Rare case of small intestine bleeding.

We present a case of a healthy 59-year-old woman who presented for a capsule endoscopy to evaluate melaena and iron deficiency anaemia. She had previously underwent an oesophagogastroduodenoscopy and colonoscopy at an outside institution which were unremarkable. Capsule endoscopy showed an ulcerated, bleeding lesion likely in the duodenum. Differential diagnosis included adenocarcinoma, carcinoid tumour, lymphoma, gastrointestinal stromal tumour and metastatic disease. A push enteroscopy was performed after which showed an ulcerated mass in the third portion of the duodenum. Biopsies confirmed adenocarcinoma. Computed tomography of the abdomen showed no signs of distant metastasis and the patient was referred to surgery for evaluation. The patient underwent a pancreaticoduodenectomy, with resection of the mass and negative lymph nodes in all nine that were removed (T3N0). The patient was classified as stage II duodenal adenocarcinoma. Duodenal adenocarcinoma is a rare but clinically significant cause of small bowel bleeding.

AFPep: an anti-breast cancer peptide that is orally active.

BACKGROUND: We have synthesized a cyclic nonapeptide (AFPep) that is effective, after being administered by parenteral routes, for the treatment or the prevention of breast cancer. To test the hypothesis that AFPep remains safe and efficacious after oral administration, three different whole-animal bioassays were utilized, and the mechanism by which AFPep functions was investigated. METHODS: Using a human breast cancer xenograft model in mice for therapeutic activity, a carcinogen-induced breast cancer model in rats for prevention efficacy, and a mouse uterus growth inhibition model of anti-estrogenic activity, AFPep was administered by oral gavage (p.o.) and its effects compared to those following intraperitoneal (i.p.) and subcutaneous (s.c.) administration. Toxicity studies evaluated body weights and organ weights in mice and rats receiving AFPep. Preliminary mechanistic studies were carried out in T47D human breast cancer cells growing in culture and evaluated the effect of AFPep on estrogen-stimulated cell growth, phosphorylation of the estrogen receptor (ER), and on level of ER-related kinases. RESULTS: Orally administered AFPep stopped the growth of human tumor xenografts in mice, decreased the incidence and multiplicity of breast cancers in carcinogen-exposed rats, and inhibited the estrogen-stimulated growth of mouse uteri. In each of these systems, orally administered AFPep produced an effect similar to that obtained for AFPep administered by either i.p or s.c. routes. In rodents, no evidence of toxicity was seen for the peptide, even at very high doses. In culture, AFPep inhibited the estrogen-stimulated growth, but not the basal growth, of T47D cells, and it inhibited the estrogen-stimulated phosphorylation of Serine 118 in the ER of these cells, which was not explainable by early changes in ER-related kinases. CONCLUSIONS: Chronic oral administration of AFPep appears to be safe and effective for the treatment or prevention of breast cancer in animal models.