
Pyogenic Granuloma of the Esophagus: A Cause of Dysphagia
Author(s) -
Ludlow David,
Thibodeaux Joel,
Nathan CherieAnn
Publication year - 2010
Publication title -
otolaryngology–head and neck surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.232
H-Index - 121
eISSN - 1097-6817
pISSN - 0194-5998
DOI - 10.1016/j.otohns.2010.06.303
Subject(s) - esophagus , dysphagia , pyogenic granuloma , medicine , granuloma , general surgery , surgery , pathology , lesion
and chemotherapy. Major causes of deaths related to head and neck squamous cell carcinoma (HNSCC) are cervical node and distant metastasis. Epithelial-mesenchymal transition (EMT) was identified to be the key role for mediating tumor invasion and metastasis of carcinomas. METHOD: The authors investigated the relationship between proinflammatory mediator and EMT in HNSCC. The author evaluated the immunohistochemical expression of interleukin-1 (IL-1 ), cyclooxygenase-2 (COX-2), Slug and E-cadherin in relationship with histologic differentiation, clinical stage and nodal status in 146 surgical specimens of HNSCC. RESULTS: There was a correlation of increased expression of IL-1 with nodal status, increased expression of COX-2 with histologic differentiation, clinical stage, and nodal status. Increased Slug expression was correlated to histologic differentiation and clinical stage. Decreased E-cadherin expression was correlated to histologic differentiation and nodal status. Significant relation was observed between IL-1 and COX-2. However, significant inverse correlation was observed between Slug and E-cadherin. Significant relation was observed between increased proinflammatory mediator IL-1 /COX-2 expression and increased EMT marker Slug/ E-cadherin expression. CONCLUSION: These results indicate that proinflammatory mediators IL-1 and COX-2 induce EMT through increase of Slug and decrease of E-cadherin. The present findings suggest some anti-inflammatory agents could be used as an adjuvant treatment modality with anti-cancer chemotherapeutic drugs in HNSCC.