Multiple Carcinoma injuries of squamous cells and Queratoacantoma on vitiligo patient

Vitiligo patients undergo a destruction of melanocytes. The melanin reduction inflicts as a risk factor for the development of skin neoplasia. Cases of malignant nonmelanocytic tumors and melanoma within the vitiligo patients is rare and isolated. This study reports the multiple injuries of the squamous cell carcinoma and keratoacanthoma within the intense vitiligo affected areas.

Comment on “A commensal strain of Staphylococcus epidermidis protects against skin neoplasia” by Nakatsuji et al.

A recent article in Science Advances described the striking discovery that the commensal Staphylococcus epidermidis strain MO34 displays antimicrobial and antitumor activities by producing a small molecule, identified as the nucleobase analog 6-N-hydroxylaminopurine (6-HAP). However, in contradiction to the literature, the authors claimed that 6-HAP is nonmutagenic and proposed that the toxic effect of 6-HAP results from its ability to inhibit, in its base form, DNA synthesis. To resolve the discrepancy, we proved by genetic experiments with bacteria and yeast that extracts of MO34 do contain a mutagenic compound whose effects are identical to chemically synthesized 6-HAP. The MO34 extract induced the same mutation spectrum as authentic 6-HAP. Notably, the toxic and mutagenic effects of both synthetic and MO34-derived 6-HAP depended on conversion to the corresponding nucleotide. The nucleobase 6-HAP does not inhibit DNA synthesis in vitro, and we conclude that 6-HAP exerts its biological activity when incorporated into DNA.

Response to Comment on “A commensal strain of Staphylococcus epidermidis protects against skin neoplasia” by Nakatsuji et al.

Kozmin et al. contend that observations previously reported regarding the antimicrobial and antitumor activities of 6-N-hydroxy aminopurine (6-HAP) were incorrect. Their conclusions rely on poorly characterized reagents and focus strictly on in vitro techniques without validation in relevant mammalian model systems. We are pleased to be able to illuminate the weaknesses in their technical comment. The totality of current results continues to support our original conclusion that a strain of the common human commensal skin bacterium, Staphylococcus epidermidis, produces 6-HAP that can inhibit tumor growth.

Tadpole serum activity (Rana catesbeiana) in caspase-3 as a marker of the role of apoptosis and total cytotoxic T lymphocytes in albino rats' epithelial cells induced by neoplasia

Aim: This study was conducted to examine the tadpole's serum activity (Rana catesbeiana) in caspase-3 as a marker of the role of apoptosis and total cytotoxic T lymphocyte (CTL) in albino rats' epithelial cells induced by neoplasia. Tadpole serumcontains thyroxine hormone that may cause the metamorphosis process and control cell proliferation. Materials and Methods: Male rats were induced by 7,12-dimethylbenz (α)anthracene (DMBA) 20 mg/rats twice every week over 5 weeks to stimulate skin neoplasia. Tadpole serum injected intracutaneously after neoplasia is known. The negative control group (C−) was not exposed to DMBA and tadpole serum, while the positive control group (C+) was exposed to DMBA. Treatment groups (T1, T2, and T3) were exposed DMBA and tadpole serum 100%, 75%, and 25%/rat/ day, respectively. Samples of skin organ were be made preparations immunohistochemistry interacted with caspase-3 and CTL antibody as the marker. Results: Based on the result, immunohistochemistry from skin neoplasia and given therapy of tadpole serum show that Treatment 1 was the highest caspase-3 and CTL expression. The result of caspase-3 expression in C−, C+, T1, T2, and T3 was 0.00c±0.000, 0.70bc±0.141, 2.00a±0.283, 1.10b±0.424, and 1.15b±0.495, respectively. The result of CTL expression in C−, C+, T1, T2, and T3 was 0.10d±0.200, 1.00c±0.230, 2.10a±0.529, 1.70ab±0.258, and 1.35bc±0.443, respectively. Conclusion: It can be concluded from the study that tadpole serum (R. catesbeiana) 100% concentration can increase caspase-3 and total CTL in albino rats' epithelial cells induced by neoplasia.