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Byeong Woo Park

Researcher at Yonsei University

Publications -  228
Citations -  7417

Byeong Woo Park is an academic researcher from Yonsei University. The author has contributed to research in topics: Breast cancer & Cancer. The author has an hindex of 45, co-authored 214 publications receiving 6208 citations. Previous affiliations of Byeong Woo Park include University Health System & Seoul National University.

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Adjuvant Capecitabine for Breast Cancer after Preoperative Chemotherapy.

TL;DR: After standard neoadjuvant chemotherapy containing anthracycline, taxane, or both, the addition of adjuvant capecitabine therapy was safe and effective in prolonging disease‐free survival and overall survival among patients with HER2‐negative breast cancer who had residual invasive disease on pathological testing.
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Expression of androgen receptors in primary breast cancer

TL;DR: AR is expressed in a significant number of breast cancers and is associated with lower tumor burden and favorable differentiation, and is significantly correlated with human epidermal growth factor receptor type 2 (HER-2) overexpression in ER-negative tumors.
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Rationally designed anti-HER2/neu peptide mimetic disables P185HER2/neu tyrosine kinases in vitro and in vivo.

TL;DR: A structure-based derivation of the AHNP represents a novel strategy for the design of receptor-specific tumor therapies for p185HER2/neu-expressing human cancers.
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Characteristics and outcomes according to molecular subtypes of breast cancer as classified by a panel of four biomarkers using immunohistochemistry

TL;DR: Molecular subtypes using four biomarkers could provide clinically useful information of tumor biology and clinical behaviors, and could be used for determining treatment and surveillance strategies.
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Up-regulation of Acetyl-CoA Carboxylase α and Fatty Acid Synthase by Human Epidermal Growth Factor Receptor 2 at the Translational Level in Breast Cancer Cells

TL;DR: In this paper, the authors determined the mechanism by which FASN and acetyl-CoA carboxylase α (ACCα) could be induced by HER2 overexpression.