Abstract
Colorectal cancer (CRC) represents the third most common type of cancer in developed countries and one of the leading causes of cancer deaths worldwide. Personalized management of CRC has gained increasing attention since there are large inter-individual variations in the prognosis and response to drugs used to treat CRC owing to molecular heterogeneity. Approximately 15% of CRCs are caused by deficient mismatch repair (dMMR) characterized by microsatellite instability (MSI) phenotype. The present review is aimed at highlighting the role of MMR status in informing prognosis and personalized treatment of CRC including adjuvant chemotherapy, targeted therapy, and immune checkpoint inhibitor therapy to guide the individualized therapy of CRC.
Highlights
Colorectal cancer (CRC) represents the third most common type of cancer in developed countries and one of the leading causes of cancer deaths worldwide [1]
Though the TNM stage remains the key determinant of CRC prognosis and treatment in clinic, there are considerable stage independent inter-individual differences in clinical outcome and therapy response of CRC patients
Status has been demonstrated as a crucial biomarker for prognosis and response to many drugs used in CRC, which helps the clinicians and patients use medications rationally to avoid dispensable treatment and reduce the burden of patients in CRC therapy
Summary
Colorectal cancer (CRC) represents the third most common type of cancer in developed countries and one of the leading causes of cancer deaths worldwide [1]. The revised Bethesda Guidelines (RBG) was developed to identify individuals at risk of LS by testing for dMMR/MSI of tumors (Box 2). Patient with CRC and CRC or Lynch Syndrome-Associated Tumor * Diagnosed in Two or More First-Degree or Second-Degree Relatives, Regardless of Age. In sporadic CRCs, dMMR occurs more frequently in stage II (~20%) and stage III (~12%) tumors, and very rare in metastatic cases (~4%), which indicates that dMMR CRC is less metastatic and MMR status detection in earlier stage is of great importance [26,27]. The vast majority of sporadic CRCs are caused by suppression of MLH1 expression (~95%) due to hypermethylation of the MLH1 promoter known as the CpG island methylator phenotype (CIMP) [28,29], and inactivation of MSH2 and MSH6 account for the small percentage (~5% and ~1%) respectively. IHC is commonly used as an alternative test when a molecular laboratory is not available and is able to pinpoint the affected gene by detecting its protein expression assisting in identifying patients with LS [33]
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