Leda Helen Raptis, Queen’s University
Department of Biomedical and Molecular Sciences
Professor
Kingston, Ontario
raptisl@queensu.ca
Office:
(613) 533-2462
Expert In
Bio/Research
Cellular interactions with neighbouring cells profoundly influence a variety of signalling events involved in mitogenesis, survival and differentiation. Unlike tissue-culture cells, cells in a tumor have extensive opportunities for adhesion to their neighbours in a three-dimensional structure, t...
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Bio/Research
Cellular interactions with neighbouring cells profoundly influence a variety of signalling events involved in mitogenesis, survival and differentiation. Unlike tissue-culture cells, cells in a tumor have extensive opportunities for adhesion to their neighbours in a three-dimensional structure, therefore in the study of these processes it is important to take into account the effect of surrounding cells. Cadherins recently emerged as a group of cell-cell adhesion molecules playing a key role in the regulation of signalling events as well as the maintenance of tissue architecture.
Our lab has recently demonstrated that engagement of E-cadherin can lead to a dramatic increase in the activity of Stat3, a protein often abnormally activated in cancer. Most importantly, Stat3 activation was independent from a number of tyrosine kinases, including the Src family, IGF1-R, EGFR and Fer, often activated in many cancers. This novel pathway could be a promising target in the treatment of cancers which may be independent from most tyrosine kinase oncogenes known to be activated in many cancers. Our recent work deals with the elucidation of this novel mechanism. We are using two different approaches:
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Our lab has recently demonstrated that engagement of E-cadherin can lead to a dramatic increase in the activity of Stat3, a protein often abnormally activated in cancer. Most importantly, Stat3 activation was independent from a number of tyrosine kinases, including the Src family, IGF1-R, EGFR and Fer, often activated in many cancers. This novel pathway could be a promising target in the treatment of cancers which may be independent from most tyrosine kinase oncogenes known to be activated in many cancers. Our recent work deals with the elucidation of this novel mechanism. We are using two different approaches:
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