Collagen triple helix repeat containing-1 (CTHRC1) expression in invasive ductal carcinoma of the breast: The impact on prognosis and correlation to clinicopathologic features

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Title
Collagen triple helix repeat containing-1 (CTHRC1) expression in invasive ductal carcinoma of the breast: The impact on prognosis and correlation to clinicopathologic features
Author(s)
J H Kim; T H Baek; H S Yim; K H Kim; S H Jeong; Ho Bum Kang; S S Oh; Hee Gu LeeJae Wha Kim; K D Kim
Bibliographic Citation
Pathology & Oncology Research, vol. 19, no. 4, pp. 731-737
Publication Year
2013
Abstract
CTHRC1 has been known as a regulator of collagen expression and cell migration. The aim of this research was to clarify the clinicopathologic significance of CTHRC1 expression in human breast cancer. 22 cases of breast cancer tissues, randomly selected from clinically diagnosed patients, showed a significant increase of CTHRC1 mRNA expression compared to the normal tissue from the same patients using RT-PCR and real-time PCR. Additionally we investigated breast cancers from 189 patients by immunohistochemistry (IHC). A high level of CTHRC1 expression was observed in 111 (58.7 %) out of 189 breast cancer patients and the expression was significantly correlated with histologic grade (P = 0.026), nodal status (P < 0.001), and TNM pathologic stage (P = 0.002). High CTHRC1 expression was associated with a shorter recurrence free survival (P = 0.008). Taken together, the results showed that CTHRC1 over-expression was significantly associated with clinicopathological factors of poor prognosis in invasive ductal carcinoma. CTHRC1 could be used as a supplementary prognostic biomarker and a potential therapeutic target in breast cancer.
Keyword
Breast cancerCTHRC1ImmunohistochemistryMetastasis
ISSN
1219-4956
Publisher
Springer
DOI
http://dx.doi.org/10.1007/s12253-013-9636-y
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Division of Biomaterials Research > Cell Factory Research Center > 1. Journal Articles
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