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Review
. 2019 Jul 23;10(19):4455-4462.
doi: 10.7150/jca.34016. eCollection 2019.

Effect of HPV Infection on the Occurrence and Development of Laryngeal Cancer: A Review

Dongli Yang  1   2 , Yong Shi  1   2 , Yemei Tang  1   2 , Hongyu Yin  1   2 , Yujia Guo  1   2 , Shuxin Wen  1   2   3 , Binquan Wang  1   2   3 , Changming An  4 , Yongyan Wu  1   2   3 , Wei Gao  1   2   3
Affiliations
Review

Effect of HPV Infection on the Occurrence and Development of Laryngeal Cancer: A Review

Dongli Yang et al. J Cancer. .

Abstract

Laryngeal cancer has the second highest incidence of head and neck malignant tumors worldwide. In recent years, studies have shown that human papillomavirus (HPV) infection may be a high-risk factor for laryngeal cancer and closely related to the development and prognosis of laryngeal cancer. The mechanism of the occurrence and development of laryngeal cancer caused by HPV infection needs investigation, as does a rapid and effective HPV detection method for effectively preventing the occurrence of laryngeal cancer and controlling its development. Many studies have explored the relation between HPV infection and laryngeal cancer. Here we review the research progress in investigating HPV infection in terms of DNA, mRNA and protein levels in the occurrence and development of laryngeal cancer and routine HPV detection methods.

Keywords: HPV Testing; Head and Neck Carcinoma, Laryngeal Carcinoma; Human Papillomavirus; Incidence.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
Mechanism of HPV infection affecting the occurrence and development of laryngeal cancer. After HPV infects laryngeal mucosal epithelial cells, its DNA is integrated into the host cell genome, thereby resulting in altered expression of a variety of proto-oncogenes and tumor suppressor genes, the overexpression of E6 and E7 mRNA and altered function of various proteins in host cells, thus leading to disordered cell metabolism and malignant proliferation.
Figure 2
Figure 2
Survival analysis of HNSCC patients with different p16 levels in tumor samples. Kaplan-Meier analysis involved using transcriptome data for HNSCC and LSCC from the TCGA database (updated on Sept. 6, 2018). A: Kaplan-Meier plot of HNSCC patients with different p16 levels (498 samples); B: Kaplan-Meier plot of LSCC patients with different p16 levels (111 samples). High or low gene expression was classified by the median of p16 level.
See this image and copyright information in PMC

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