**1. Introduction**

Colorectal cancer (CCR) is the third most common cancer in men, the second in women and the third most prevalent cause of mortality in the world. It was estimated more than 1.8 million new cases in 2018 according to American Institute for Cancer Research and Continuous Update project panel. It is linked to the transition nutrition to the western lifestyle, consuming processed meat, red meat and alcoholic drinks, greater body fatness and adult height increase the risk of the disease. The incidence of the disease continues to rise especially in low and middle income countries and it is considered one of the clearest markers for rapid societal and economic changes that are associated with cancer development [1].

Genetic knowledge is essential for understanding of carcinogenic colorectal cancer, and can develop strategies for prevention, diagnosis and treatment. A list of genes in which mutations are capable of interfering with both cancer creation and treatment, has grown a lot in recent years, helping to understand risks for cancer formation and identifying several promising therapeutic targets. Today focused on a best treatment, but research on colorectal cancer genetics began with a focus on diagnosis, much of our understanding of pathogenesis came from study of hereditary syndromes of colorectal diseases that advanced into cancer, showing a huge diversity in types of colorectal cancer and genetic involvement.

In 1882 W. Harrison Cripps associated in his work that multiple intestinal polyposis had hereditary nature and also potentially malignant nature. Subsequently in 1913 Aldred S. Warthin reported on 1600 cases of carcinoma treated at University of Michigan for 19 years, collecting detailed family histories of approximately 500 patients and mapping a predisposition to gastrointestinal and endometrial carcinogenesis of three generations. In 1950, Eldon J. Gardner at University of Utah conducted a long genetic study in patient families with multiple polyps and established a link between this event and a predisposition to carcinomatosis only in 1986 Herrera et al. described a case of a patient with polyposis and multiple carcinomatosis, with an amputation in a long arm of chromosome 5, suggesting a location of tumor suppressor gene. Subsequent studies in families with polyps have identified the 5q21 region as adenomatous polyposis coli or APC gene. Since then, we have identified numerous genetic defects and genetic expressions showing a diversity of mutations with distinct pathways of progression [2].

There have been significant advances in the last years and more than understanding the risk factors for CCR, recent progress in the field of molecular biology, has allowed us to identify the oncogenesis basis to the development of the disease. Then apply these knowledge in the research of new drugs that lead to better outcomes even in the advanced disease.
