Total mesorectal excision (TME) appears to be associated with a reduced local recurrence rate following surgery for rectal cancer. Of 20 patients with rectal cancer in whom TME was performed, adenocarcinoma was found in the distal mesorectum in four. Distal mesorectal spread often extended further than intramural spread. Patients with tumour in the distal mesorectum had a worse outcome at 4-year follow-up, a greater risk of local recurrence and an increased frequency of distant metastasis. Distal tumour spread is, therefore, a marker of poor prognosis in rectal cancer. This study provides further evidence that incomplete excision of the mesorectum contributes to local recurrence in a proportion of patients with rectal cancer, particularly in those with tumours in the middle and lower third of the rectum.

The 'intestinal' form of gastric cancer, which is the commonest type, develops against a background of chronic gastritis, atrophy, and intestinal metaplasia.1 2 Helicobacter pylori is the cause of (type B) chronic gastritis and has been shown in epidemiological studies to be a major risk factor for the development of gastric cancer.3-6 Increased mucosal cell proliferation increases the likelihood of the development of a neoplastic clone of epithelial cells7 where there is chronic epithelial injury associated with H pylori positive gastritis. However, little is known about cell proliferation in H pyloni associated gastritis. The aims of the study were, firstly, to compare antral mucosal cell proliferation in normal gastric mucosa with H pylori positive and negative chronic gastritis and, secondly, to determine the effect of H pylori eradication treatment on cell proliferation. MethodsPatients undergoing routine diagnostic endoscopy were recruited after informed consent. Those taking non-steroidal anti-inflammatory drugs, H2 antagonists, proton pump inhibitors, or bismuth salts, or those who had undergone gastric surgery, were excluded from the study. Using standard biopsy forceps, tissue specimens were taken from the gastric antrum (three) and corpus (two) for histological and immunohistochemical studies. The study was approved by the hospital ethical committee. HISTOLOGYTwo antral and two corpus biopsy specimens from each site were routinely processed, and stained with haematoxylin and eosin.H PYLORI H pylori status was determined using a modified Giemsa stain on the antral and corpus sections and a biopsy urease test (CLO/DeltaWest) on the third antral biopsy specimen. To establish eradication of the micro-organism, both tests had to be negative. IMMUNOHISTOCHEMISTRYTwo antral biopsy specimens for immunostaining were put immediately into RPMI (without L-Glutamine) (Gibco) containing bromodeoxyuridine (5 mg/10 ml). They were immersed in a waterbath for 60 minutes at 37°C then placed on filter paper and fixed in 346 on 10 May 2018 by guest. Protected by copyright.

No abstract

Patients who have undergone gastric resection are at higher risk of developing gastric carcinoma than normal subjects, and bile reflux is believed to play a role in carcinogenesis. An Little is known of the cell kinetics of the gastric corpus mucosa in H pylori gastritis or after gastric resection. This study aimed to measure mucosal cell proliferation in H pylori gastritis affecting the corpus and to compare this with cell proliferation in the gastric corpus after surgical resection. MethodsPatients undergoing routine diagnostic endoscopy were recruited after they had given informed consent. Those taking H2 antagonists, proton pump inhibitors, non-steroidal anti-inflammatory drugs, antibiotics, or bismuth salts were excluded from the study. At endoscopy, using standard forceps, biopsy specimens were taken from the antrum (2) and corpus (3) of the intact stomach. In patients who had undergone gastric resection, biopsy specimens (3) were taken from a point approximately 5-10 cm from the anastomosis, or 10 cm from the pylorus in the intact resected stomach, on the greater curve. Two biopsy specimens from each site were placed in 10% formalin, routinely processed, and stained with haematoxylin and eosin. A modified Giemsa stain was used to detect H pylori. The third biopsy from the corpus or gastric remnant was taken for in vitro bromodeoxyuridine labelling. Only biopsy specimens of the gastric remnant that were of body type mucosa were included in the study. The study was approved by the hospital ethics committee. BROMODEOXYURIDINE LABELLINGThe corpus/remnant biopsy specimen for immunostaining was put immediately into RPMI 1640 (without L-Glutamine) (Gibco) containing bromodeoxyuridine (5 mg/10 ml), incubated in a waterbath for 60 minutes at 370C, then placed on filter paper and fixed in formalin. Using a three step immunoperoxidase technique, sections were stained with anti-bromodeoxyuridine (DAKOPATT) antibody (1:20 dilution) for 60 minutes. Only sections that were complete and orientated were counted. For the purpose of counting, the gastric mucosa was divided into three zones: zone 1=surface and gastric pit; zone 2 = isthmus; zone 3=gland base. The number of cells to be counted was determined by counting consecutive high power fields until the continuous mean varied by less than 5%. Five hundred cells were found to be necessary.