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SAFETY OF RED LIGHT FOR TISSUES WITH CANCER 555 Tumor area measured across time. No statistically significant difference was observed by repeated measures ANOVA. Mean – SEM is shown. The control mice showed typical sickness behavior including a semicollapsed posture, shivering as a sign of being cold, lack of movement, and lack of grooming. This observation is consistent with our earlier report of beneficial effects of LLLT on immune response and sepsis.15 Discussion The use of phototherapy in the treatment of cancer pa- tients has been controversial. Current recommendations suggest that therapy should be carefully considered and used cautiously in patients with cancer, and that treatment in areas bearing tumors should be avoided. This empiric advice is based on our current knowledge of the experimental ac- celeration of cellular proliferation and stimulation of wound healing and tissue repair as demonstrated in both animal models and clinical scenarios.16–18 There have been few studies that have investigated the influence of LLLT on tumors and tumor growth. The hamster cheek pouch DMBA-induced oral SCC has been recently investigated by Monteiro et al.10 The authors treated the oral cavity with 660 nm LLLT after induction of tumors. Histo- logical evaluation demonstrated an increase in the progres- sion and severity of SCC.10 Liebow et al. had also demonstrated an apparent stimu- lation of tumor induction and growth after CO2 laser inci- sions were created in cheek pouch tissue that had been transformed as a result of DMBA painting.19,20 Both the Montiero and Liebow investigations involved manipulations of tissue that had been manipulated into a transformed field as a result of DMBA induction. This process inevitably re- sults in tumor formation and it is well known that scalpel incisions and other perturbations of the epithelium can stimulate tumor induction. It is also well known that these tumors are dependent upon epidermal growth factor (EGF) for growth.21 Saliva contains significant concentrations of EGF and other growth factors and cytokines. Inflammation results in consumption and degradation of these growth factors, and processes that reduce or modulate the inflam- matory response similarly affect tumor development in these tissues. CO2 laser use results in a reduction and delay in the inflammatory response.22–25 This particular laser is capable of inducing heat shock proteins by a mechanism similar to that observed in modification of wound healing and scar formation in laser-assisted-scar-healing (LASH) in hu- mans.26,27 Similarly, phototherapy at 660nm is known to reduce inflammation.28 Both of these studies demonstrate that the local milieu is important in the induction and proliferation of malignant lesions. However, it would not be appropriate to make generalizations about all types of cancers based on this very specific model and tumor system. The model We chose a model that can produce a large number of malignant cutaneous lesions economically and automatically (Fig. 2), provides a way to irradiate them with red light au- tomatically (Fig. 3), and allows us to monitor the growth of these tumors daily. This experimental model (Fig. 1) induces spontaneous and genetically heterogeneous nonmelanoma skin cancers on the backs of hairless mice after UV damage. The induction of cancer by UV exposure is a random process and involves a combination of randomly induced mutations in multiple genes per tumor. The tumors produced by this model are heterogeneous, which is more representative of a wider range of clinically observed cancers as contrasted to models that use genetically homogeneous cancer cell lines. Although nonmelanoma skin cancer is not as deadly as other cancers in humans, it is a true cancer genetically and func- tionally and therefore with the effects of red light, LLLT in the presence of these neoplasms is relevant to the potential effects of red light therapy on other types of cancer. The advantage of SKH-1 mouse cancer model is that the cells producing cancer in the overwhelming majority are epidermal keratinocytes, that is the fast-dividing keratino- cytes of the lowest layer of epidermis, which is very thin in mice, less than 0.05 mm. Therefore, the tumors grow on the surface of the skin and a very minor part of each tumor is below the surface.29–33 Early investigations using the SKH-1 model documented the high degree of histologic similarity in the numerous cutaneous malignant lesions produced in this model.29–33 In addition, the high throughput method of periodic photographing the tumors and measuring their diameter on the photographs, a well-established method of measurement, fosters the analysis of hundreds of tumors longitudinally, which is not possible with other end-point methods, such as histology. The majority of the research studies utilizing this SKH-1 cancer model use the size of the visible tumor as a function of time as a measure of tumor proliferation.12,34–41 The sensitivity of the model to detect small therapeutic effects is limited by the fact that the tumors in treatment and control groups are by their nature different genetically, as each tumor is a result of random mutagenic events. Al- though this difference is of no significance, because of large numbers of medium-sized tumors in both groups, the indi- vidual random mutations resulting in the induction of small numbers of large fast growing tumors potentially affected the overall statistical results. This limitation can be overcome in the future by increasing the number of mice treated or by FIG. 8.PDF Image | Preliminary Study of the Safety of Red Light Phototherapy Cancer
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