RT Journal Article
SR Electronic
T1 Absence of Endothelial Cells, Central Necrosis, and Fibrosis Are Associated with Aggressive Inflammatory Breast Cancer
JF Cancer Research
JO Cancer Res
FD American Association for Cancer Research
SP 445
OP 451
VO 61
IS 2
A1 Shirakawa, Kazuo
A1 Tsuda, Hitoshi
A1 Heike, Yuji
A1 Kato, Kazunori
A1 Asada, Rumiko
A1 Inomata, Motoko
A1 Sasaki, Hiroki
A1 Kasumi, Fujio
A1 Yoshimoto, Masataka
A1 Iwanaga, Toshihiko
A1 Konishi, Fumio
A1 Terada, Masaaki
A1 Wakasugi, Hiro
YR 2001
UL http://cancerres.aacrjournals.org/content/61/2/445.abstract
AB We recently established a new human inflammatory breast cancer (IBC) xenograft (WIBC-9) originating from a patient with IBC. The graft was transplantable in BALB/c nude and severe combined immunodeficient (SCID) mice. WIBC-9 was frequently accompanied by lung metastasis and exhibited erythema of the overlying skin, reflecting its human counterpart. Histological study of the original tumor and WIBC-9 revealed invasive ductal carcinoma with a hypervascular structure of solid nests and marked lymphatic permeation in the overlying dermis. In the central part of the solid nests, absence of endothelial cells, central necrosis, and fibrosis were observed. In vitro, WIBC-9 formed tube-like structures and loops, reflecting its in vivo feature and its human counterpart. WIBC-9 exhibited aneuploidy, ErbB-2 gene amplification, and an absence of estrogen receptor and progesterone receptor, which is consistent with IBC. Comparative studies of WIBC-9, three established non-IBC xenografts, and a human breast cancer cell line (SK-BR3) by reverse transcription-PCR, ELISA, and immunohistochemistry indicated that certain human genes (interleukin 8, vascular epidermal growth factor, basic fibroblast growth factor, angiopoietin 13, Flt-1, Tie-2, and Tie-1) and certain murine genes (integrin αvβ3, flt-1, tie-2, vascular epidermal growth factor, and CD31) were overexpressed in exposure to tumor cells. The molecular basis and these unique histological features may be associated with aggressive IBC on angiogenic and nonangiogenic pathways. ©2001 American Association for Cancer Research.