This book reaches out to a wide variety of professionals in the biomedical field with an interest in inflammatory bowel disease (IBD). Enormous progress has been made in the last few years since the publication of the first edition in the study of complex diseases and IBD, with hundreds of genomic regions identified that are associated with increased risk. Authored by leading clinical and research scientists in the field, the book includes state-of-the art synopses of recent genetic findings, and their interpretation for current and future exploitation in translational approaches to personalized medicine in IBD. The book also covers risk prediction, improved diagnostic and therapeutic precision, dissection of disease phenotypes and subtypes, identification of biomarkers, and host gene-microbiota interactions of clinical relevance.

This book reaches out to a wide variety of professionals in the biomedical field with an interest in inflammatory bowel disease (IBD). Enormous progress has been made in the last few years since the publication of the first edition in the study of complex diseases and IBD, with hundreds of genomic regions identified that are associated with increased risk. Authored by leading clinical and research scientists in the field, the book includes state-of-the art synopses of recent genetic findings, and their interpretation for current and future exploitation in translational approaches to personalized medicine in IBD. The book also covers risk prediction, improved diagnostic and therapeutic precision, dissection of disease phenotypes and subtypes, identification of biomarkers, and host gene-microbiota interactions of clinical relevance.

Research in Crohn's disease (CD) and ulcerative colitis (UC), together known as the inflammatory bowel diseases (IBD), has truly seen a revolution in the last 5-10 years. This book examines how these genetic discoveries have led to the identification of biological functions not previously associated with IBD pathophysiology (e.g. autophagy), how multiple genetic risk factors for IBD converge on given biological functions and that together the identified variants in these genes have predisposing and protective roles (e.g. the multiple variants in the receptor for the IL23 cytokine and its signaling cascade), and how having such a large number of known genetic risk factors has changed our understanding not only about the genetic and molecular overlap between CD and UC, but also between these diseases and other chronic inflammatory diseases (e.g. psoriasis, multiple sclerosis, type 1 diabetes and many others).

Research in Crohn's disease (CD) and ulcerative colitis (UC), together known as the inflammatory bowel diseases (IBD), has truly seen a revolution in the last 5-10 years. This book examines how these genetic discoveries have led to the identification of biological functions not previously associated with IBD pathophysiology (e.g. autophagy), how multiple genetic risk factors for IBD converge on given biological functions and that together the identified variants in these genes have predisposing and protective roles (e.g. the multiple variants in the receptor for the IL23 cytokine and its signaling cascade), and how having such a large number of known genetic risk factors has changed our understanding not only about the genetic and molecular overlap between CD and UC, but also between these diseases and other chronic inflammatory diseases (e.g. psoriasis, multiple sclerosis, type 1 diabetes and many others).