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Akira Morimiya

Researcher at Indiana University

Publications -  16
Citations -  1349

Akira Morimiya is an academic researcher from Indiana University. The author has contributed to research in topics: Breast cancer & Cancer. The author has an hindex of 13, co-authored 16 publications receiving 1261 citations. Previous affiliations of Akira Morimiya include Indiana University – Purdue University Indianapolis.

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NF-κB represses E-cadherin expression and enhances epithelial to mesenchymal transition of mammary epithelial cells: potential involvement of ZEB-1 and ZEB-2

TL;DR: It is shown that NF-κB suppresses the expression of epithelial specific genes E-cadherin and desmoplakin and induces theexpression of the mesenchymal specific gene vimentin and the dependence of MCF10A/p65 cells to Z EB-1 and ZEB-2 for cell cycle progression or survival is suggested.
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FOXA1 expression in breast cancer - Correlation with luminal subtype A and survival

TL;DR: FoxA1 expression correlates with luminal subtype A breast cancer and it is significant predictor of cancer-specific survival in patients with ER-positive tumors and prognostic ability of FOXA1 in these low-risk breast cancers may prove to be useful in clinical treatment decisions.
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Forkhead box A1 expression in breast cancer is associated with luminal subtype and good prognosis

TL;DR: Based on this study in patients treated with surgery followed by adjuvant anthracycline-based chemotherapy, FOXA1 expression is associated with good prognosis, and could possibly serve as a clinical marker for luminal subtype A.
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Microsomal prostaglandin E2 synthase-1 in breast cancer: a potential target for therapy.

TL;DR: Targeting mPGES‐1 might prove to be an alternative therapeutic strategy to inhibit PGE2 production, as its expression in breast cell lines and normal and malignant breast tissues indicated its potential as a target for therapy.
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Lymphangiogenesis does not occur in breast cancer.

TL;DR: Lymphangiogenesis was not evident when studied by lymphatic vessel density or by lymph vessel endothelial proliferation, in contrast to the strong expression seen in adjacent tumor cells and blood vessel endothelium.