Scholarlink

Background <p>Oropharyngeal squamous cell carcinoma (OPSCC) is the second largest contributor to cancer in the head and neck region. The typical ENT cancer patient—an elderly male smoker and drinker—is becoming less common. In part fueled by the decline in smoking prevalence, there is a growing new group of younger patients with human papillomavirus (HPV)-associated tumors and a&#xa0;significantly better prognosis. Since the eighth Union for International Cancer Control (UICC) tumor classification, HPV-positive and HPV-negative OPSCC have been treated as separate entities.</p> Methods <p>We performed a&#xa0;selective literature search in the PubMed database to establish the current state of knowledge regarding viral and non-viral carcinogenesis of OPSCC.</p> Results <p>Most HPV infections abate within 1&#xa0;year. However, if a&#xa0;high-risk HPV type remains active, it can lead to an HPV-positive cancer decades later. The oncoproteins E6 (suppression of p53) and E7 (inactivation of retinoblastoma protein) play a&#xa0;central role in this mechanism by influencing the cell cycle. While HPV-negative tumors lack these oncoproteins, mutations in <i>CDKN2A</i> and <i>TP53</i> often lead to similar effects. In addition, the tumor microenvironment (TME) has effects on carcinogenesis: HPV-positive OPSCC is characterized by an immunoactive TME, whereas HPV-negative OPSCC has a&#xa0;more suppressed environment. Some details of the complex interplay between immune and tumor cells are already known; however, many central questions remain unanswered and the research requirement is high.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Virale und nichtvirale Karzinogenese bei Oropharynxkarzinomen – humane Papillomaviren als Karzinogen

  • 期刊论文

  • 发表日期：

    2025年10月28日

查看全文
  • Raphaela Graessle,
  • Markus Wirth

摘要

Background

Oropharyngeal squamous cell carcinoma (OPSCC) is the second largest contributor to cancer in the head and neck region. The typical ENT cancer patient—an elderly male smoker and drinker—is becoming less common. In part fueled by the decline in smoking prevalence, there is a growing new group of younger patients with human papillomavirus (HPV)-associated tumors and a significantly better prognosis. Since the eighth Union for International Cancer Control (UICC) tumor classification, HPV-positive and HPV-negative OPSCC have been treated as separate entities.

Methods

We performed a selective literature search in the PubMed database to establish the current state of knowledge regarding viral and non-viral carcinogenesis of OPSCC.

Results

Most HPV infections abate within 1 year. However, if a high-risk HPV type remains active, it can lead to an HPV-positive cancer decades later. The oncoproteins E6 (suppression of p53) and E7 (inactivation of retinoblastoma protein) play a central role in this mechanism by influencing the cell cycle. While HPV-negative tumors lack these oncoproteins, mutations in CDKN2A and TP53 often lead to similar effects. In addition, the tumor microenvironment (TME) has effects on carcinogenesis: HPV-positive OPSCC is characterized by an immunoactive TME, whereas HPV-negative OPSCC has a more suppressed environment. Some details of the complex interplay between immune and tumor cells are already known; however, many central questions remain unanswered and the research requirement is high.