Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Mod Pathol. 2022 Feb;35(2):274-282. doi: 10.1038/s41379-021-00942-3. Epub 2021 Oct 14.
Squamous cell carcinomas of the lower female genital tract may be human papillomavirus-associated or independent. We studied the HPV status, mutational repertoire, histology, and clinical data of 28 samples from 26 patients, 65% with a vulvar primary and 35% with a vaginal primary. These represented invasive vulvovaginal squamous cell carcinomas that underwent clinical tumor-normal targeted massively parallel sequencing analysis. HPV status was determined using the HPV high-risk RNA ISH assay and/or by MSK-IMPACT. Eleven patients had HPV-associated squamous cell carcinoma (four vulvar and seven vaginal) and 15 patients had HPV-independent SqCC (13 vulvar and 2 vaginal). Well-differentiated squamous cell carcinomas were always HPV-independent. HPV-independent moderately and poorly differentiated carcinomas frequently had alterations in the NOTCH signaling pathway (6/7), which were also associated with increased tumor budding (P: 0.002). HPV-associated vulvovaginal squamous cell carcinoma had PIK3CA activating mutations (7/11, 64%) as the most common genomic event, while TERT gene alterations, mainly TERT promoter mutations (14/15 cases, 93%) featured significantly in HPV-independent carcinomas. Other common abnormalities in HPV-independent tumors were TP53 mutations (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1 mutations (7/15, 47% each). A subset of both HPV-associated and -independent tumors had NOTCH pathway alterations (6/11, 55% and 10/15, 67% respectively), but different genes in this pathway were altered in these tumors. In summary, TERT, TP53, CDKN2A, and NOTCH1 gene alterations strongly point away from an HPV-driven process (odds ratios: 0.01, 0.07, 0, and 0, respectively with p values < 0.02 for all four genes), while PIK3CA activating mutations without the other mutations strongly favors an HPV-driven tumor (odds ratio: 10.12, p value: 0.016). HPV-independent carcinomas are more likely to be moderately-poorly differentiated with intermediate to high tumor cell budding. Cancer cell fraction analysis of HPV-independent squamous carcinomas suggests that TERT and/or NOTCH1 alterations along with TP53 alterations can be the initiating event in these tumors.
下生殖道鳞状细胞癌可能与人类乳头瘤病毒(HPV)相关,也可能不相关。我们研究了 26 名患者的 28 个样本的 HPV 状态、突变谱、组织学和临床数据,其中 65%的患者为外阴原发性,35%的患者为阴道原发性。这些样本代表了接受临床肿瘤-正常靶向大规模平行测序分析的侵袭性外阴阴道鳞状细胞癌。HPV 状态通过 HPV 高危 RNA ISH 检测和/或 MSK-IMPACT 来确定。11 名患者患有 HPV 相关的鳞状细胞癌(4 名外阴和 7 名阴道),15 名患者患有 HPV 无关的 SqCC(13 名外阴和 2 名阴道)。分化良好的鳞状细胞癌总是与 HPV 无关。HPV 无关的中、低分化癌常发生 NOTCH 信号通路改变(7/7),并且与肿瘤芽生增加相关(P:0.002)。HPV 相关的外阴阴道鳞状细胞癌中 PIK3CA 激活突变(11/11,64%)是最常见的基因组事件,而 TERT 基因改变,主要是 TERT 启动子突变(15 例中的 14 例,93%)在 HPV 无关的癌中特征显著。HPV 无关肿瘤中其他常见的异常包括 TP53 突变(13/15,87%)、CDKN2A 改变(10/15,67%)和 NOTCH1 和 FAT1 突变(7/15,各 47%)。一部分 HPV 相关和 HPV 无关的肿瘤都存在 NOTCH 通路改变(6/11,55%和 10/15,67%),但这些肿瘤中改变的是该通路中的不同基因。总之,TERT、TP53、CDKN2A 和 NOTCH1 基因改变强烈指向 HPV 驱动的过程(优势比分别为 0.01、0.07、0 和 0,所有四个基因的 p 值均<0.02),而没有其他突变的 PIK3CA 激活突变强烈支持 HPV 驱动的肿瘤(优势比:10.12,p 值:0.016)。HPV 无关的癌更有可能是中-低分化,具有中等至高的肿瘤细胞芽生。HPV 无关的鳞状细胞癌的癌细胞分数分析表明,TERT 和/或 NOTCH1 改变以及 TP53 改变可能是这些肿瘤的起始事件。