This study examined the nature of the inflammatory response in the oral cavity as assessed by inflammatory markers in saliva. Both periodontal disease and diabetes mellitus were independently associated with the oral inflammatory burden, in which the effect of periodontal disease was more pronounced.

Head and neck angiosarcomas (HN-AS) are rare malignancies with a poor prognosis relative to other soft tissue sarcomas. To date, the HN-AS literature has been limited to short reports and single-institution experiences. This study evaluated patients registered with the Surveillance, Epidemiology, and End Results (SEER) program who had been diagnosed with a primary HN-AS. Predictors were drawn from demographic and baseline tumor characteristics. Outcomes were survival months and cause of death. Kaplan-Meier analyses were used to estimate overall (OS) and disease-specific survival (DSS) rates. Cox proportional hazards regression models were used for multivariate analyses. A total of 1250 patients (mean age 73.3 years) were identified, and nearly all lesions (93.5%) were cutaneous. Two-and 5-year OS rates were 47.3% (95% CI 44.3-50.3) and 26.5% (95% CI 23.7-29.3), while 2-and 5-year DSS rates were 66.6% (95% CI 63.6-69.6) and 48.3% (95% CI 44.5-52.1). In the univariate analyses, age, race, tumor grade, tumor size, AJCC stage, SEER historic stage, and surgery were significant predictors of both OS and DSS. Multivariate regression revealed that independent predictors of poor OS and DSS were older age [OS: HR 1.04 (95% CI 1.02-1.05), p < 0.01; DSS: HR 1.03 (95% CI 1.01-1.05), p < 0.01], increased tumor size [OS: HR 1.01 (95% CI 1.01-1.01), p < 0.01; DSS: HR 1.01 (95% CI 1.01-1.02), p < 0.01], and distant disease [OS: HR 2.97 (95% CI 1.65-5.34), p < 0.01; DSS: HR 4.99 (95% CI 2.50-9.98), p < 0.01]. Age, tumor size, and disease extent were determinants of HN-AS survival. When all other factors were controlled, lower histologic grade and surgery did not improve the risk of death.

Esophageal cancers comprise adenocarcinoma and squamous cell carcinoma, two distinct histologic subtypes. Both are difficult to treat and amongst the deadliest human malignancies. We describe protocols to initiate, grow, passage and characterize patient-derived organoids (PDO) of esophageal cancers as well as squamous cell carcinomas of oral/head-and-neck and anal origin. Formed rapidly (< 14 days) from a single cell suspension embedded in basement membrane matrix, esophageal cancer PDO recapitulate the histology of the original tumors. Additionally, we provide guidelines for morphological analyses and drug testing coupled with functional assessment of cell response to conventional chemotherapeutics and other pharmacological agents in concert with emerging automated imaging platforms.

BackgroundFor early‐stage oral squamous cell carcinoma (OSCC), there is no existing risk‐stratification modality beyond conventional TNM staging system to identify patients at high risk for cancer‐specific mortality.MethodsA total of 568 early‐stage OSCC patients who had surgery only and also with available 5‐year clinical outcomes data were identified. Signature microRNAs (miRNAs) were discovered using deep sequencing analysis and validated by qRT‐PCR. The final 5‐plex prognostic marker panel was utilized to generate a cancer‐specific mortality risk score using the multivariate Cox regression analyses. The prognostic markers were validated in the internal and external validation cohorts.ResultsThe risk score from the 5‐plex marker panel consisting of miRNAs‐127‐3p, 4736, 655‐3p, TNM stage and histologic grading stratified patients into four risk categories. Compared to the low‐risk group, the high‐risk group had 23‐fold increased mortality risk (hazard ratio 23, 95% confidence interval 13‐42), with a median time‐to‐recurrence of 6 months and time‐to‐death of 11 months (vs >60 months for each among low‐risk patient; p < .001).ConclusionThe miRNA‐based 5‐plex marker panel driven mortality risk score formula provides clinically practical and reliable measures to assess the prognosis of patients assigned to an early‐stage OSCC.