Cutaneous melanoma is the most serious form of skin cancer and is curable only if it is detected early. The most effective treatment for the melanoma is surgical excision of the lesion. Traditionally, wide margins of excision have been used for effective treatment, but are not always desirable due to increased risk of infection and esthetic reasons. Besides, safe surgical margins of the lesion are not always correlated well with the size of the lesions. We have previously developed a system using elastic light single-scattering spectroscopy to differentiate cancerous tissue from non-cancerous tissue and tested it in vitro.The goal of this study was, therefore, to determine the effectiveness of this system ex vivo by using a mouse model of melanoma. First, a melanoma cell line; B16F10 were injected subcutaneously at right mid flank region of C57BL6 mice (n=5) and allowed to develop for two weeks. Tumors were dissected and spectra were taken on tumor tissue and on normal looking skin tissue that was 10 mm distant from the incision. Since these tumors become markedly necrotic in the middle, spectra of necrotic area was also taken. Slopes of the spectra were positive taken on non-cancerous skin tissues that were later verified by histological examination. On the other hand, it gave negative slopes on melanomas.Increased sizes of the nuclei correlated with the negative slope while smaller nuclei found in non-cancerous tissue gave positive slope. Spectrum taken from necrotic area differed from both cancerous and non-cancerous tissue such that it gave a U-shaped spectrum.These results demonstrate that elastic light single-scattering spectroscopy system can differentiate cancerous tissue from non-cancerous and has potential to be used intraoperatively to determine the surgical margins.
Background/aim Nonalcoholic fatty liver is one of the most common forms of liver disease and role of microRNAs (miRNAs) on this illness is currently unclear. It was aimed to evaluate the predictive role of circulating miR-33a and mir-200c on high fructose corn syrup (HFCS)-induced fatty liver and vitamin D 3 supplementation-related hepatic changes. Materials and methods Twenty-four rats were randomized into three groups: sham (n = 8), experimental fatty liver group (n = 8), and fatty liver + vitamin D 3 supplementation group (n = 8). In the treatment group, 10 μg/kg/week of vitamin D 3 was given by orogastric tube weekly for 4 weeks in addition to a high fructose diet. Serum AST, ALT, TNF-α, and MDA levels were tested. Liver tissue samples were examined using hematoxylin/eosin, periodic acid-Schif (PAS) and Masson’s Trichrome staining. Circulating miR-33a and mir-200c were quantified by qRT-PCR method. Moreover, in silico analyses were accomplished. Results In the vitamin D 3 group, results of biochemical parameters were significantly different than those of the fatty liver group (p < 0.001). Moreover, significant differences in serum levels of circulating miR-33a and mir-200c were identified among all groups (p < 0.05). Finally, more favorable histopathological changes were noticed in the vitamin D 3 supplementation group. The expressions of Ki-67 were also considerably reduced in the vitamin D 3 group. According to KEGG pathway analysis, mir-33a and mir-200c were found to play a common role in the Hippo signaling pathway, lysine degradation, and protein processing. Conclusion Our current experimental fatty liver study showed that, in a specified dose, vitamin D 3 supplementation could alleviate adverse undesirable hepatic effects of HFCS via miR-33a and mir-200c.
Fizyolojik ve patolojik durumlarda, işleyişleri farklı, nekroz ve apoptoz olarak adlandırılan iki ana hücre ölümü meydana gelir. Apoptoz basamaklarındaki disregülasyonun kanser veya otoimmüniteyi tetiklediği bildirilmiş olup, aşırı apoptoz ise dejeneratif hastalıklarla ilişkilendirilmektedir. Proliferasyon artışıyla karakterize edilen kanserin tedavisi için hücrelerin apoptozdan kurtulma yolları araştırılmaktadır. Bununla ilişkili olarak kanser hücrelerinde Bcl-2, Bcl-xL ve Mcl-1 gibi antiapoptotik proteinlerin arttığı, proapoptotik proteinlerin ise azaldığı belirlenmiştir. Hücre ölümünde görev alan birçok protein ve protein kompleksleri arasında bir diğer önemli grubu apoptoz inhibitörü (IAP) protein ailesi oluşturmaktadır. IAP’lar apoptozda hem intrinsik hem de ekstrinsik yolağı baskılayabilen endojen kaspaz inhibitörleri olarak fonksiyon görmekte olup, apoptoz dışında hücre bölünmesi ve immün regülasyonda da rol almaktadırlar. Bcl-2 ve IAP ailesi üyeleri gibi aşırı ekspresyonu tespit edilen proteinler, hem tanı koyma hem de tedavi aşamasında yarar sağlamaktadır. Günümüzde sadece kanser hücresini hedefleyen ilaçlar tedavi protokolleri arasına girmiş bulunmaktadır. Bu derlemede apoptotik yolaklara ait moleküler mekanizmalar ve onlarla ilişkili hedefe yönelik yeni tedavi yaklaşımları genel hatlarıyla irdelenmektedir.
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