REVIEW ARTICLE Helicobacter pylori: Gastric Cancer and Extragastric Intestinal Malignancies Michael Selgrad,* 1 Jan Bornschein,* 1 Theodore Rokkas † and Peter Malfertheiner* *Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke-University of Magdeburg, Magdeburg, Germany, † Gastroenterology Clinic, Henry Dunant Hospital, Athens, Greece Keywords gastric cancer, colorectal cancer, pepsinogen EMR, atrophic gastritis. Reprint requests to: Peter Malfertheiner, Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke- University of Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany. E-mail: peter. malfertheiner@med.ovgu.de 1 These authors equally contributed to this manuscript. Abstract The greatest challenge in Helicobacter pylori–related diseases continues to remain prevention of gastric cancer. New evidence supports the beneficial effect of H. pylori eradication not only on prevention of gastric cancer but also on the regression of preneoplastic conditions of the gastric mucosa. Con- cerning early detection of gastric cancer there are still no adequate means and there is urgent need to define appropriate markers, for example, by gen- ome-wide research approaches. Currently, the best available method is the “serologic” biopsy based on pepsinogen I and the pepsinogen I/II ratio for identification of patients with severe gastric atrophy at increased risk for gas- tric cancer development. The treatment of early gastric cancer by endoscopic techniques can be performed safely and efficiently, but patients need metic- ulous follow-up for detection of metachronous lesions. In case of advanced disease, laparoscopically assisted surgical procedures are safe and favorable compared to open surgery. Two phase III trials support the role of adjuvant systemic treatment with different regimens. Unfortunately, there is still only slow progress in the development of palliative treatment regimens or modifi- cation of the existing therapy protocols. There is accumulating evidence for a role of H. pylori infection also in colorectal carcinogenesis. Seropositive individuals are at higher risk for the development of colorectal adenomas and consequently adenocarcinomas of this anatomical region. This phenom- enon can partly be attributed to the increase of serum gastrin as response to atrophic changes of the gastric mucosa. In 2012, the infection with Helicobacter pylori remains one of the most challenging infectious diseases of the world, causing high morbidity and mortality. The major burden in global health care is still given by H. pylori representing the main risk factor for gastric cancer (GC), the second leading cause of cancer-related death. During the past years, the progress in the clinical management of GC has been modest. Innovations are limited to modifications of the existing chemotherapy regimens in either palliative or perioperative settings. Furthermore, new data have been gained concerning the endoscopic treatment of early GC. This review summarizes recent clinical- and research- related advances in the field of H. pylori and GC that have been published between April 2011 and April 2012, including also recent insights concerning the association between H. pylori infection and colorectal neoplasias. Prevention and Screening of Gastric Cancer H. pylori infection leads in all infected individuals to a chronic active gastritis, which can proceed, via the so-called Correa cascade, to gastric mucosal atrophy and intestinal metaplasia (IM), and finally to the devel- opment of GC. Thus, atrophy and IM are considered as precancerous conditions, and H. pylori eradication ther- apy is considered as preventive for GC [1]. Several studies have proven that eradication therapy also improves, or at least prevents, progression of gastric atrophy and IM; however, some did not show a benefit [2–5]. A recent study therefore evaluated the gastric mucosa of patients that underwent eradication therapy in a long-term follow-up [6]. A total of 118 patients have been monitored after successful eradication ther- © 2012 Blackwell Publishing Ltd, Helicobacter 17 (Suppl. 1): 30–35 30 Helicobacter ISSN 1523-5378 doi: 10.1111/j.1523-5378.2012.00980.x