Abstract:
:Breast cancer is one of the common malignant diseases among women in Japan as well as in western countries, and its incidence continues to increase. Normal mammary duct epithelial cells exhibit a well-organized apicobasal polarity, which forms the basis for their specific structure and function. Although the loss of epithelial cell polarity is one of the major changes that occur during the progression of tumor cells, including breast cancer, the underlying molecular mechanisms for this, as well as their relationship to other changes such as increased proliferation and metastasis, remain to be elucidated. The atypical protein kinase C lambda/iota (aPKC lambda/iota) is involved in several signal transduction pathways, including the establishment of epithelial cell polarity. In this study we evaluated the expression and localization of aPKC lambda/iota in breast cancer by immunohistochemistry and compared our findings with the clinicopathologic factors associated with the tumor specimens. We detected aPK Clambda/iota protein overexpression in 88 of the 110 breast cancer cases (80.0%) under study, expect for decreased expression in a few cases. The immunoreactivity of aPK Clambda/iota was generally weak in ductal carcinoma in situ, but strong in invasive ductal carcinoma (IDC; P = .022). The correlation between apical or cytoplasmic aPKC lambda/iota localization and tumor pathologic type (ie, atypical ductal hyperplasia, ductal carcinoma in situ. or IDC) was also demonstrated (P < .001). These results thus indicate that the normal apicobasal polarity is lost upon the progression of a breast lesion to IDC. This is also the first evidence to show aPKC lambda/iota overexpression in breast cancer and demonstrates that its localization is associated with the trend of pathologic type of the tumor.
journal_name
Hum Patholjournal_title
Human pathologyauthors
Kojima Y,Akimoto K,Nagashima Y,Ishiguro H,Shirai S,Chishima T,Ichikawa Y,Ishikawa T,Sasaki T,Kubota Y,Inayama Y,Aoki I,Ohno S,Shimada Hdoi
10.1016/j.humpath.2007.11.001subject
Has Abstractpub_date
2008-06-01 00:00:00pages
824-31issue
6eissn
0046-8177issn
1532-8392pii
S0046-8177(07)00603-Xjournal_volume
39pub_type
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