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Intestinal and non-intestinal nasal cavity adenocarcinoma: Impact of wood dust exposure.
European Annals of Otorhinolaryngology, Head and Neck Diseases 2018 September 8
The aim of the present study was to investigate the role of wood dust exposure in intestinal (ITAC) and non-intestinal type (non-ITAC) nasal adenocarcinoma, so as to improve understanding of the oncogenic mechanisms in the light of the recent literature and of evo-devo concepts.
MATERIALS AND METHODS: All consecutive patients operated in our institution for nasal adenocarcinoma diagnosed on anatomopathology between May 2004 and February 2014 were included. Surgical specimens were examined twice by independent pathologists, blind to wood dust exposure status. Clinical and demographic data, including wood dust exposure, were collected for the two groups (ITAC and non-IATC).
RESULTS: 90 patients (84 ITAC, 6 non-ITAC) were included. No non-ITAC patients had history of wood dust exposure, versus 83/84 cases (99%) in ITAC (mean exposure duration: 30±16 years; range 2-65 years). Only 12 ITAC patients (18%) were still exposed at diagnosis. ITAC may develop long after the end of wood dust exposure (up to 60 years). Eight patients (12%) had exposure durations of less than 5 years. Latency between onset of exposure and onset of disease did not decrease with exposure duration.
CONCLUSION: Exposure to wood dust, even for short periods of time, incurs a risk of developing ITAC, usually after a long latency period. Any exposure requires lifetime follow-up, to ensure prompt treatment. Factors leading to the development of nasal ITAC and non-ITAC are probably different. The analogy with Barret's esophagus and esophageal adenocarcinoma may shed light on the oncogenesis of nasal ITAC.
MATERIALS AND METHODS: All consecutive patients operated in our institution for nasal adenocarcinoma diagnosed on anatomopathology between May 2004 and February 2014 were included. Surgical specimens were examined twice by independent pathologists, blind to wood dust exposure status. Clinical and demographic data, including wood dust exposure, were collected for the two groups (ITAC and non-IATC).
RESULTS: 90 patients (84 ITAC, 6 non-ITAC) were included. No non-ITAC patients had history of wood dust exposure, versus 83/84 cases (99%) in ITAC (mean exposure duration: 30±16 years; range 2-65 years). Only 12 ITAC patients (18%) were still exposed at diagnosis. ITAC may develop long after the end of wood dust exposure (up to 60 years). Eight patients (12%) had exposure durations of less than 5 years. Latency between onset of exposure and onset of disease did not decrease with exposure duration.
CONCLUSION: Exposure to wood dust, even for short periods of time, incurs a risk of developing ITAC, usually after a long latency period. Any exposure requires lifetime follow-up, to ensure prompt treatment. Factors leading to the development of nasal ITAC and non-ITAC are probably different. The analogy with Barret's esophagus and esophageal adenocarcinoma may shed light on the oncogenesis of nasal ITAC.
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