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首页> 外文期刊>Toxicologic pathology >Differential tumor biology effects of double-initiation in a mouse skin chemical carcinogenesis model comparing wild type versus protein kinase Cepsilon overexpression mice.
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Differential tumor biology effects of double-initiation in a mouse skin chemical carcinogenesis model comparing wild type versus protein kinase Cepsilon overexpression mice.

机译：小鼠皮肤化学致癌模型中两次启动的差异肿瘤生物学效应，将野生型与蛋白激酶Cepsilon过表达小鼠进行了比较。

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Our previous studies showed that protein kinase Cepsilon (PKCepsilon) verexpression in mouse skin resulted in metastatic squamous cell carcinoma (SCC) elicited by single 7,12-dimethylbenz(a)anthracene (DMBA)-initiation and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promotion in the absence of preceding papilloma formation as is typically observed in wild type mice. The present study demonstrates that double-DMBA initiation modulates tumor incidence, multiplicity, and latency period in both wild type and PKCepsilon overexpression transgenic (PKCepsilon-Tg) mice. After 17 weeks (wks) of tumor promotion, a reduction in papilloma multiplicity was observed in double- versus single-DMBA initiated wild type mice. Papilloma multiplicity was inversely correlated with cell death indices of interfollicular keratinocytes, indicating decreased papilloma formation was caused by increased cell death and suggesting the origin of papillomas is in interfollicular epidermis. Double-initiated PKCepsilon-Tg mice had accelerated carcinoma formation and cancer incidence in comparison to single-initiated PKCepsilon-Tg mice. Morphologic analysis of mouse skin following double initiation and tumor promotion showed a similar if not identical series of events to those previously observed following single initiation and tumor promotion: putative preneoplastic cells were observed arising from hyperplastic hair follicles (HFs) with subsequent cancer cell infiltration into the dermis. Single-initiated PKCepsilon-Tg mice exhibited increased mitosis in epidermal cells of HFs during tumor promotion.
机译：我们以前的研究表明，蛋白激酶Cepsilon（PKCepsilon）在小鼠皮肤中的正常表达导致单个7,12-二甲基苯并（a）蒽（DMBA）的起始和12-O-十四烷酰佛波-13-引起的转移性鳞状细胞癌（SCC）。不存在先前的乳头瘤形成的情况下，通常在野生型小鼠中观察到乙酸（TPA）促进作用。本研究表明，在野生型和PKCepsilon过表达转基因（PKCepsilon-Tg）小鼠中，双DMBA起始可调节肿瘤发生率，多样性和潜伏期。肿瘤促进17周后（wks），在双DMBA和单DMBA引发的野生型小鼠中观察到乳头状瘤多样性降低。乳头状瘤的多样性与小泡间角质形成细胞的细胞死亡指数呈负相关，表明乳头状瘤形成的减少是由于细胞死亡的增加引起的，提示乳头状瘤的起源是在小泡间表皮。与单次启动的PKCepsilon-Tg小鼠相比，双次启动的PKCepsilon-Tg小鼠具有更快的癌症形成和癌症发生率。两次启动和肿瘤促进后对小鼠皮肤的形态学分析显示，与先前单次启动和肿瘤促进后发生的事件相似甚至不同：观察到假定的前肿瘤细胞是由增生的毛囊（HFs）产生，随后癌细胞浸润真皮。在肿瘤促进过程中，单启动PKCepsilon-Tg小鼠在HF的表皮细胞中显示出增加的有丝分裂。

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