Gastric Cancer Following Bariatric Surgery: a Review

Background Bariatric procedures can induce a massive weight loss, that lasts more than 15 years after surgery; in addition they achieve important metabolic effects including diabetes resolution in the majority of morbidly obese patients. However some bariatric interventions may cause gastroesophageal reflux disease and other serious complications. The aim of our study is to evaluate the risk of cancer after bariatric surgery. Methods We performed a review of literature about the cases of gastric cancer arising after any bariatric procedure, including a case of adenocarcinoma incidentally discovered by the authors six months after Laparoscopic Adjustable Gastric Banding. Results Globally 17 case reports describing 18 patients were retrieved, including the case of the authors. The diagnosis of tumor was at mean of 8,6 years after bariatric surgery, respectively 9,3 after RYGB and 8,1 after restrictive procedures. The adenocarcinoma represented most cases (15 patients - 83%). In the patients with RYGB the adenocarcinoma was localized in the excluded stomach in 5 (83%) and in the pouch in 1 (17%). After a restrictive procedure the cancer was localized in the pouch in 5 patients (62,5%), in the pylorus in 2 patients (25%) and in lesser curvature only in 1 (12,5%). Conclusion Nowadays there is a lack of evidence about a connection between the late occurrence of gastric adenocarcinoma and the bariatric surgery. For this reason while the preoperative upper endoscopy is still mandatory, there is no need for a regular endoscopic evaluation of patients after surgery

Apoptosis inhibition in cancer cells: a novel molecular pathway that involves BAG3 protein

Stress-induced apoptosis regulates neoplasia pathogenesis and response to therapy. Indeed, cell transformation induces a stress response, that is overcome, in neoplastic cells, by alterations in apoptosis modulators; on the other hand, antineoplastic therapies largely trigger the apoptosis stress pathway, whose impairment results in resistance. Therefore, the study of the roles of apoptosis- modulating molecules in neoplasia development and response to therapy is of key relevance for our understanding of these processes. Among molecules that regulate apoptosis, a role is emerging for BAG3, a member of the BAG co-chaperone protein family. Proteins that share the BAG domain are characterized by their interaction with a variety of partners (heat shock proteins, steroid hormone receptors, Raf-1 and others), involved in regulating a number of cellular processes, including proliferation and apoptosis. BAG3, also known as CAIR-1 or Bis, forms a complex with the heat shock protein (Hsp) 70. This assists polypeptide folding, can mediate protein delivery to proteasome and is able to modulate apoptosis by interfering with cytochrome c release, apoptosome assembly and other events in the death process. It has been recently shown that, in human primary lymphoid and myeloblastic leukemias and other neoplastic cell types, BAG3 expression sustains cell survival and underlies resistance to therapy, through downmodulation of apoptosis. This review summarizes findings that assign an apoptotic role to BAG3 in some neoplastic cell types and identify the protein as a candidate target of therapy. © 2007 Elsevier Ltd. All rights reserved