BackgroundWestern diets increase colon cancer risk. Epidemiological evidence and experimental studies suggest that ginseng can inhibit colon cancer development. In this study we asked if ginseng could inhibit Western diet (20% fat) promoted colonic tumorigenesis and if compound K, a microbial metabolite of ginseng could suppress colon cancer xenograft growth.MethodsMice were initiated with azoxymethane (AOM) and, two weeks later fed a Western diet (WD, 20% fat) alone, or WD supplemented with 250-ppm ginseng. After 1 wk, mice received 2.5% dextran sulfate sodium (DSS) for 5 days and were sacrificed 12 wks after AOM. Tumors were harvested and cell proliferation measured by Ki67 staining and apoptosis by TUNEL assay. Levels of EGF-related signaling molecules and apoptosis regulators were determined by Western blotting. Anti-tumor effects of intraperitoneal compound K were examined using a tumor xenograft model and compound K absorption measured following oral ginseng gavage by UPLC-mass spectrometry. Effects of dietary ginseng on microbial diversity were measured by analysis of bacterial 16S rRNA.ResultsGinseng significantly inhibited colonic inflammation and tumorigenesis and concomitantly reduced proliferation and increased apoptosis. The EGFR cascade was up-regulated in colonic tumors and ginseng significantly reduced EGFR and ErbB2 activation and Cox-2 expression. Dietary ginseng altered colonic microbial diversity, and bacterial suppression with metronidazole reduced serum compound K following ginseng gavage. Furthermore, compound K significantly inhibited tumor xenograft growth.ConclusionsGinseng inhibited colonic inflammation and tumorigenesis promoted by Western diet. We speculate that the ginseng metabolite compound K contributes to the chemopreventive effects of this agent in colonic tumorigenesis.

Angiogenesis has an important role in the carcinogenesis of esophageal adenocarcinoma, however, the diagnostic and prognostic utility of microvascular density counts have not been clinically established. The aim of this study is to assess the correlation between microvascular density and disease progression of non-dysplastic Barrett's esophagus, low-grade dysplasia, high-grade dysplasia and invasive carcinoma in the superficial aspects of the tissue. Archival histological specimens from two referral centers for Barrett's esophagus and esophageal cancer were selected for review. A total of 160 regions marked according to histological grade were assessed with digitally interactive software to measure microvascular density. This was quantified in three levels: 0-50, 50-100 and 100-150 lm. In the areas of gastric cardia, Barrett's esophagus, low-grade dysplasia, high-grade dysplasia and cancer, microvascular density was significantly different (Po0.0001) among the five groups in the most superficial 150 lm of the mucosa. Furthermore, when examining the pairwise difference between the groups, there was a significant difference between cancer and each of the lower grades of histology (Po0.05) and between high-grade dysplasia and each of the lower grades of histology (Po0.05). These statistically significant differences were preserved in examining the depth at the most superficial 50 lm. We have used digital pathology to demonstrate a significant and stepwise increase in microvascular density, which supports the hypothesis that angiogenesis has a key role in Barrett's carcinogenesis. Furthermore, the differences in the most superficial mucosal layers are consistent with findings of increased vascularity by depth-restricted imaging modalities. Modern Pathology (2013) 26, 125-130; doi:10.1038/modpathol.2012 published online 24 August 2012 Keywords: angiogenesis; Barrett's esophagus; esophageal cancer; microvascular density Angiogenesis has an important role in the carcinogenesis of esophageal adenocarcinoma, however, the diagnostic and prognostic utility of microvascular density counts have not been clinically established. 1,2 Esophageal adenocarcinoma arises from Barrett's esophagus in a metaplasia-dysplasia-carcinoma sequence. Intestinal metaplasia and dysplasia have been studied in terms of microvascular density, and neoangiogenesis is thought to begin in these precursor lesions. [3][4][5][6][7]

Infantile hepatic hemangioendothelioma (IHE) is a rare angiogenic tumour with diverse clinical presentations and varied course ranging from spontaneous regression to life-threatening complications. The authors report a 2-year boy who presented with respiratory distress and was identified as a case of inoperable multi-focal hepatic IHE. He showed a transient response to trans-arterial-chemo-embolisation and liver resection but had progressive disease despite chemotherapy (prednisolone/vicristine/ifosfamide/cisplatin). Thereafter, he was successfully managed with metronomic therapy using cyclophosphamide and tamoxifen.

Objective:The objective was to analyze the demography, clinical presentation, and management of spinal intradural schwannomas in pediatric population.Materials and Methods:This retrospective study includes 21 pediatric patients (under 18 years of age) who underwent surgery for spinal intradural schwannomas from January 1998 to April 2008. The medical records were reviewed retrospectively and the information regarding clinical presentation, tumor location, operative findings, and postoperative status and functional outcome were analyzed.Results:A total of 21 patients (14 females and 7 males) were operated for spinal schwannomas. Six patients had associated neurofibromatosis (five were NF I and one was NF II) at presentation. The most common presenting symptom was progressive myelopathy (86%). The tumor location was either cervical or dorsal in 18 cases. All patients underwent surgery. Gross total excision was achieved in 20 cases. The median follow-up was 38 months. All the patients had neurological improvement in both power and bladder symptoms.Conclusion:Pediatric spinal neurofibromas/schwannomas are an uncommon but completely treatable group of tumors. Complete surgical excision gives excellent outcome.

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