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致癌性人乳头瘤病毒导致三分之一的鼻窦鳞状细胞癌，且与基因突变并非相互排斥。

Oncogenic Human Papillomaviruses Drive One-Third of Sinonasal Squamous Cell Carcinoma and Are Not Mutually Exclusive for Gene Mutations.

作者信息

Henrion Maxime, Costes-Martineau Valérie, Bravo Ignacio González, Boulle Nathalie, Solassol Jérôme, Vendrell Julie, Garrel Renaud, Trinquet Aude, Lacheretz-Szablewski Vanessa

机构信息

Departement de Pathologie, Centre Hospitalo-Universitaire Montpellier, Montpellier, France.

Laboratoire MIVEGEC, Centre National de la recherche Scientifique (CNRS), Montpellier, France.

出版信息

Head Neck. 2025 Jun;47(6):1726-1735. doi: 10.1002/hed.28084. Epub 2025 Jan 25.

DOI:10.1002/hed.28084
PMID:39865501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12068539/
Abstract

BACKGROUND

The detection rate of oncogenic human papillomaviruses (HPVs) in sinonasal squamous cell carcinomas (SNSCCs) varies among studies. The mutational landscape of SNSCCs remains poorly investigated.

METHODS

We investigated the prevalence and prognostic significance of HPV infections based on p16 protein expression, HPV-DNA detection, and E6/E7 mRNA expression using immunohistochemistry, polymerase chain reaction, and in situ hybridization, respectively. In addition, we evaluated the genetic mutations in 59 patients using next-generation sequencing.

RESULTS

One-third of the SNSCCs were truly oncogenic HPV-driven tumors associated with a nonkeratinizing morphology (p = 0.01) and did not correlate with the prognosis. The following gene mutations were detected: TP53, PIK3CA, CDKN2A, EGFR, and FGFR3. These mutations occurred alone, in association with, or with oncogenic HPV.

CONCLUSION

One-third of SNSCCs were high-risk HPV driven lesions. However, gene mutations and HR-HPV infections are not mutually exclusive. Further studies are required to analyze the prognostic value of these associations.

摘要

背景

鼻窦鳞状细胞癌（SNSCCs）中致癌性人乳头瘤病毒（HPVs）的检出率在不同研究中有所差异。SNSCCs的突变图谱仍未得到充分研究。

方法

我们分别使用免疫组织化学、聚合酶链反应和原位杂交技术，基于p16蛋白表达、HPV-DNA检测和E6/E7 mRNA表达来研究HPV感染的患病率和预后意义。此外，我们使用下一代测序技术评估了59例患者的基因突变情况。

结果

三分之一的SNSCCs是真正由致癌性HPV驱动的肿瘤，与非角化形态相关（p = 0.01），且与预后无关。检测到以下基因突变：TP53、PIK3CA、CDKN2A、EGFR和FGFR3。这些突变单独出现、与致癌性HPV共同出现或与致癌性HPV同时出现。

结论

三分之一的SNSCCs是高危HPV驱动的病变。然而，基因突变和高危型HPV感染并非相互排斥。需要进一步研究来分析这些关联的预后价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/fe0af68859f5/HED-47-1726-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/bae661c778b2/HED-47-1726-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/28dfd2f100e1/HED-47-1726-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/eb6cb2cc7c38/HED-47-1726-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/53dc99d246c3/HED-47-1726-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/fe0af68859f5/HED-47-1726-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/bae661c778b2/HED-47-1726-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/28dfd2f100e1/HED-47-1726-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/eb6cb2cc7c38/HED-47-1726-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/53dc99d246c3/HED-47-1726-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da59/12068539/fe0af68859f5/HED-47-1726-g002.jpg

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本文引用的文献

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Exome sequencing reveals candidate mutations implicated in sinonasal carcinoma and malignant transformation of sinonasal inverted papilloma.外显子组测序揭示了与鼻窦癌和鼻窦内翻性乳头状瘤恶变相关的候选突变。
Oral Oncol. 2022 Jan;124:105663. doi: 10.1016/j.oraloncology.2021.105663. Epub 2021 Dec 13.
3
p16 overexpression and Rb loss correlate with high-risk HPV infection in oropharyngeal squamous cell carcinoma.
p16 过表达和 Rb 缺失与口咽鳞状细胞癌中高危 HPV 感染相关。
Histopathology. 2021 Sep;79(3):358-369. doi: 10.1111/his.14337. Epub 2021 May 6.
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Genomic Sequencing of Cancer-related Genes in Sinonasal Squamous Cell Carcinoma and Coexisting Inverted Papilloma.鼻窦鳞状细胞癌及共存的内翻性乳头状瘤相关基因的基因组测序。
Anticancer Res. 2021 Jan;41(1):71-79. doi: 10.21873/anticanres.14752.
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Clinicopathologic Significance of EGFR Mutation and HPV Infection in Sinonasal Squamous Cell Carcinoma.鼻窦鳞状细胞癌中 EGFR 突变和 HPV 感染的临床病理意义。
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Cancers (Basel). 2020 Aug 9;12(8):2224. doi: 10.3390/cancers12082224.
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