Abstract
Although a decline in colorectal cancer (CRC) incidence rate has been registered, attributed to increases in screening adhesion rates and linked detection and removal of precancerous lesions, CRC remains one of the most common cancers (1,2). By its frequency, CRC ranks third in men and second in women worldwide. Originally depicted as a multi-step dynamical disease (3,4), it is now recognized that CRC develops slowly over several years and progresses through benign and malignant states, from single crypt lesions through adenoma, to malignant carcinoma with the potential for local invasion and distant metastasis. CRC is a heterogeneous disease; it encompasses different genetic pathways and cellular entities with a wide range of clinical behaviors (5,6). The response to treatment is variable between patients, even when they are diagnosed at the same clinical stage. Such clinical heterogeneity remains an obstacle to the optimization of treatment for each individual.
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