{'fraction_non_alphanumeric': 0.037374221370388115, 'fraction_numerical': 0.022041207474844275, 'mean_word_length': 5.566037735849057, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Evaluation of the Prognostic Role of pSTAT3 Expression in Temporal Bone Squamous Cell Carcinoma

Objective Temporal bone squamous cell carcinoma (SCC) accounts for less than 0.2% of all head and neck tumors. Although some progress has been made in treating this aggressive tumor, the prognosis in advanced cases remains poor. More effective therapeutic strategies need to be considered, including receptor-mediated carcinoma-targeted therapy. Phosphorylated STAT3 (pSTAT3) regulates many genes that are necessarily expressed in cancer initiation, development, and progression, being involved in proliferation, anti-apoptosis, invasion, angiogenesis, and immune surveillance evasion. The aim of the present study was to preliminarily investigate the potential prognostic role of pSTAT3 expression in temporal bone SCC. Study Design Retrospective clinicopathologic investigation. Setting Tertiary referral centers. Patients Twenty-five consecutively operated patients with primary temporal bone SCC. Intervention pSTAT3 immunohistochemical expression in primary temporal bone SCCs was assessed with the aid of computer-based image analysis. Main Outcome Measures Conventional clinicopathologic parameters and pSTAT3 expression were correlated with SCC prognosis. Results pT, stage, and surgical margin status were significantly related with recurrence rate (p = 0.002, p = 0.01, and p = 0.047, respectively) and disease-free survival (DFS) (p = 0.0049, p = 0.031, and p = 0.035, respectively). pT classification was also related with disease-specific survival (DSS) (p = 0.035). The SCC recurrence rate did not correlate with pSTAT3 expression. Statistical analyses ruled out any significant difference in DFS or DSS when patients were stratified by pSTAT3 expression (>80.0% or ⩽80.0%). Conclusion Despite our preliminary results, the role of pSTAT3 in temporal bone SCC warrants further investigation in larger series because there is increasing evidence in preclinical models to indicate that inhibiting STAT3 phosphorylation can be a useful addition to different anticancer strategies.