Fiche publication
Date publication
novembre 2013
Auteurs
Membres identifiés du Cancéropôle Est :
Pr JANKOWSKI Roger
,
Pr VIGNAUD Jean-Michel
,
Pr GAUCHOTTE Guillaume
,
Pr GALLET Patrice
Tous les auteurs :
Gauchotte G, Marie B, Gallet P, Nguyen DT, Grandhaye M, Jankowski R, Vignaud JM
Lien Pubmed
Résumé
Respiratory epithelial adenomatoid hamartoma (REAH) is regarded as a rare tumor of the nasal cavity. The mechanisms driving the development of REAH are unknown, and its nature as a benign tumor, hamartoma, or reactive inflammatory process is still open to discussion. A total of 150 consecutive patients operated on for nasal polyposis (NP) were extensively checked for the diagnosis of REAH. The profile of REAH occurring in association with NP was compared with solitary REAH in a series of 19 cases. The possible role of tryptase-producing mast cells (MC) and of metalloproteinases MMP2 and MMP9 in REAH development was investigated by immunohistochemistry. REAH lesions were identified in 35% of patients who had surgery for NP (53/150). The distribution of the lesions suggested that REAH originated in the olfactory cleft. Solitary REAH occurred about 20 times less frequently than those observed in an NP context but shared the same microscopic characteristics. Tryptase-producing MCs were recruited at high density in REAH (135/10 hpf), compared with inflammatory polyps (45/10 hpf; P
Référence
Am J Surg Pathol. 2013 Nov;37(11):1678-85
