Head & Neck最新文献

{"title":"iPLA2β regulates the dual effects of arachidonic acid in thyroid cancer","authors":"Yu Zhang, Wei Su, Zhou Yang, Dan Zhao, Qing Guan, Tian Liao, Duanshu Li, Baijie Feng, Yunjun Wang, Yu Wang, Jun Xiang","doi":"10.1002/hed.27937","DOIUrl":"https://doi.org/10.1002/hed.27937","url":null,"abstract":"BackgroundAbnormal arachidonic acid metabolism in the tumor microenvironment is closely related to cancer progression; however, thyroid cancer was rarely researched.MethodsThrough lipidomic analysis, we disclosed that dysregulated arachidonic acid metabolism plays dual effects on thyroid cancer. The promoting role of arachidonic acid in the progression of thyroid cancer cells was evaluated utilizing cell viability (CCK‐8 assay) and transwell invasion assays, confirmed by corresponding inhibitors. Lipid peroxidation and the use of various cell death inhibitors confirmed that arachidonic acid confers vulnerability to ferroptosis in thyroid cancer. The roles of arachidonic acid and ferroptosis inducer in thyroid cancer were assessed in a xenograft mouse model.ResultsOn one hand, arachidonic acid promotes the progression of thyroid cancer through the cyclooxygenase/prostaglandin pathway; on another hand, arachidonic acid confers vulnerability to ferroptosis through lipoxygenases. Moreover, iPLA2β drives converse roles of arachidonic acid between cancer‐progression and ferroptosis vulnerability through releasing free arachidonic acid from the cell membrane. Finally, we confirmed high arachidonic acid diet promotes the development of thyroid cancer in vivo, whereas ferroptosis inducer sulfasalazine dramatically reduced tumor growth of mice with feeding arachidonic acid.ConclusionsOur research demonstrated the roles of iPLA2β in conversing dual effects of arachidonic acid in thyroid cancer and provides ferroptosis inducer as a potential therapeutic strategy.","PeriodicalId":501638,"journal":{"name":"Head & Neck","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond complete remission: A comparative analysis of long‐term laryngeal function in patients with hypopharyngeal and laryngeal cancer following radiotherapy and concurrent chemoradiation","authors":"Gene Huh, Eun‐Jae Chung, Won Shik Kim, Seong Keun Kwon, Myung‐Whun Sung, Bhumsuk Keam, Hong‐Gyun Wu, Joo Ho Lee, Jin Ho Kim, Soon‐Hyun Ahn","doi":"10.1002/hed.27935","DOIUrl":"https://doi.org/10.1002/hed.27935","url":null,"abstract":"BackgroundThis study evaluates functional larynx preservation in patients with hypopharyngeal cancer (HPC) and laryngeal cancer (LC) who achieved complete remission following radiotherapy (RT) or concurrent chemoradiation (CCRT).MethodsHPC and LC patients treated with RT/CCRT from 1999 to 2017 were retrospectively analyzed. Severe late dysphagia and tracheostomy cases were assessed to determine laryngeal function. Long‐term preservation rate of functional larynx and associated factors were evaluated.ResultsOf 152 patients (55 HPC, 97 LC), nine developed severe dysphagia, occurring on average 58.2 months post‐treatment. HPC and cervical node metastasis significantly increased the risk of laryngeal function impairment (<jats:italic>p</jats:italic> &lt; 0.001 and <jats:italic>p</jats:italic> = 0.014, respectively), presenting a continued decline in functional larynx preservation rate beyond 10 years.ConclusionsPatients with HPC and cervical node metastasis demonstrate an increased risk for long‐term laryngeal function impairment despite successful oncologic outcomes. This risk extends beyond 10 years, underscoring the need for prolonged monitoring and comprehensive support.","PeriodicalId":501638,"journal":{"name":"Head & Neck","volume":"15 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering the impact of STAT3 activation mediated by PTPRT promoter hypermethylation as biomarker of response to paclitaxel‐plus‐cetuximab in patients with recurrent or metastatic squamous cell carcinoma of the head and neck","authors":"Beatriz Cirauqui Cirauqui, Adrià Bernat Peguera, Ariadna Quer Pi‐Sunyer, Angelica Ferrando‐Díez, Jose Luis Ramírez Serrano, Marta Domenech Viñolas, Iris Teruel García, Vanesa Quiroga García, Imane Chaib Oukadour, Andrea González Valencia, Pilar Hernández Vergara, Itziar de Aguirre