Colorectal cancer is the third most common cancer worldwide, and in many parts of the western world, it is the second leading cause of cancer-related deaths.

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Introduction; N. Beauchemin, J. Huot1. The Metastatic Process: an Overview; N.Porquet, S. Guot, J. Huot1.1 Models of metastasis 1.1.1 The progression model 1.1.2 The transient compartment model 1.1.3 The early oncogenesis model 1.1.4 The fusion model 1.1.5 The gene transfer models 1.1.6 The genetic predisposition model1.2 Metastatic steps 1.2.1 Development of the primary colorectal cancer 1.2.1.1 Initiation of the primary neoplasm 1.2.1.2 Influence of stromal cells 1.2.1.3 Influence of the extracellular matrix 1.2.1.4 Epithelial-Mesenchymal transition 1.2.1.5 Angiogenesis and lymphangiogenesis 1.2.2 Intravasation 1.2.3 Circulation of cancer cells 1.2.4 Extravasation 1.2.4.1 The adhesion on endothelial cells and the homing concept of metastasis 1.2.4.2 The passage across the endothelium1.2.5 Colonization of the secondary sites1.3 Concluding RemarksReferences2. Physiopathology of Colorectal Metastasis; C. Ferrario, M. Basik2.1 Mechanisms of metastatic spread 2.1.1 Circulatory spread 2.1.1.1 Lymphatic spread 2.1.1.2 Hematogenous spread 2.1.2 Local spread 2.1.3 Tumour dormancy2.2 Sites of metastasis and consequences of spread 2.2.1 Liver 2.2.1.1 Steps in liver invasion 2.2.1.2 Development of liver failure 2.2.2 Lungs 2.2.3 Peritoneum 2.2.4 Bone and bone marrow 2.2.5 Brain metastasis2.3 factors contributing to metastatic spread 2.3.1 Tumour factors 2.3.1.1 Tissue Factor 2.3.1.2 EGFR 2.3.2 Host factors 2.3.2.1 Immunity 2.3.2.2 Diet, exercise and liver disease 2.3.3 Iatrogenic factors2.4 ConclusionReferences3. The Genetic of Colorectal Cancer; A.M. Kaz, W.M. Grady3.1 Introduction3.2 The Adenoma-to-Carcinoma Sequence3.3 Genomic Instability 3.3.1 Overview 3.3.2 Chromosome Instability 3.3.3 DNA Mismatch Repair Inactivation and Microsatellite Instability 3.3.4 Base Excision Repair Defects/MYH3.4 Common Deregulated Signalling Pathways 3.4.1 Wingless/Wnt Signalling Pathway 3.4.1.1 APC 3.4.1.2 B-Catenin (CTNNB1) 3.4.2 KRAS, BRAF and RAS-RAF-MAPK Signalling Pathway 3.4.2.1 K-RAS 3.4.2.2 BRAF 3.4.3 p53 (TP53) 3.4.4 The Phosphatidylinositol 3-kinase (PI3K) Pathway 3.4.4.1 PIK3CA 3.4.4.2 PTEN 3.4.5 TGF-B Signalling Pathways 3.4.5.1 TGFBR2 3.4.5.2 The SMAD Family of Genes 3.4.5.3 TGF-B Superfamily Receptors: ACVR2 and BMPR1A3.5 Genome-Wide Analyses of Colorectal Cancer Genes3.6 Metastasis Genes3.7 ConclusionsReferences4. Epigenetics of Colorectal Cancer; F.J. Carmona, M. Esteller4.1 Introduction4.2 DNA methylation defects in colorectal cancer 4.2.1 Hypomethylation of DNA4.3 Inactivation of tumour suppressor genes by CpG island hypermethylation4.4 Epigenetic regulation of microRNA in cancer4.5 MicroRNAs as metastasis switches4.6 Histone modification defects in colon cancer4.7 Epigenetic contribution to co