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Grant: Operating Grant - Priority Announcement: Breast Cancer

University of Alberta

$650,485.00

Regulation of EGFR-mediated Cell Signaling and Endocytosis during Mitosis

EF 2010-11

Résumé
Cell growth is controlled by various growth factors. Growth factors bind to their receptors at cell surface to stimulate cell growth by activating these receptors. Over-activation of these receptors will cause the over-growth of the cells, leading to cancer development. The growth factor and its receptor involved in this grant are called epidermal growth factor (EGF) and EGF receptor (EGFR). EGFR over-activation happens in many cancers especially in breast cancer, ovarian cancer, skin cancer and lung cancer. EGFR over-activation correlates to poor prognosis, drug resistance, cancer metastasis and lower survival rate. All these make EGFR the top choice as a target for developing cancer therapies. Cell division is the most dramatic period of the cell cycle, involving a major reorganization of virtually all cell components. A major difference between cancer cells and normal cells is that the cancer cells are much more mitogenic and frequently enter mitosis for proliferation. Therefore, most cancer drugs are designed to specifically target the mitotic cells. However, the role of growth factor receptor during cell division is very rarely and poorly studied. In this proposal we plan to study how the growth factor receptor controls cell signalling during cell division, what is the molecular mechanism regulating the internalization and trafficking of the receptor during cell division, and how the internalization of the receptor controls the receptor activity during cell division. The results generated from our research will certainly strengthen our ability to develop better therapeutic treatment for various cancers.
Programme
Operating Grant - Priority Announcement: Breast Cancer
Bénéficiaire
Emplacement
Alberta, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database

Tel que publié

Id
215438
Name
Wang Zhixiang
Region
Alberta
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Cell Biology & Mechanisms of Disease
Projecttitle
Regulation of EGFR-mediated Cell Signaling and Endocytosis during Mitosis
Programtype2
Operating Grants
Orgnameinp2
University of Alberta
Cihramount2
$650,485
Cihrequipment2
$0
Programname2
Operating Grant - Priority Announcement: Breast Cancer
Keyworddelim
Cell Cycle; Dimerization; Egf Receptor; Endocytosis; Endocytosis Motif; Kinase Activity; Mitosis
Abstract
Cell growth is controlled by various growth factors. Growth factors bind to their receptors at cell surface to stimulate cell growth by activating these receptors. Over-activation of these receptors will cause the over-growth of the cells, leading to cancer development. The growth factor and its receptor involved in this grant are called epidermal growth factor (EGF) and EGF receptor (EGFR). EGFR over-activation happens in many cancers especially in breast cancer, ovarian cancer, skin cancer and lung cancer. EGFR over-activation correlates to poor prognosis, drug resistance, cancer metastasis and lower survival rate. All these make EGFR the top choice as a target for developing cancer therapies. Cell division is the most dramatic period of the cell cycle, involving a major reorganization of virtually all cell components. A major difference between cancer cells and normal cells is that the cancer cells are much more mitogenic and frequently enter mitosis for proliferation. Therefore, most cancer drugs are designed to specifically target the mitotic cells. However, the role of growth factor receptor during cell division is very rarely and poorly studied. In this proposal we plan to study how the growth factor receptor controls cell signalling during cell division, what is the molecular mechanism regulating the internalization and trafficking of the receptor during cell division, and how the internalization of the receptor controls the receptor activity during cell division. The results generated from our research will certainly strengthen our ability to develop better therapeutic treatment for various cancers.
Competitiondate
201009
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Wang, Zhixiang
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $650,485~ $0~