26 - World Journal of Gastroenterology

More documents

Recommendations

Info

Murray KF, Abrams SH, Rosenthal P, Sanyal AJ, Robuck PR, Brunt EM, Unalp A, Tonascia J. Treatment of nonalcoholic fatty liver disease in children: TONIC trial design. Contemp Clin Trials 2010; 31: 62-70 96 Lavine JE, Schwimmer JB, Molleston JP, Chalasani NP, Rosenthal P, Murray KF, Abrams SH, Scheimann AO, Sanyal AJ, Brunt EM, Kleiner DE, Robuck PR,Van Natta M, Unalp A, Tonascia J. Vitamin E, Metformin or placebo for treatment of nonalcoholic fatty liver disease in children. Hepatology 2010; 52 Supp l: 110A 97 Sanyal AJ, Chalasani N, Kowdley KV, McCullough A, Diehl AM, Bass NM, Neuschwander-Tetri BA, Lavine JE, Tonascia J, Unalp A, Van Natta M, Clark J, Brunt EM, Kleiner DE, Hoofnagle JH, Robuck PR. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med 2010; 362: 1675-1685 98 Armstrong MJ, Houlihan DD, Rowe IA. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med 2010; 363: 1185; author reply 1186 99 Maggard MA, Shugarman LR, Suttorp M, Maglione M, Sugerman HJ, Livingston EH, Nguyen NT, Li Z, Mojica WA, Hilton L, Rhodes S, Morton SC, Shekelle PG. Meta-analysis: surgical treatment of obesity. Ann Intern Med 2005; 142: 547-559 100 Sjöström L, Lindroos AK, Peltonen M, Torgerson J, Bouchard C, Carlsson B, Dahlgren S, Larsson B, Narbro K, Sjöström WJG|www.wjgnet.com Pacifico L et al . Pediatric NAFLD and cardiovascular risk CD, Sullivan M, Wedel H. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med 2004; 351: 2683-2693 101 Mathurin P, Hollebecque A, Arnalsteen L, Buob D, Leteurtre E, Caiazzo R, Pigeyre M, Verkindt H, Dharancy S, Louvet A, Romon M, Pattou F. Prospective study of the long-term effects of bariatric surgery on liver injury in patients without advanced disease. Gastroenterology 2009; 137: 532-540 102 Pratt JS, Lenders CM, Dionne EA, Hoppin AG, Hsu GL, Inge TH, Lawlor DF, Marino MF, Meyers AF, Rosenblum JL, Sanchez VM. Best practice updates for pediatric/adolescent weight loss surgery. Obesity (Silver Spring) 2009; 17: 901-910 103 Pardee PE, Lavine JE, Schwimmer JB. Diagnosis and treatment of pediatric nonalcoholic steatohepatitis and the implications for bariatric surgery. Semin Pediatr Surg 2009; 18: 144-151 104 Nadler EP, Youn HA, Ren CJ, Fielding GA. An update on 73 US obese pediatric patients treated with laparoscopic adjustable gastric banding: comorbidity resolution and compliance data. J Pediatr Surg 2008; 43: 141-146 105 Nadler EP, Reddy S, Isenalumhe A, Youn HA, Peck V, Ren CJ, Fielding GA. Laparoscopic adjustable gastric banding for morbidly obese adolescents affects android fat loss, resolution of comorbidities, and improved metabolic status. J Am Coll Surg 2009; 209: 638-644 S- Editor Tian L L- Editor O’Neill M E- Editor Ma WH 3091 July 14, 2011|Volume 17|Issue 26|
Online Submissions: http://www.wjgnet.com/1007-9327office wjg@wjgnet.com doi:10.3748/wjg.v17.i26.3092 REVIEW Intestinal inflammation and colorectal cancer: A doubleedged sword? Angelamaria Rizzo, Francesco Pallone, Giovanni Monteleone, Massimo Claudio Fantini Angelamaria Rizzo, Francesco Pallone, Giovanni Monteleone, Massimo Claudio Fantini, Department of Internal Medicine, University of Rome “Tor Vergata”, Rome, Italy Author contributions: Rizzo A, Pallone F, Monteleone G and Fantini MC equally contributed to generating the ideas for this review and writing this manuscript. Supported by “Associazione Italiana per la Ricerca sul Cancro”, AIRC, MFAG-9353 and “Fondazione Umberto di Mario”, Rome Correspondence to: Massimo Claudio Fantini, MD, PhD, Department of Internal Medicine, University of Rome “Tor Vergata”, Via Montpellier 1, 00133, Rome, Italy. m.fantini@med.uniroma2.it Telephone: +39-6-72596150 Fax: +39-6-72596391 Received: August 14, 2010 Revised: September 30, 2010 Accepted: October 7, 2010 Published online: July 14, 2011 Abstract Chronic inflammation is thought to be the leading cause of many human cancers including colorectal cancer (CRC). Accordingly, epidemiologic and clinical studies indicate that patients affected by ulcerative colitis and Crohn’s disease, the two major forms of inflammatory bowel disease, have an increased risk of developing CRC. In recent years, the role of immune cells and their products have been shown to be pivotal in initiation and progression of colitis-associated CRC. On the other hand, activation of the immune system has been shown to cause dysplastic cell elimination and cancer suppression in other settings. Clinical and experimental data herein reviewed, while confirming chronic inflammation as a risk factor for colon carcinogenesis, do not completely rule out the possibility that under certain conditions the chronic activation of the mucosal immune system might protect from colonic dysplasia. © 2011 