Egaña, Cristina Queralt Herrero, Oscar Mesía Carbonell, Assumpció López Paradís, Anna Esteve, Mireia Margelí Vila, Rafael Rosell, Anna Martínez‐Cardús, Ricard Mesía","doi":"10.1002/hed.27892","DOIUrl":"https://doi.org/10.1002/hed.27892","url":null,"abstract":"BackgroundSquamous cell carcinoma of the head and neck (SCCHN) is an aggressive disease with poor prognosis. It is known that the activation of STAT3 signaling pathways promotes the development and progression of this neoplasia and it has been described the role of PTPRT as a negative regulator of STAT3. Then, we have evaluated the impact of them as biomarkers of outcome in a series of patients with recurrent and/or metastatic SCCHN treated with weekly paclitaxel‐plus‐cetuximab (ERBITAX) regimen.Patients and methodsBetween 2008 and 2017, 52 patients with recurrent/metastatic SCCHN were treated with ERBITAX at our center, 34 of whom had available tumor samples. Phosphorylated STAT3 (pSTAT3) protein expression was analyzed by immunohistochemistry, <jats:italic>STAT3</jats:italic> mRNA expression by qPCR, and <jats:italic>PTPRT</jats:italic> promoter methylation by methylation‐specific PCR. Molecular results were correlated with response rate (RR), progression‐free survival (PFS), and overall survival (OS).ResultspSTAT3 overexpression was detected in 67% and <jats:italic>PTPRT</jats:italic> promoter hypermethylation in 41% of tumor samples. <jats:italic>PTPRT</jats:italic> promoter hypermethylation showed a trend towards an association with lower RR (21% vs. 60%; <jats:italic>p</jats:italic> = 0.06). A lower RR was also observed in patients with pSTAT3 overexpression (36% vs. 54%) and in those with high <jats:italic>STAT3</jats:italic> mRNA levels (43% vs. 64%), but these differences did not reach statistical significance. <jats:italic>PTPRT</jats:italic> promoter hypermethylation correlated with pSTAT3 overexpression (<jats:italic>p</jats:italic> = 0.009) but not with <jats:italic>STAT3</jats:italic> mRNA overexpression. OS and PFS was shorter in patients with activated STAT3, but the difference did not reach statistical significance.ConclusionsAlthough this was a relatively small retrospective study, it provides preliminary indications of the potential role of the STAT3 pathway on outcome in SCCHN and confirms that PTPRT acts as a negative regulator of STAT3. Our findings warrant investigation in a larger patient cohort to determine if inactivating this pathway through specific targeted treatments could improve outcomes in recurrent/metastatic SCCHN patients.","PeriodicalId":501638,"journal":{"name":"Head & Neck","volume":"94 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141776787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recurrence after primary salivary gland carcinoma: Frequency, survival, and risk factors","authors":"Lisa Nachtsheim, L. Jansen, S. Shabli, C. Arolt, A. Quaas, J. P. Klussmann, M. Mayer, P. Wolber","doi":"10.1002/hed.27880","DOIUrl":"https://doi.org/10.1002/hed.27880","url":null,"abstract":"BackgroundPrimary salivary gland carcinomas (SGC) are rare neoplasms that present therapeutic challenges especially in recurrent tumors. The aim of this study was to investigate the incidence and distribution of tumor recurrence, associated risk factors, and survival.MethodsThis analysis includes data from 318 patients treated for SGC between 1992 and 2020. Survival analysis was performed using the Kaplan–Meier method. Univariate and multivariate analyses were used to identify risk factors associated with recurrence.Results21.7% of the patients developed recurrent disease after a mean of 38.2 months. In multivariate analysis, positive‐resection margins, vascular invasion, and tumor localization in the submandibular gland and small salivary glands were independent factors for recurrence. The 5‐year overall survival was 67%, the 5‐year disease‐free survival was 54%.ConclusionTumor recurrence in SGC occurred in one out of five patients. In highly aggressive entities and patients with risk factors, treatment intensification should be considered.","PeriodicalId":501638,"journal":{"name":"Head & Neck","volume":"61 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141776786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}