Kathryn Lawson, Ph.D.

Associate Professor


Dr. Kathryn LawsonMidwestern University 
Arizona College of Osteopathic Medicine
Department of Biochemistry
Agave 201N
19555 N. 59th Ave.
Glendale, AZ 85308

Office: (623) 572-3238
email: klawso@midwestern.edu

 

EDUCATION

Ph.D. Biochemistry University of Arizona   1998
B.S.  Microbiology University of Arizona 1992

RESEARCH SUMMARY

The worldwide incidence of oral and oropharyngeal cancer is estimated at 400,000 new cases per year.  Early detection is critical, as the survival rate for oral cancer drops significantly once tumors have become invasive.  In many tissues, including tissues of the oral cavity, tumor development is accompanied by alterations in a group of calcium-dependent cell adhesion proteins called cadherins.  Alterations in expression of P-cadherin occupy a unique position within the spectrum of events associated with oral tumor development. The prototypical epithelial adhesion protein E-cadherin, noted to function as a tumor suppressor, is downregulated during oral tumor progression.  In contrast,  the related epithelial protein, P-cadherin, appears by histological analysis to undergo an upregulation during early oral dysplasia, only to be displaced or lost in later-stage cancers. The majority of studies of P-cadherin dysplastic progression are anecdotal in nature, and few studies have yet been performed to analyze the molecular contributions of P-cadherin to the establishment/progression of early stage cancers.  The goal of the proposed research is to determine the role of P-cadherin in facilitating oral tumor development.    To this end, my laboratory uses a tissue culture-based approach using genetically altered oral precancer and oral tumor lines to examine the role of P-cadherin in facilitating oral tumor development.

Project I: A major focus of the laboratory is the role of P-cadherin in oral dysplasia, in which cells abnormally proliferate but are not yet considered to be cancerous.  The increase in P-cadherin seen oral tissue during dysplasia, and the subsequent loss of  P-cadherin in malignant carcinomas suggests a key role for P-cadherin in driving oral tumor progression. We are utilizing a dysplastic human oral cell model system with altered levels of P-cadherin to identify the effects of altered cadherin expression on cellular aggression, including motility, invasion, and apoptosis.  

Project II: A second avenue of investigation in the laboratory is the influence of P-cadherin in growth-factor receptor-mediated signaling pathways.  We have previously shown that P-cadherin alters Epidermal Growth Factor and Insulin-like Growth Factor signaling pathways in dysplastic cells and oral tumor cells, respectively.  Current work in the laboratory is aimed at elucidating the mechanism(s) by which P-cadherin alters ligand-induced signaling pathways, and characterizing the effects of these alterations on cell aggressiveness.

Select Publications

P-cadherin potentiates ligand-dependent EGFR and IGF-1R signaling in dysplastic and malignnant oral keratinocytes.  
Lysne D, Johns J, Walker A, Ecker R, Fowler C, Lawson KR.  Oncol Rep 2014 Dec; 32(6):2541-8.  
PMID: 25322858

The cytoplasmic domain of N-cadherin modulates MMP-9 induction in oral squamous carcinoma cells.  
Walker A, Frei R, Lawson KR.   Int J Oncol. 2014 Oct; 45(4):1699-706.  
PMID: 25175499