Human papillomavirus prevalence in a Mid‐European oral squamous cell cancer population: A cohort study

Torre, Daniel Dalla; Burtscher, Doris; Soelder, Elisabeth; Offermanns, Vincent; Rasse, Michael; Puelacher, Wolfgang

doi:10.1111/odi.12882

Cited by 15 publications

(17 citation statements)

References 30 publications

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“…Altogether, these findings support the hypothesis that the traditional risk factors can be responsible for just a small proportion of cases of oral cancer among young people and that factors other than tobacco and alcohol are implicated (Al‐Amad, Awad, & Nimri, 2014; Dalla Torre et al., 2018; Fan et al., 2014; Guidry, Birdwell, & Scott, 2018; Lee et al., 2020; Llewellyn, Linklater, Bell, Johnson, & Warnakulasuriya, 2003; Llewellyn, Bell, Johnson, & Warnakulasuriya, 2004; Purwanto et al., 2020; Toporcov et al., 2015; Vidal Loustau et al., 2019).…”

Section: Have You Ever Had a Diagnosis Of Genital Herpes? Have You Evsupporting

confidence: 73%

Oral Human Papillomavirus (HPV) and sexual behaviors in a young cohort of oral cancer survivors

et al. 2020

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Section: Have You Ever Had a Diagnosis Of Genital Herpes? Have You Evsupporting

confidence: 73%

Oral Human Papillomavirus (HPV) and sexual behaviors in a young cohort of oral cancer survivors

et al. 2020

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“…Head and neck squamous cell carcinomas comprise a diverse group of tumors, which are classified into anatomical subsites including oral cavity, oropharynx, hypopharynx, larynx, and nasopharynx. Cancers of different subsites are known to have unique epidemiology, anatomy, clinical behavior, and association with human papilloma virus (HPV) infection [1, 2]. In this review, we will focus on HPV-driven oropharyngeal squamous cell carcinoma (OPSCC), which has become a matter of growing clinical urgency as its incidence has dramatically increased in recent years.…”

Section: Introductionmentioning

confidence: 99%

HPV-driven oropharyngeal cancer: current knowledge of molecular biology and mechanisms of carcinogenesis

2018

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Understanding of oropharyngeal squamous cell carcinoma has significantly progressed over the last decades, and the concept that this disease can be subdivided into two distinct entities based on human papilloma virus (HPV) status has gained acceptance. To combat the constantly growing epidemic of HPV+ oropharyngeal cancer, further investigation and characterization the unique features of the disease, along with the development and implementation of new, targeted therapies, is crucial. In this review, we summarize the etiology, pathogenesis, diagnosis, treatment, and molecular characteristics of HPV-associated oropharyngeal squamous cell carcinoma.

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“…Head and neck squamous cell carcinomas (HNSCCs) comprise a diverse group of tumors, which are classified into various anatomical sites (e.g. oral cavity, oropharynx, hypopharynx, larynx, and nasopharynx), with unique epidemiology, anatomy, clinical behavior, and association with human papilloma virus (HPV) or Epstein-Barr Virus infection [1, 2]. HPV-negative (HPV(−)) head and neck cancers are strongly associated with tobacco and alcohol use and are most commonly found in the oral cavity and larynx [3].…”

Section: Introductionmentioning

confidence: 99%

NSD1 mutations by HPV status in head and neck cancer: differences in survival and response to DNA-damaging agents

et al. 2019

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Background Compared to HPV-negative head and neck squamous cell carcinomas (HNSCCs), HPV-positive HNSCCs are associated with a favorable prognosis in part due to their improved treatment sensitivity. Inactivating mutations in NSD1 were shown to be a favorable prognostic biomarker in laryngeal cancers. Here, we characterize NSD1 mutations from the expanded The Cancer Genome Atlas (TCGA) HNSCC cohort (n = 522) and examine their prognostic implications based on HPV status of the tumor. We also begin to examine if NSD1 regulates response to platinum-based drugs and other DNA-damaging agents. Methods TCGA HNSCC samples were segregated by HPV and NSD1 mutations using cBioPortal and patient survival was determined. Pathogenicity of mutations was predicted using UMD-Predictor. NSD1-depleted cell lines were established by transfection with control or shRNAs against NSD1, followed by puromycin selection, and confirmed by qRT-PCR. Cell sensitivity to DNA damaging agents was assessed using short-term proliferation and long-term clonogenic survival assays. Results Among 457 HPV(−) tumors, 13% contained alterations in the NSD1 gene. The majority (61.3%) of NSD1 gene alterations in HPV(−) specimens were truncating mutations within or before the enzymatic SET domain. The remaining alterations included homozygous gene deletions (6.7%), missense point mutations (30.7%) and inframe deletions (1.3%). UMD-Predictor categorized 18 of 23 missense point mutations as pathogenic. For HPV(+) HNSCC (n = 65), 6 NSD1 mutations, comprised of two truncating (33%) and 4 missense point (66%) mutations, were identified. Three of the 4 missense point mutations were predicted to be pathogenic or probably pathogenic by UMD-Predictor. Kaplan-Meier survival analysis determined significantly improved survival of HPV(−) HNSCC patients whose tumors harbored NSD1 gene alterations, as compared to patients with wild-type NSD1 tumors. Interestingly, the survival effect of NSD1 mutations observed in HPV-negative HNSCC was reversed in HPV(+) tumors. Proliferation and clonogenic survival of two HPV(−) cell lines stably expressing control or NSD1 shRNAs showed that NSD1-depleted cells were more sensitive to cisplatin and carboplatin, but not to other DNA damaging drugs. Conclusions Genetic alterations in NSD1 hold potential as novel prognostic biomarkers in HPV(−) head and neck cancers. NSD1 mutations in HPV(+) cancers may also play a prognostic role, although this effect must be examined in a larger cohort. NSD1 downregulation results in improved sensitivity to cisplatin and carboplatin, but not to other DNA-damaging agents, in epithelial cells. Increased sensitivity to platinum-based chemotherapy agents associated with NSD1 depletion may contribute to improved survival in HPV(−) HNSCCs. Further studies are needed to determine mechanisms through which NSD1 protects HPV(−) HNSCC cells from platinum-based therapy, as well as confirmation of NSD1 effect in HPV(+...

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Human papillomavirus prevalence in a Mid‐European oral squamous cell cancer population: A cohort study

Cited by 15 publications

References 30 publications

Oral Human Papillomavirus (HPV) and sexual behaviors in a young cohort of oral cancer survivors

Oral Human Papillomavirus (HPV) and sexual behaviors in a young cohort of oral cancer survivors

HPV-driven oropharyngeal cancer: current knowledge of molecular biology and mechanisms of carcinogenesis

NSD1 mutations by HPV status in head and neck cancer: differences in survival and response to DNA-damaging agents

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