Accession Number : ADA463709


Title :   Molecular Characterization of Squamous Cell Carcinomas From Recessive Dystrophic Epidermolysis Bullosa


Descriptive Note : Final rept. 29 May 2002-31 Aug 2006


Corporate Author : THOMAS JEFFERSON UNIV PHILADELPHIA PA


Personal Author(s) : Mahoney, My G ; Rodeck, Ulrich ; Uitto, Jouni


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/a463709.pdf


Report Date : Sep 2006


Pagination or Media Count : 93


Abstract : Patients with recessive dystrophic epidermolysis bullosa (ROEB) frequently present with squamous cell carcinomas (SCCs) probably as a result of chronic blistering and extensive scarring. These tumors are clinically aggressive as they metastasize readily. The metastasis-associated protein (MTA)-1, a transcription suppressor, is overexpressed in several epithelial neoplasms including SCCs. Our preliminary results demonstrate that MTA1 expression is induced by activation of the epidermal growth factor receptor (EGFR). As deregulation of EGFR signaling is frequently observed in aggressive epithelial neoplasms we propose to study the role of EGFR signaling and MTA1 expression in SCCs derived in ROEB patients. Our Specific Aims are to establish cell lines derived from SCCs in non-ROEB and ROEB patients, characterize the malignant phenotype of these cells as it relates to EGFR expression and signaling and to expression of MTA1, examine the contribution of EGFR/MTA1 to proliferation, invasiveness, and cell survival and identity EGFRdependent signaling pathways contributing to MTA1 expression in these cells. The results from this research will provide invaluable tools for future analysis of the pathology of carcinoma cells and will ascertain whether EGFR/MTA1 signaling pathways contributes significantly to the metastasis and invasiveness of SCC derived from ROEB patients.


Descriptors :   *EPITHELIUM , *PROTEINS , *CANCER , *SCARS , SIGNAL PROCESSING , EPIDERMIS , METASTASIS , NEOPLASMS , SURVIVABILITY , ACTIVATION


Subject Categories : Biochemistry
      Medicine and Medical Research


Distribution Statement : APPROVED FOR PUBLIC RELEASE