This book is the proceedings of the Falk Symposium 158, on Intestinal Inflammation and Colorectal Cancer, held in Seville, Spain, in March 2007. It covers the current understanding of inflammation-driven colon carcinogenesis, highlights the most relevant mechanisms and discusses measures to interfere with this process. This is a true translational topic which will attract both basic scientists and clinicians, specifically those who can make a difference in preventing this type of cancer.
The past 15 years have brought significant progress in the molecular understanding of colon carcinogenesis and tumor progression. In contrast, the functional relationship between inflammation and the origin of cancer is not new. Highlighted by over 400 scientific reports, the role model of inflammation-driven carcinogenesis is colorectal cancer in ulcerative colitis. Today, this relationship between chronic inflammation and carcinogenesis is well established by epidemiological data and has become widely accepted. In addition, we have just started to learn how cancer may create an inflammation-like environment that augments disease progression and metastasis.
Clinicians, researchers, graduate students, academics
Table of contents
List of principal contributors
List of chairpersons
SECTION I: EPIDEMIOLOGY OF THE VILLAIN.- 1 Colorectal cancer in patients with inflammatory bowel disease: influence of nutritional.- 2 Inflammatory bowel disease high-risk groups.-
SECTION II: NOT ALL COLORECTAL CANCERS ARE THE SAME.- 3 Getting familiar with familial colon cancer.- 4 The adenomatous polyposis coli tumour-suppressor protein in normal gut tissue maintenance and cancer.- 5 Mismatch repair competency predicts 5-fluorouracil effectiveness on patient survival.- 6 Inflammatory bowel disease-related cancer – just the same as sporadic? – Pro.- 7 Differences between sporadic and colitis-associated colorectal cancer.-
SECTION III: SCREENING AND SURVEILLANCE.- 8 Endoscopic guidelines for hereditary non-polyposis colorectal cancer, familial adenomatous polyposis, inflammatory bowel disease and sporadic colorectal cancer.- 9 Which new techniques will replace classical surveillance?.- 10 How to deal with dysplasia and adenomatous polyps in inflammatory bowel disease.-
SECTION IV: TAKING DYSPLASIA TO THE MOLECULAR LEVEL.- 11 Inflammation-driven carcinogenesis: the players.- 12 Cancer originating from bone marrow stems cells: can we extrapolate from gastritis to colitis?.- 13 Translating laboratory findings into clinics: of mice and man.-
SECTION V: HOW CAN WE PREVENT?.- 14 Inner and outer environment.- 15 Can we prevent inflammatory bowel disease-related colorectal cancer with 5-aminosalicylic acid, azathioprine, or 6-mercaptopurine? The clinical evidence.- 16 How can we prevent colorectal cancer with ursodeoxycholic acid?.-
SECTION VI: MOLECULAR ACTIONS OF 5-ASA – THE MAGIC BULLETT.- 17 5-Aminosalicylic acid and replication fidelity.- 18 New mechanisms of action of 5-aminosalicylic acid: PPAR-gamma: how it decreases inflammation and cancer.- 19 Mesalazine and the prevention of colorectal cancer in inflammatory bowel disease.- 20 Mesalazine and cell cycle progression.- 21 Chemopreventive role of mesalazine in inflammatory bowel disease-associated colorectal cancer: the role of DNA methylation.- 22 Molecular actions of 5-aminosalicylic acid: the magic bullet on epidermal growth factor receptor signalling.-
SECTION VII: STATE-OF-THE-ART LECTURE.- 23 State-of-the Art-Lecture: Infection, inflammation and cancer – the future.-
SECTION VIII: PROGRESSION OF CANCER THROUGH INFLAMMATORY MECHANISMS.- 24 An integrating concept of malignant progression in colorectal cancer.- 25 The balance between survival and apoptosis.- 26 The tumour microenvironment regulates components of the fucose biosynthesis pathways in colorectal cancer cells.-