title: Evaluation of the prognostic role of pSTAT3 expression in temporal bone squamous cell carcinoma.
abstract: 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.
  
  
  METHODS
  Retrospective clinicopathologic investigation.
  
  
  METHODS
  Tertiary referral centers.
  
  
  METHODS
  Twenty-five consecutively operated patients with primary temporal bone SCC.
  
  
  METHODS
  pSTAT3 immunohistochemical expression in primary temporal bone SCCs was assessed with the aid of computer-based image analysis.
  
  
  METHODS
  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%).
  
  
  CONCLUSIONS
  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.
authors.affiliation: *Department of Neurosciences, Otolaryngology Section, Padova University Hospital, Padova; †Otorhinolaryngology Division, Legnano Hospital, Legnano; ‡Department of Medicine DIMED, §Pediatric Onco-Hematology Unit, and ∥Department of Neurosciences, Otosurgery Unit, Padova University Hospital, Padova; and ¶Anatomic Pathology Division, Legnano Hospital, Legnano, Italy.
authors.forename: Gino
authors.initials: G
authors.lastname: Marioni
authors.forename: Raoul
authors.initials: R
authors.lastname: Nucci
authors.forename: Filippo
authors.initials: F
authors.lastname: Marino
authors.forename: Rocco
authors.initials: R
authors.lastname: Cappellesso
authors.forename: Marta
authors.initials: M
authors.lastname: Pillon
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Zanoletti
authors.forename: Luciano
authors.initials: L
authors.lastname: Giacomelli
authors.forename: Sebastiano
authors.initials: S
authors.lastname: Franchella
authors.forename: Paola
authors.initials: P
authors.lastname: Billo
authors.forename: Roberto
authors.initials: R
authors.lastname: Pareschi
authors.forename: Alessandro
authors.initials: A
authors.lastname: Martini
mesh_terms: D000368:Aged; D002294:Carcinoma, Squamous Cell / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D018572:Disease-Free Survival; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009364:Neoplasm Recurrence, Local / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D010766:Phosphorylation; D011379:Prognosis; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D012888:Skull Neoplasms / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D015996:Survival Rate; D013701:Temporal Bone / Q000378:metabolism* / Q000473:pathology
chemical_list: D050796:STAT3 Transcription Factor