Objective(s): To delineate the somatic mutational landscape of follicular thyroid carcinoma (FTC) from a large, real-world cohort to identify molecular subtypes and actionable targets for personalized therapeutic interventions. Methods: Genomic and clinical data for 168 FTC samples were retrieved from the AACR Project GENIE^® registry via cBioPortal. This study assessed mutation frequencies, copy number alterations, and subgroup differences (primary vs. metastatic; adult vs. pediatric) using statistical tests. Results: NRAS was the most common mutation (33.9%), followed by TERT (22.6%), DICER1 (15.5%), HRAS (11.9%), and PTEN (10.7%). DICER1 mutations were significantly enriched in pediatric cases (44.4% vs. 4.6% in adults, p < 0.001), while TERT mutations were exclusive to adults (42%). NRAS mutations were more frequent in metastatic tumors (42.4%) than primary tumors (29.2%). Conclusions: FTC tumorigenesis is driven by distinct molecular pathways, with significant heterogeneity between pediatric and adult patients as well as primary and metastatic disease. These findings underscore the necessity of molecular profiling for patient stratification and provide a strong rationale for developing personalized treatment strategies to improve clinical outcomes.

For centuries, infectious diseases have represented a leading cause of global morbidity and mortality, with high transmissibility posing persistent public health challenges. Because early physiological changes often precede overt clinical symptoms, continuous physiological monitoring may provide opportunities for earlier recognition of illness and timely intervention. In this study, we developed and evaluated a wireless wearable device capable of measuring microvascular tissue oxygen saturation, respiratory rate, respiratory rhythm, breathing depth, heart rate, and pulse strength. Device performance was assessed in a clinical study involving healthy participants performing breath-holding, paced breathing, and mild hypercapnia tasks. Breathing rate and heart rate derived from the wearable device were compared with corresponding measurements obtained from commercial physiological monitoring systems. Chest tissue oxygen saturation measured by the wearable device was additionally evaluated alongside peripheral blood oxygen saturation measured using a commercial pulse oximeter. Across all tasks, wearable-derived breathing rate and heart rate demonstrated strong agreement with commercial systems, with small biases (≤0.19 breaths/min for breathing rate and ≤0.47 beats/min for heart rate). Chest tissue oxygen saturation exhibited distinct and rapid responses during breath-holding and mild hypercapnia, whereas peripheral oxygen saturation showed delayed or inconsistent changes. During breath-holding, changes in tissue oxygenation preceded peripheral desaturation by approximately 10 seconds. Collectively, these findings demonstrate the feasibility of the wearable device for real-time, continuous monitoring of cardiorespiratory parameters and microvascular tissue oxygenation, and suggest that tissue-level oxygenation measurements may provide complementary physiological information relevant to early respiratory stress in both general health and infectious disease research contexts.

Objective: We aimed to characterize the somatic mutational landscape of oropharyngeal squamous cell carcinoma (OPSCC) and identify potential genomic drivers of tumor progression and therapeutic resistance using the AACR GENIE database. Study Design: Retrospective genomic analysis was employed. Setting: We used publicly available data from the American Association for Cancer Research (AACR) Project GENIE database accessed via cBioPortal. Methods: We analyzed 412 tumor samples from 401 patients diagnosed with OPSCC. Somatic mutations, clinical variables and tumor characteristics were extracted and analyzed. Statistical comparisons of mutation frequencies across gender and tumor stage (primary vs. metastatic) were conducted. Co-occurrence and mutual exclusivity analyses were performed to identify significant genomic patterns. Results: The most frequently mutated genes included TP53 (30.1%), PIK3CA (26.0%), and KMT2D (21.6%). Gender-specific analyses suggested potential enrichment of TP53 and MET mutations in females and of ZNF750 in males. Distinct mutation patterns were observed between primary and metastatic tumors; primary tumors were enriched for mutations in TP53 and CDKN2A, while metastatic lesions harbored unique alterations in genes like CBLB and BUB1B, suggesting pathways involved in immune evasion and chromosomal instability may drive disease progression. Co-occurrence was noted between PIK3CA and FBXW7, and mutual exclusivity between TP53 and CYLD. Conclusions: This study identifies distinct genomic signatures in OPSCC subgroups, highlighting candidate biomarkers in pathways like PI3K/AKT signaling that warrant further investigation. Validating these markers in prospective trials is a critical next step to translate these findings into personalized therapeutic strategies for OPSCC patients.