Introduction to Oropharyngeal Carcinomas

What is/are Oropharyngeal Carcinomas?

Oropharyngeal Carcinomas - The authors also emphasize the need for determining HPV status for all oropharyngeal carcinomas. ^[1] Genetically, at least one subgroup resembles oropharyngeal carcinomas rather than those of the upper GI tract. ^[2] Methods this was a cross-sectional study of 41 patients with oropharyngeal carcinomas seen over a 2-year period. ^[3] The high-risk subtype Human Papillomaviruses (hrHPVs), including HPV16, HPV18, HPV31, HPV33, and HPV45, infect and oncogenically transform epithelial cells and cause squamous cell carcinomas and adenocarcinomas associated with the development of cervical cancer and subsets of vulvar, vaginal, penile, and anogenital cancers, as well as head-and-neck oropharyngeal carcinomas which often have poor clinical prognoses. ^[4] Introduction Many types of research have been performed to improve the diagnosis, therapy, and prognosis of oropharyngeal carcinomas (OP-SCCs). ^[5] Of the 42 solid tumors half were non-melanoma skin cancers and 7 epidermoid oropharyngeal carcinomas. ^[6] HPV positive oropharyngeal carcinomas have a very different outcome to HPV negative malignancies and are therefore considered a separate disease entity. ^[7] The present study aimed to evaluate whether human papilloma virus (HPV) infection, epidermal growth factor receptor (EGFR) and its pathway-related gene mutations, known to be sensitive biomarkers of oropharyngeal carcinomas, could be used as biomarkers for the prediction of the prognosis of patients with CESCC. ^[8] Squamous cell carcinomas (SCC) account for the majority of all primary oropharyngeal carcinomas. ^[9] Background/Aim: While in many Western countries the number of tonsillectomies decreases significantly, there is an increasing incidence of oropharyngeal carcinomas. ^[10] This case demonstrates the importance of tumor morphology and immunohistochemical testing in HPV-related oropharyngeal carcinomas, despite the overall good prognosis of such tumors, due to the possibility of synchronous or colliding primary neoplasms. ^[11] In the 8th Edition TNM Classification for Head and Neck Cancer, the classification for carcinoma of unknown primary (CUP) changed in addition to oropharyngeal carcinomas. ^[12] Discovering the key role HPV plays in head and neck carcinogenesis has revolutionized our approach to cancers such as oropharyngeal carcinomas. ^[13] The majority of human papillomavirus (HPV)–associated oropharyngeal carcinomas are squamous cell carcinomas; however, there are rare reports of HPV–associated neuroendocrine carcinomas (HPV‐NECs) in the upper aerodigestive tract. ^[14] Thus, guidance about human papillomavirus testing in oropharyngeal carcinomas and Epstein-Barr virus testing in nasopharyngeal carcinomas is highlighted. ^[15] Both regions are sites of some of the most well-studied viral-associated malignancies, including human papillomavirus-related oropharyngeal carcinomas and Epstein-Barr virus-related nasopharyngeal carcinomas. ^[16] Background: Late detection and diagnosis of oral and oropharyngeal carcinomas are responsible for the related increased morbidity and mortality. ^[17] 8% oropharyngeal carcinomas) were analyzed. ^[18] We demonstrate the concept for early T-stage oropharyngeal carcinomas and their spread to ipsilateral lymph node levels Ib to IV. ^[19] Almost all cervical carcinomas (squamous cell carcinoma and adenocarcinoma) and a significant proportion of other anogenital carcinomas (vulvovaginal, anal, penile carcinomas) and oropharyngeal carcinomas are attributed to HPV infections. ^[20] BACKGROUND The incidence of oropharyngeal carcinomas associated with human papillomavirus (HPV) is continuously increasing. ^[21] HPV status was evaluated for patients with oropharyngeal carcinomas. ^[22] Prevention: Subtypes of the human papilloma virus (HPV) have been identified as causative agent for HPV-driven oropharyngeal carcinomas nearly two decades ago. ^[23] Purpose The present retrospective multicenter study intended to investigate the factors associated with severe oral mucositis and candidiasis in patients undergoing radiotherapy for oral and oropharyngeal carcinomas. ^[24] SUMMARY The incidence of human papilloma virus (HPV)-associated head and neck squamous cell carcinoma (HNSCC) is increasing and implicated in more than 60% of all oropharyngeal carcinomas (OPSCCs). ^[25] There are significant staging differences for each anatomic site within the head and neck when lymph node sampling is considered, most importantly related to human papillomavirus-associated oropharyngeal carcinomas and mucosal melanomas. ^[26] The vast majority of cervical and 75% of oropharyngeal carcinomas are triggered by infection with a type of high-risk oncogenic human papillomavirus (HPV). ^[27] After excluding human papillomavirus-associated oropharyngeal carcinomas, two risk categories were classified as “p53 adverse function” and “p53 favorable function” based on TP53 mutation status and p53 protein phenotype. ^[28] Cyfra21-1 assay showed significant differences between tumors of different sites with prominent elevation being found in oropharyngeal carcinomas and between patients with p16 positive and p16 negative HNSCC (p=0. ^[29] Human Papillomaviruses (HPV) 16 and 18 are recognized as causative factors in 4-5% of all human cancers, including the majority of cervical and oropharyngeal carcinomas. ^[30] The purpose of our study was to assess the efficacy and safety of TLM for the treatment of early oropharyngeal carcinomas. ^[31] Primary surgery could also be the preferred modality of treatment for most early (T1–T2, N0) laryngeal and hypo/oropharyngeal carcinomas when this strategy offers an opportunity to reserve radiotherapy for a potential recurrence or second primary tumor. ^[32] The patient population consisted of 19 oropharyngeal carcinomas and four floor of the mouth cancers, all of which had stage cT4 (six female and 17 male patients), and with an average patient age of 59. ^[33]

Associated Oropharyngeal Carcinomas

The majority of human papillomavirus (HPV)–associated oropharyngeal carcinomas are squamous cell carcinomas; however, there are rare reports of HPV–associated neuroendocrine carcinomas (HPV‐NECs) in the upper aerodigestive tract. ^[1] There are significant staging differences for each anatomic site within the head and neck when lymph node sampling is considered, most importantly related to human papillomavirus-associated oropharyngeal carcinomas and mucosal melanomas. ^[2] After excluding human papillomavirus-associated oropharyngeal carcinomas, two risk categories were classified as “p53 adverse function” and “p53 favorable function” based on TP53 mutation status and p53 protein phenotype. ^[3]

Related Oropharyngeal Carcinomas

This case demonstrates the importance of tumor morphology and immunohistochemical testing in HPV-related oropharyngeal carcinomas, despite the overall good prognosis of such tumors, due to the possibility of synchronous or colliding primary neoplasms. ^[1] Both regions are sites of some of the most well-studied viral-associated malignancies, including human papillomavirus-related oropharyngeal carcinomas and Epstein-Barr virus-related nasopharyngeal carcinomas. ^[2]