| Sumario: | We read with interest the recent study by Hu et al., in which they described an approach to elucidate the genomic landscape of synchronous colorectal cancer (SCRC). They used a cohort of paired tumors located in different sites of the colon (right and left colon) and analyzed single nucleotide variation, somatic mutation, and copy number alteration by whole-exome sequencing. The authors finally suggested the heterogeneity between lesions and the polyclonal origin of the paired tumors in the same individual (Hu et al., 2021). They added other previous studies also reporting the heterogeneity and independent genetic origin of SCRC (Cereda et al., 2016; Wang et al., 2018), but without focusing on the location of the paired tumors. On the contrary, to the best of our knowledge, we previously analyzed the largest series of SCRC in exploring clonality, composed by 104 paired SCRCs from 52 consecutive patients without hereditary forms of CRC, using initially a single-nucleotide polymorphism array and a subsequent statistical application to define them according to clonality. Moreover, we used parameters like the mutational concordance and CpG island methylator phenotype (CIMP) status, to confirm our clonality results, and developed a classification according to clonality and paired tumor location, showing clinical correlations. Our results suggested heterogeneity in 64.4% of cases (Figure 1A) but the presence of clonality in 35.6% of cases (Figure 1B) (Perea et al., 2019).
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