Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
Cancer Res. 2013 Jan 1;73(1):150-9. doi: 10.1158/0008-5472.CAN-12-2670. Epub 2012 Oct 29.
Field cancerization refers to areas of grossly normal epithelium that exhibit increased risk for tumor occurrence. Unfortunately, elucidation of the locoregional changes that contribute to increased tumor risk is difficult due to the inability to visualize the field. In this study, we use a noninvasive optical-based imaging approach to detail spatiotemporal changes in subclinical hyperemia that occur during experimental cutaneous carcinogenesis. After acute inflammation from 10 weeks of UVB irradiation subsides, small areas of focal hyperemia form and were seen to persist and expand long after cessation of UVB irradiation. We show that these persistent early hyperemic foci reliably predict sites of angiogenesis and overlying tumor formation. More than 96% of the tumors (57 of 59) that developed following UVB or 7,12-dimethylbenz(a)anthracene/phorbol 12-myristate 13-acetate (DMBA/PMA) treatment developed in sites of preexisting hyperemic foci. Hyperemic foci were multifocal and heterogeneously distributed and represented a minor fraction of the carcinogen-treated skin surface (10.3% of the imaging area in vehicle-treated animals). Finally, we also assessed the ability of the anti-inflammatory agent, celecoxib, to suppress hyperemia formation during photocarcinogenesis. The chemopreventive activity of celecoxib was shown to correlate with its ability to reduce the area of skin that exhibit these hyperemic foci, reducing the area of imaged skin containing hyperemic foci by 49.1%. Thus, we propose that a hyperemic switch can be exploited to visualize the cancerization field very early in the course of cutaneous carcinogenesis and provides insight into the chemopreventive activity of the anti-inflammatory agent celecoxib.
“Field cancerization”是指大体正常的上皮区域存在肿瘤发生风险增加的现象。不幸的是,由于无法可视化“field”,因此很难阐明导致肿瘤风险增加的局部变化。在这项研究中,我们使用非侵入性的基于光学的成像方法详细描述了实验性皮肤癌变过程中发生的亚临床充血的时空变化。在 10 周的 UVB 照射引起的急性炎症消退后,会形成小面积的局灶性充血,并且在停止 UVB 照射后很久仍持续存在并扩大。我们表明,这些持续的早期充血焦点可靠地预测了血管生成和表面肿瘤形成的部位。在 UVB 或 7,12-二甲基苯并蒽/佛波醇 12-肉豆蔻酸 13-乙酸酯(DMBA/PMA)处理后发展的肿瘤中,超过 96%(57/59)的肿瘤出现在预先存在的充血焦点部位。充血焦点呈多灶性且分布不均,仅占致癌剂处理皮肤表面的一小部分(载体处理动物的成像区域的 10.3%)。最后,我们还评估了抗炎药塞来昔布在光致癌过程中抑制充血形成的能力。塞来昔布的化学预防活性与其抑制皮肤出现充血焦点的能力相关,将包含充血焦点的成像皮肤面积减少了 49.1%。因此,我们提出可以利用充血开关来在皮肤癌变过程的早期可视化癌化场,并深入了解抗炎药塞来昔布的化学预防活性。