Abstract

G A A b st ra ct s MSI (38% vs 22%). However, AA patients showed significantly higher FHIT methylation in both MSI (52% vs 26%) and MSS (32% vs 18%) CRCs. Conclusions: We have firstly identified a subset of genes that are aberrantly expressed in CRC tissues from AA patients, which provides new insight into the molecular signatures that distinguish this disease in these two ethnic populations. We also provide evidence that frequent loss of FHIT expression via methylation-induced silencing in AA patients may be one of the molecular events that accounts for the poorer prognosis in CRC among AA patients.

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