Endoscopic submucosal dissection of scar-embedded rectal polyps: a prospective study (Esd in scar-embedded rectal polyps).

BACKGROUND & AIMS: Endoscopic submucosal dissection (ESD) was developed for en bloc resection of superficial neoplasm of the digestive tract. We evaluated feasibility and safety of ESD, as a salvage therapy of large refractory rectal polyps, in a tertiary care setting. METHODS: We prospectively enrolled in the present study and treated by ESD 11 consecutive patients with rectal polyps (median diameter 3.5 cm; range 2-5 cm), who had previously undergone several attempts of endoscopic resection and not suitable for further standard endoscopic treatment. The ESD was carried out with a standard needle knife. Follow up examinations were scheduled at 3, 6, 12 and 24 months. RESULTS: We achieved apparently complete resection of polyps in 10/11 patients. In one patient ESD was interrupted and the pathology of the resected fragment showed deep submucosal infiltration; this patient underwent surgery. Deep and lateral margins were shown to be free of neoplasm (radical resection) in six out of 11 patients. However all the 10 patients with apparently complete resection were free of recurrence after a mean follow up of 19.2 months (12-24). A T1 adenocarcinoma was radically resected by ESD, with no recurrence. We recorded 2 cases of subcutaneous emphysema, both treated conservatively. CONCLUSIONS: Radical resection is difficult to be achieved by ESD in patients with rectal scar-embedded polyps. Nevertheless ESD may be proposed as a definitive treatment of selected patients with refractory polyps, avoiding surgery in the majority of them.

Major hepatectomy in patients with synchronous colorectal liver metastases: whether or not a contraindication to simultaneous colorectal and liver resection?

OBJECTIVE: Synchronous hepatic lesions account for 15-25% of newly diagnosed colorectal cancer and its optimal timing to surgery is not completely defined, but simultaneous colorectal and liver resection is recently gaining acceptance, at least in patients with a right colonic primary and liver metastases that need a minor hepatectomy to be fully resected. METHOD: From September 2002 to December 2004, 16 patients underwent simultaneous resection as treatment of synchronous colorectal liver resection; in 10 patients (62.5%) a major hepatectomy was performed. RESULTS: The mean duration of intervention was 322.5 +/- 59.5 min, operative mortality and morbidity rates was 0% and 25% respectively; the hospitalization was 14.4 (range 8-60) days on average. Mean follow-up was 14 months and actuarial survival was 76.5% at 1 year and 63.5% at 2 years. CONCLUSION: We concluded that simultaneous colonic and liver resection should be undertaken in selected patients with synchronous colorectal liver resection regardless of the extent of hepatectomy; major liver resection, in fact, seems capable of providing better oncological results, allowing resection of liver micrometastases that, in almost one-third of the patients, are located in the same liver lobe of macroscopic lesions, without increased morbidity rates.

Carcinogen metabolism, DNA damage repair and oral head and neck squamocellular carcinoma (HNSCC). A review.

Head and neck squamocellular carcinoma (HNSCC) has now become the 6th most common cancer among men in the developed world and affects the oral cavity, salivary glands, larynx and pharynx. Tobacco chewing, alcohol consumption and last but not least, smoking seem to be the most important risk factors. In particular in non-drinkers, smoke increases the relative risk (RR) of developing HNSCC of the oral cavity and pharynx from 2 to 20 fold; especially in the oral cavity, the association between alcohol and smoke could have a multiplier effect. Cancer arises from damage to DNA of genes located at various points of the short (p) and long (q) arms of a number of chromosomes, caused by exposure to various carcinogens. Thus, the carcinogenic process requires continuous exposure to environmental carcinogens (i.e., longstanding history of smoking and drinking), an increased susceptibility to carcinogens (induced by xenobiotic metabolizing enzyme polymorphism) and an impaired DNA repair capacity (both inherited and acquired). Our purpose in this paper is to review advances in the understanding of the role of the European or Caucasian genetic aberrations that affect carcinogen metabolism and DNA repair genes in oral HNSCC development: we consider that those abnormalities will be useful in assessing individuals at risk.