Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA.
Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Mod Pathol. 2021 Feb;34(2):280-290. doi: 10.1038/s41379-020-0617-x. Epub 2020 Jul 6.
The DNA cytosine deaminase APOBEC3B (A3B) is a newly recognized endogenous source of mutations in a range of human tumors, including head/neck cancer. A3B inflicts C-to-T and C-to-G base substitutions in 5'-TCA/T trinucleotide motifs, contributes to accelerated rates of tumor development, and affects clinical outcomes in a variety of cancer types. High-risk human papillomavirus (HPV) infection causes A3B overexpression, and HPV-positive cervical and head/neck cancers are among tumor types with the highest degree of APOBEC signature mutations. A3B overexpression in HPV-positive tumor types is caused by the viral E6/E7 oncoproteins and may be an early off-to-on switch in tumorigenesis. In comparison, less is known about the molecular mechanisms responsible for A3B overexpression in HPV-negative head/neck cancers. Here, we utilize an immunohistochemical approach to determine whether A3B is turned from off-to-on or if it undergoes a more gradual transition to overexpression in HPV-negative head/neck cancers. As positive controls, almost all HPV-positive oral epithelial dysplasias and oropharyngeal cancers showed high levels of nuclear A3B staining regardless of diagnosis. As negative controls, A3B levels were low in phenotypically normal epithelium adjacent to cancer and oral epithelial hyperplasias. Interestingly, HPV-negative and low-grade oral epithelial dysplasias showed intermediate A3B levels, while high-grade oral dysplasias showed high A3B levels similar to oral squamous cell carcinomas. A3B levels were highest in grade 2 and grade 3 oral squamous cell carcinomas. In addition, a strong positive association was found between nuclear A3B and Ki67 scores suggesting a linkage to the cell cycle. Overall, these results support a model in which gradual activation of A3B expression occurs during HPV-negative tumor development and suggest that A3B overexpression may provide a marker for advanced grade oral dysplasia and cancer.
DNA 胞嘧啶脱氨酶 APOBEC3B(A3B)是一系列人类肿瘤(包括头颈部癌症)中突变的新发现的内源性来源。A3B 在 5'-TCA/T 三核苷酸基序中造成 C 到 T 和 C 到 G 碱基取代,促进肿瘤发展的加速,并影响多种癌症类型的临床结局。高危型人乳头瘤病毒(HPV)感染导致 A3B 过表达,HPV 阳性的宫颈和头颈部癌症是 APOBEC 特征性突变程度最高的肿瘤类型之一。HPV 阳性肿瘤类型中的 A3B 过表达是由病毒 E6/E7 癌蛋白引起的,可能是肿瘤发生的早期开关。相比之下,HPV 阴性头颈部癌症中导致 A3B 过表达的分子机制知之甚少。在这里,我们利用免疫组织化学方法来确定 A3B 是从关闭到开启,还是在 HPV 阴性头颈部癌症中经历更渐进的过表达转变。作为阳性对照,几乎所有 HPV 阳性口腔上皮异型增生和口咽癌都表现出高水平的核 A3B 染色,无论诊断如何。作为阴性对照,癌旁表型正常的上皮和口腔上皮增生中 A3B 水平较低。有趣的是,HPV 阴性和低级别口腔上皮异型增生显示出中间水平的 A3B,而高级别口腔异型增生显示出与口腔鳞状细胞癌相似的高水平 A3B。A3B 水平在 2 级和 3 级口腔鳞状细胞癌中最高。此外,还发现核 A3B 与 Ki67 评分之间存在强烈的正相关,提示与细胞周期有关。总体而言,这些结果支持在 HPV 阴性肿瘤发展过程中 A3B 表达逐渐激活的模型,并表明 A3B 过表达可能为高级别口腔异型增生和癌症提供标志物。