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Abstract Summary and conclusion Colorectal cancers (CRC) is the third most commonly diagnosed malignancy and the fourth leading cause of cancer-related deaths worldwide, and its burden is expected to increase by 60% to more than 2.2 million new cases and 1.1 million cancer deaths by 2030. The development of CRC is a complex and heterogeneous process arising from an interaction between multiple etiological factors, including genetic factors and environmental factors such as diet and life style. Despite on-going efforts to establish an early preventive screening of the disease, 25% of CRC patients present metastasis at initial diagnosis and 50% will develop metastasis after diagnosis. Like other types of human solid tumors, CRC genomes harbor various types of genomic alterations ranging from small-scale changes (i.e., point mutations or small indels) to large-scale chromosomal copy number changes or rearrangements. Some of these alterations may contribute to colorectal carcinogenesis as oncogenic drivers, but the full spectrum of driver genomic alterations in CRC genomes is still incomplete. NGS technology appeared at the beginning of the current century as an alternative to Sanger sequencing. Its major advantage is to dramatically increase the sequence through put by performing several thousands of sequencing reactions simultaneously. |