Baishideng. All rights reserved. Key words: Colorectal cancer; Inflammation; T cells; Cytokines; Immunosurveillance WJG|www.wjgnet.com 3092 World J Gastroenterol 2011 July 14; 17(26): 3092-3100 ISSN 1007-9327 (print) ISSN 2219-2840 (online) © 2011 Baishideng. All rights reserved. Peer reviewers: Ole Høie, MD, PhD, Department of Gastroenterology, Sørlandet Hospital, Arendal, N-4809, Norway; Alexander Becker, MD, Department of Surgery, Haemek Medical Center, Afula 18000, Israel Rizzo A, Pallone F, Monteleone G, Fantini MC. Intestinal inflammation and colorectal cancer: A double-edged sword? World J Gastroenterol 2011; 17(26): 3092-3100 Available from: URL: http://www.wjgnet.com/1007-9327/full/v17/i26/3092.htm DOI: http://dx.doi.org/10.3748/wjg.v17.i26.3092 INTRODUCTION Chronic inflammation is thought to be the leading cause of many human cancers including colorectal cancer (CRC). Ulcerative colitis (UC) and Crohn’s disease (CD), the two major forms of inflammatory bowel disease (IBD), are associated with an increased risk of developing colitisassociated colorectal cancer (CAC). The risk of CRC in UC patients is 2% after 10 years, 8% after 20 years and 18% after 30 years of active disease [1] . Although more recently other studies have estimated a lower risk in this class of patients, the overall incidence rate ratio for developing CRC calculated in UC patients was found by Bernstein et al [2] to be 2.75 [95% confidence interval (95% CI), 1.91-3.97] compared to the general population. While the relationship between UC and CRC is well established, the risk associated with CD has been unclear until recently. Indeed, the heterogeneous nature of CD which can involve any part of the gut in a non-continuous way, with many patients having no colonic involvement, makes it difficult to estimate the actual risk of developing CRC in these patients. A milestone Swedish study demonstrated a relative risk of CRC of 5.6 for CD patients with exclusive localization in the colon and 3.2 for patients with ileo-colitis [3] . In contrast, patients with exclusive ileal localization of the disease had no increased risk. A meta-analysis of CRC risk in CD revealed an overall relative risk of 2.5 (95% CI, 1.3-4.7) [4] . In the subset of patients with exclusive colonic July 14, 2011|Volume 17|Issue 26|
Page 1 and 2: World Journal of Gastroenterology W
Page 3 and 4: Robert JL Fraser, Daw Park Jacob Ge
Page 5 and 6: Italy Donato F Altomare, Bari Piero
Page 7 and 8: Fernando Azpiroz, Barcelona Ramon B
Page 9 and 10: S Contents EDITORIAL REVIEW ORIGINA
Page 11 and 12: Contents APPENDIX FLYLEAF EDITORS F
Page 16 and 17: of HCC. Multimodal approaches with
Page 18 and 19: 15S): A4577 63 Gruenwald V, Wilkens
Page 20 and 21: cause of liver disease in pediatric
Page 22 and 23: Table 1 Published studies on the as
Page 24 and 25: genesis through the presence of abn
Page 26 and 27: Manini R, Natale S, Vanni E, Villan
Page 30 and 31: localization, the risk was 4.5 (95%
Page 34 and 35: The role of chemokines in CAC is fu
Page 36 and 37: MM, Rotter JI, Nicolae DL, Cho JH.
Page 38 and 39: Online Submissions: http://www.wjgn
Page 40 and 41: HO-1 Donor liver CO induced exclusi
Page 42 and 43: Table 1 Upregulation of heme oxygen
Page 44 and 45: N, Takamiya Y, Yamaguchi T, Ishimur
Page 48 and 49: Table 1 Clinical characteristics of
Page 50 and 51: A CCL20 mRNA expression relative to
Page 53 and 54: Rubie C et al . FOLFOX and CCL20/CC
Page 55 and 56: Strickertsson JAB et al . Interfero
Page 57 and 58: Table 1 Fundic somatostatin mRNA in
Page 59 and 60: A Ghrelin mRNA, arb expression C Pl
Page 61 and 62: Strickertsson JAB et al . Interfero
Page 65 and 66: Pompili M et al . PEI treatment of
Page 67 and 68: Cum survival Pompili M et al . PEI
Page 69 and 70: Pompili M et al . PEI treatment of
Page 71 and 72: Deng SX et al . Colorectal cancer s
Page 79 and 80:
Li GL et al . Biliary complications
Page 81 and 82:
Li GL et al . Biliary complications
Page 83:
Gao F et al . Combined therapy for
Page 86 and 87:
esponse of the tumor was seen in on
Page 88 and 89:
Online Submissions: http://www.wjgn
Page 90 and 91:
Clostridium; PY Agar for Clostridiu
Page 92 and 93:
C A i h g f e d c b a M WJG|www.wjg
Page 94 and 95:
tion-based study. J Clin Gastroente
Page 96 and 97:
and the subsequent blood transfusio
Page 99 and 100:
Wang HQ et al . Vascular occlusion
Page 101 and 102:
Wang HQ et al . Vascular occlusion
Page 104 and 105:
After reviewing the medical literat
Page 106 and 107:
Extradigestive manifestations of He
Page 108 and 109:
Page 110 and 111:
Page 112 and 113:
Page 114 and 115:
System at: http://www.wjgnet.com/10
Page 116 and 117:
Books Personal author(s) 10 Sherloc
show all

26 - World Journal of Gastroenterology

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?