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Cutaneous neoplasia is invariably preceded by expanding areas of increased hyperemia that is suppressed by topical celecoxib treatment
Author(s) -
Konger Raymond L,
Sahu Ravi P,
Xu Zhengbin,
Kim Young L.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb317
Subject(s) - celecoxib , medicine , hyperplasia , pathology , reactive hyperemia , blood flow
Previous studies using biophotometric imaging with spectroscopic analysis and back‐directional gating have shown that hyperemia is a feature of neoplastic lesions and is also present in otherwise normal epithelium in the surrounding tissue field. We utilized this methodology in mouse models of chemical and photocarcinogenesis to show that hyperemia invariably precedes the appearance of grossly visible tumors. While all tumors developed in areas of high Hgb content, not all hyperemic areas developed tumors. In ultraviolet B (UVB) studies, mice were irradiated for 10 weeks with UVB 3 times/week and treated topically with either acetone or celecoxib (0.5 mg/0.2 ml) after each UV treatment. UVB treatments were discontinued at 10 weeks, but celecoxib treatments continued for 30 weeks. Importantly, focal areas of hyperemia continued to increase in size after cessation of the UVB treatments suggesting a self‐sustaining mechanism. Celecoxib treatment reduced tumor occurrence by 40% and also markedly suppressed the formation of hyperemic areas. At 30 weeks, areas of high and low Hgb content without visible tumors were assessed histologically. High Hgb content was associated with marked epidermal hyperplasia/dermal inflammation and frequent small endophytic tumors. Our data suggests that hyperemia, possibly due to a self‐sustaining inflammatory angiogenesis is a feature of the premalignant microenvironment. Thus, this imaging approach may be useful for identifying areas of subclinical or pre‐neoplastic disease, to assess the efficacy of chemopreventive strategies and to identify focal areas resistant to chemopreventive approaches. Supported by NIH R03 CA153982 & R01 HL062996 grants.