TY - JOUR
T1 - A novel mouse monoclonal antibody targeting ErbB2 suppresses breast cancer growth
AU - Kawa, Seiji
AU - Matsushita, Hirohisa
AU - Ohbayashi, Hirokazu
AU - Semba, Kentaro
AU - Yamamoto, Tadashi
N1 - Funding Information:
We thank The NIH Fellows Editorial Board for editing suggestions. This work was supported by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science, and Technology of Japan.
PY - 2009/7/3
Y1 - 2009/7/3
N2 - Overexpression of ErbB2 in breast cancer is associated with increased recurrence and worse prognosis. Accumulating evidences suggest that molecular targeted therapy is a promising anticancer strategy. In this study, we produced a novel anti-ErbB2 monoclonal antibody, 6G10, that recognized an epitope distinct from the trastuzumab binding site. 6G10 induced aggregation of BT474 breast cancer cells and inhibited proliferation of various breast cancer cell lines including BT474. A growth inhibition assay showed that 6G10 had EC50 values comparable to trastuzumab, indicating that the drugs have a similar level of potency. Furthermore, intraperitoneal administration of 6G10 completely inhibited the growth of xenografted tumors derived from BT474 and SK-BR-3 cells. These data suggested that 6G10 has great therapeutic potential and could be administered to patients alternatively, or synergistically, with trastuzumab.
AB - Overexpression of ErbB2 in breast cancer is associated with increased recurrence and worse prognosis. Accumulating evidences suggest that molecular targeted therapy is a promising anticancer strategy. In this study, we produced a novel anti-ErbB2 monoclonal antibody, 6G10, that recognized an epitope distinct from the trastuzumab binding site. 6G10 induced aggregation of BT474 breast cancer cells and inhibited proliferation of various breast cancer cell lines including BT474. A growth inhibition assay showed that 6G10 had EC50 values comparable to trastuzumab, indicating that the drugs have a similar level of potency. Furthermore, intraperitoneal administration of 6G10 completely inhibited the growth of xenografted tumors derived from BT474 and SK-BR-3 cells. These data suggested that 6G10 has great therapeutic potential and could be administered to patients alternatively, or synergistically, with trastuzumab.
KW - 6G10
KW - Breast cancer
KW - ErbB2
KW - Molecular therapeutics
KW - Preclinical study
KW - Trastuzumab
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U2 - 10.1016/j.bbrc.2009.04.118
DO - 10.1016/j.bbrc.2009.04.118
M3 - Article
C2 - 19409371
AN - SCOPUS:65649112936
SN - 0006-291X
VL - 384
SP - 329
EP - 333
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -
