, P.I., Anne Alvarez, Co-P.I. Paul Patek et al.