Absence of endothelial cells, central necrosis, and fibrosis are associated with aggressive inflammatory breast cancer

Citation
K. Shirakawa et al., Absence of endothelial cells, central necrosis, and fibrosis are associated with aggressive inflammatory breast cancer, CANCER RES, 61(2), 2001, pp. 445-451
Citations number
20
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
CANCER RESEARCH
ISSN journal
0008-5472 → ACNP
Volume
61
Issue
2
Year of publication
2001
Pages
445 - 451
Database
ISI
SICI code
0008-5472(20010115)61:2<445:AOECCN>2.0.ZU;2-G
Abstract
We recently established a new human inflammatory breast cancer (IBC) xenogr aft (WIBC-9) originating from a patient with IBC, The graft was transplanta ble 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 th e original tumor and WIBC-9 revealed invasive ductal carcinoma with a hyper vascular structure of solid nests and marked lymphatic permeation in the ov erlying dermis. In the central part of the solid nests, absence of endothel ial cells, central necrosis, and fibrosis were observed. In vitro, WIBC-9 f ormed tube-like structures and loops, reflecting its irt who feature and it s human counterpart. WIBC-9 exhibited aneuploidy, ErbB-2 gene amplification , and an absence of estrogen receptor and progesterone receptor, which is c onsistent with IBC, Comparative studies of WIBC-9, three established non-IB C xenografts, and a human breast cancer cell line (SK-BR3) by reverse trans cription-PCR, ELISA, and immunohistochemistry indicated that certain human genes (interleukin 8, vascular epidermal growth factor, basic fibroblast gr owth factor, angiopoietin 13, Flt-1, Tie-2, and Tie-1) and certain murine g enes (integrin alpha (v)beta (3), flt-1, tie-2, vascular epidermal growth f actor, and CD31) were overexpressed in exposure to tumor cells. The molecul ar basis and these unique histological features may be associated with aggr essive IBC on angiogenic and nonangiogenic pathways.