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首页> 外文期刊>Cell cycle >BRAF and RKIP aberrations in actinic keratosis and non-melanoma skin cancers.
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BRAF and RKIP aberrations in actinic keratosis and non-melanoma skin cancers.

机译：光化性角化病和非黑素瘤皮肤癌中的BRAF和RKIP畸变。

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摘要

This issue of Cell Cycle presents an important article on the mutation and expression status of the genes BRAF and RKIP in pre-cancerous lesions, such as actinic keratosis (AK) and non-melanoma skin tumors such as cutaneous squamous cell carcinoma (SCC). In their article entitled "BRAF and RKIP are significantly decreased in cutaneous squamous cell carcinoma," Zaravinos et al., indicated that BRAF does not appear to be frequently mutated in AK and SCC. BRAF is a kinase that activates the RAF/MEK/ERK signal transduction cascade and gene mutations, especially the T to A missense transversion at nucleotide 1799 (leading to a V600E amino acid change in the BRAF protein), thereby causing constitutive activation of the BRAF kinase activity, independently of RAS activation, by converting BRAF into a dominant transforming protein. Thus, BRAF gene mutations have been proposed to contribute to cancer development. T1799A mutations have been observed in 80% of the malignant melanoma tumors and cell lines. Although, we have previously investigated the incidence of BRAF gene mutations within exons 11 and 15 in basal cell carcinoma (BCC), no mutations were detected.
机译：本期《细胞周期》提供了有关BRAF和RKIP基因在癌前病变（例如光化性角化病（AK）和非黑素瘤皮肤肿瘤，例如皮肤鳞状细胞癌（SCC））中突变和表达状态的重要文章。 Zaravinos等人在其题为“ BRAF和RKIP在皮肤鳞状细胞癌中显着降低”的文章中指出，BRAF在AK和SCC中似乎不经常发生突变。 BRAF是一种激酶，可激活RAF / MEK / ERK信号转导级联和基因突变，特别是核苷酸1799处的T到A错义转化（导致BRAF蛋白中的V600E氨基酸改变），从而引起BRAF的组成型活化通过将BRAF转化为显性转化蛋白，激酶活性独立于RAS激活。因此，已经提出BRAF基因突变有助于癌症的发展。在80％的恶性黑色素瘤肿瘤和细胞系中已观察到T1799A突变。尽管我们之前已经调查了基底细胞癌（BCC）外显子11和15内BRAF基因突变的发生率，但未发现突变。

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