Expression of platelet derived growth factor family members and the potential role of imatinib mesylate for cervical cancer

Despite significant achievements in the treatment of cervical cancer, it is still a deadly disease; hence newer therapeutical modalities are needed. Preliminary investigations suggest that platelet-derived growth factor (PDGF) might have a role in the development of cervical cancer, therefore it is...

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Published in:Cancer cell international Vol. 6; no. 1; p. 22
Main Authors: Taja-Chayeb, Lucia, Chavez-Blanco, Alma, Martínez-Tlahuel, Jorge, González-Fierro, Aurora, Candelaria, Myrna, Chanona-Vilchis, Jose, Robles, Elizabeth, Dueñas-Gonzalez, Alfonso
Format: Journal Article
Language:English
Published: England National Library of Medicine - MEDLINE Abstracts 02-10-2006
BioMed Central Ltd
BioMed Central
BMC
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Summary:Despite significant achievements in the treatment of cervical cancer, it is still a deadly disease; hence newer therapeutical modalities are needed. Preliminary investigations suggest that platelet-derived growth factor (PDGF) might have a role in the development of cervical cancer, therefore it is important to determine whether this growth factor pathway is functional and its targeting with imatinib mesylate leads to growth inhibition of cervical cancer cells. PDGF receptors (PDGFR) and their ligands are frequently expressed in cervical cancer and the majority exhibited a combination of family members co-expression. A number of intronic and exonic variations but no known mutations in the coding sequence of the PDGFRalpha gene were found in cancer cell lines and primary tumors. Growth assays demonstrated that PDGFBB induces growth stimulation that can be blocked by imatinib and that this tyrosine kinase inhibitor on its own inhibits cell growth. These effects were associated with the phosphorylation status of the receptor. The PDGFR system may have a role in the pathogenesis of cervical cancer as their members are frequently expressed in this tumor and cervical cancer lines are growth inhibited by the PDGFR antagonist imatinib.
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ISSN:1475-2867
1475-2867
DOI:10.1186/1475-2867-6-22