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Conference Paper: DNA hypermethylation of TIMP3 gene in invasive breast ductal carcinoma

TitleDNA hypermethylation of TIMP3 gene in invasive breast ductal carcinoma
Authors
KeywordsTIMP3
Invasive ductal carcinoma
Methylation
Issue Date2005
PublisherElsevier France, Editions Scientifiques et Medicales. The Journal's web site is located at http://www.elsevier.com/locate/biopha
Citation
Proceedings of the 1st Annual Conference of OOTR COX-2 and Angiogenesis in Oncology, Hong Kong, 15-16 October 2004. In Biomedicine & Pharmacotherapy, v. 59 n. suppl. 2, p. S363-S365 How to Cite?
AbstractBackground. - Neoplastic cells often display aberrant methylation and silencing of multiple genes, including tumor suppressor genes (TSGs) that regulate critical processes such as cell cycle control, DNA repair and angiogenesis. Tissue inhibitor of metalloproteinase-3 (TIMP3) is an extracellular matrix-bound protein which regulates matrix composition and affects tumor growth, invasion and angiogenesis. It mediates vascular endothelial growth factor (VEGF) by blocking the binding of VEGF to VEGF receptor-2 and inhibits downstream signaling. This study focused on the hypermethylation status of the TIMP3 gene with clinical parameters in invasive breast ductal carcinoma (IDC) samples. Materials and methods. - DNA extraction and methylation specific PCR (MSP) was performed on 173 patients with invasive breast carcinoma. Both specific methylated and unmethylated primers for each gene were used for PCR and the products were visualized on agarose gel. The methylation status of TIMP3 was then compared with corresponding patients' clinicopathologic characteristics. Results. - Methylation frequencies of TIMP3 in the breast cancer samples were 20.81 %. Among the hypermethylated cancers, 50% were tumor grade II-III, 44.44% were positive in lymph node involvement (LN), 36.11% were positive in lymphovascular permeation (LVP); 44.44%, 22.22% and 47.22% for the overexpressions in estrogen receptor (ER), progesterone receptor(PR) and c-erbB2, respectively. Conclusion. - The result demonstrated that hypermethylation of TIMP3 in IDC might be associated with high tumor grading and lymph nodes metastasis, and overexpression of ER, PR and c-erbB2, respectively.
DescriptionThis article belongs to a special issue 'Proceedings of the 1st Annual Conference of OOTR COX-2 and Angiogenesis in Oncology'
Persistent Identifierhttp://hdl.handle.net/10722/205646
ISSN
2015 Impact Factor: 2.326
2015 SCImago Journal Rankings: 0.787
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLui, ELH-
dc.contributor.authorLoo, WTY-
dc.contributor.authorZhu, L-
dc.contributor.authorCheung, MNB-
dc.contributor.authorChow, LWC-
dc.date.accessioned2014-09-26T02:13:28Z-
dc.date.available2014-09-26T02:13:28Z-
dc.date.issued2005-
dc.identifier.citationProceedings of the 1st Annual Conference of OOTR COX-2 and Angiogenesis in Oncology, Hong Kong, 15-16 October 2004. In Biomedicine & Pharmacotherapy, v. 59 n. suppl. 2, p. S363-S365-
dc.identifier.issn0753-3322-
dc.identifier.urihttp://hdl.handle.net/10722/205646-
dc.descriptionThis article belongs to a special issue 'Proceedings of the 1st Annual Conference of OOTR COX-2 and Angiogenesis in Oncology'-
dc.description.abstractBackground. - Neoplastic cells often display aberrant methylation and silencing of multiple genes, including tumor suppressor genes (TSGs) that regulate critical processes such as cell cycle control, DNA repair and angiogenesis. Tissue inhibitor of metalloproteinase-3 (TIMP3) is an extracellular matrix-bound protein which regulates matrix composition and affects tumor growth, invasion and angiogenesis. It mediates vascular endothelial growth factor (VEGF) by blocking the binding of VEGF to VEGF receptor-2 and inhibits downstream signaling. This study focused on the hypermethylation status of the TIMP3 gene with clinical parameters in invasive breast ductal carcinoma (IDC) samples. Materials and methods. - DNA extraction and methylation specific PCR (MSP) was performed on 173 patients with invasive breast carcinoma. Both specific methylated and unmethylated primers for each gene were used for PCR and the products were visualized on agarose gel. The methylation status of TIMP3 was then compared with corresponding patients' clinicopathologic characteristics. Results. - Methylation frequencies of TIMP3 in the breast cancer samples were 20.81 %. Among the hypermethylated cancers, 50% were tumor grade II-III, 44.44% were positive in lymph node involvement (LN), 36.11% were positive in lymphovascular permeation (LVP); 44.44%, 22.22% and 47.22% for the overexpressions in estrogen receptor (ER), progesterone receptor(PR) and c-erbB2, respectively. Conclusion. - The result demonstrated that hypermethylation of TIMP3 in IDC might be associated with high tumor grading and lymph nodes metastasis, and overexpression of ER, PR and c-erbB2, respectively.-
dc.languageeng-
dc.publisherElsevier France, Editions Scientifiques et Medicales. The Journal's web site is located at http://www.elsevier.com/locate/biopha-
dc.relation.ispartofBiomedicine & Pharmacotherapy-
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in <Journal title>. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in PUBLICATION, [VOL#, ISSUE#, (DATE)] DOI#-
dc.subjectTIMP3-
dc.subjectInvasive ductal carcinoma-
dc.subjectMethylation-
dc.titleDNA hypermethylation of TIMP3 gene in invasive breast ductal carcinomaen_US
dc.typeConference_Paperen_US
dc.identifier.emailChow, LWC: lwcchow@hkucc.hku.hk-
dc.identifier.doi10.1016/S0753-3322(05)80079-4-
dc.identifier.pmid16507410-
dc.identifier.hkuros114699-
dc.identifier.volume59-
dc.identifier.issuesuppl. 2-
dc.identifier.spageS363-
dc.identifier.epageS365-
dc.identifier.isiWOS:000234423600040-
dc.publisher.placeFrance-
dc.description.otherProceedings of the 1st Annual Conference of OOTR COX-2 and Angiogenesis in Oncology, Hong Kong, 15-16 October 2004. In Biomedicine & Pharmacotherapy, v. 59 n. suppl. 2, p. S363-S365-

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