Despite major advances in therapy, cancer continues to be a leading cause of mortality. In addition, toxicities of traditional therapies pose a significant challenge to tolerability and adherence. TTFields, a noninvasive anticancer treatment modality, utilizes alternating electric fields at specific frequencies and intensities to selectively disrupt mitosis in cancerous cells. TTFields target proteins crucial to the cell cycle, leading to mitotic arrest and apoptosis. TTFields also facilitate an antitumor immune response. Clinical trials of TTFields have proven safe and efficacious in patients with glioblastoma multiforme (GBM), and are FDA approved for use in newly diagnosed and recurrent GBM. Trials in other localized solid tumors are ongoing. Clin Cancer Res; 24(2); 266-75. Ó2017 AACR.

Most patients with hepatitis C virus have been treated or will be treated with direct-acting antivirals. It is important that we can model the risk of hepatocellular carcinoma in these patients, so that we develop the optimum screening strategy that avoids unnecessary screening, while adequately screening those at increased risk. Herein, we have developed and validated models that are available as web-based tools that can be used to guide screening strategies.

Background and aimsHepatocellular carcinoma (HCC) risk is high in cirrhosis. We sought to describe differences in HCC risk, predictors and trends over time according to etiology of cirrhosis.MethodsWe identified 116,404 patients with cirrhosis diagnosed between 2001–2014 in the VA healthcare system and determined incident HCC cases occurring from the date of cirrhosis diagnosis until 01/31/2017. Patients were divided by cirrhosis etiology into hepatitis C virus (HCV, n = 52,671), alcoholic liver disease (ALD, n = 35,730), nonalcoholic fatty liver disease (NAFLD, n = 17,354), or OTHER (n = 10,649).ResultsDuring a mean follow-up of 4.3 years, 10,042 new HCC cases were diagnosed. Patients with HCV had >3 times higher incidence of HCC (3.3 per 100 patient-years) than patients with ALD (0.86/100 patient-years), NAFLD (0.90/100 patient-years) or OTHER (1.0/100 patient-years), an association that persisted after adjusting for baseline characteristics. HCC incidence was 1.6 times higher in patients with cirrhosis diagnosed in 2008–2014 (2.47/100 patient-years) than in 2001–2007 (1.55/100 patient-years).Independent predictors of HCC among all cirrhosis etiologies included: age, male sex, Hispanic ethnicity, high serum alpha fetoprotein, alkaline phosphatase and AST/√ALT ratio and low serum albumin and platelet count. Diabetes was associated with HCC in ALD-cirrhosis and NAFLD-cirrhosis, and BMI in ALD-cirrhosis.ConclusionsHCC risk is 3 times greater in cirrhotic patients with HCV than ALD or NAFLD. HCC risk continues to increase over time in analyses extending to 2017 in cirrhosis of all etiologies. Multiple readily available risk factors for HCC were identified that were influenced by cirrhosis etiology and could be used to develop HCC risk estimation models.

There are no significant differences between DAA regimens in HCC risk after antiviral treatment. This suggests that DAAs do not have direct carcinogenic effects as it would be unlikely that different DAAs would have identical carcinogenic effects.

Endoscopic full-thickness resection (EFTR) has emerged as a viable technique in the management of mucosal and subepithelial lesions of the gastrointestinal tract (GIT) not amenable to conventional therapeutic approaches. While various devices and techniques have been described for EFTR, a single, combined full-thickness resection and closure device (full-thickness resection device, FTRD system, Ovesco Endoscopy AG, Tuebingen, Germany) has become commercially available in recent years. Initially, the FTRD system was limited to use in the colorectum only. Recently, a modified version of the FTRD has been released for EFTR in the upper GIT as well. This review provides a broad summary of the FTRD, highlighting recent advances and current challenges.

A 72-year-old man with recently diagnosed metastatic appendiceal adenocarcinoma undergoing chemotherapy with capecitabine plus oxaliplatin presented with lower abdominal pain and watery, large-volume diarrhea up to 15 times per day for the previous 3 weeks. His diarrhea was nonbloody, woke him up from sleep, was accompanied by crampy abdominal pain, and was not associated with nausea or vomiting. The diarrhea persisted despite treatment with combinations of loperamide, atropine/diphenoxylate, colestipol, and tincture of opium. He required repeated intravenous infusions for fluid and electrolyte repletion. His physical examination results revealed normal vital signs and a mildly tender abdomen with hyperactive bowel sounds, but no peritoneal signs. His laboratory workup results were notable for severe hypokalemia and hypomagnesemia, as well as positive fecal lactoferrin and elevated fecal calprotectin levels of 646 μg/g. His infectious workup results were unremarkable. A computed tomography scan of the abdomen/pelvis revealed diffuse longsegment wall thickening involving nearly the entire terminal ileum (Figure , A). An ileocolonoscopy revealed erythematous and congested mucosa with scattered erosions and ulcerations throughout the examined terminal ileum (Figure , B). Targeted biopsies were obtained (Figure , C). Histopathology C Colonoscopy B Contrasted computed tomography A Figure. Contrasted computed tomography of the abdomen and pelvis (A), colonoscopy (B), and histopathology (hematoxylin-eosin, original magnification ×100) (C). WHAT IS YOUR DIAGNOSIS? A. Cytomegalovirus ileitis B. Capecitabine-induced terminal ileitis C. Ileal metastasis D. Small bowel carcinoid tumor Clinical Review & Education