Abstract

To compare protein expression levels, gene mutation and survival among Right-Sided Colon Cancer (RSCC), Left-Sided Colon Cancer (LSCC) and rectal cancer patients, 57 cases of RSCC, 87 LSCC and 145 rectal cancer patients were included retrospectively. Our results demonstrated significant differences existed among RSCC, LSCC and rectal cancer regarding tumor diameter, differentiation, invasion depth and TNM stage. No significant difference was identified in expression levels of MLH1, MSH2, MSH6, PMS2, β-Tubulin III, P53, Ki67 and TOPIIα, and gene mutation of KRAS and BRAF among three groups. Progression Free Survival (PFS) of RSCC was significantly lower than that of LRCC and rectal cancer. In univariate analyses, RSCC, preoperative chemoradiotherapy, poor differentiation, advanced TNM stage, elevated serum CEA and CA19-9 level, tumor deposit, perineural and vascular invasion were found to be predictive factors of shorter PFS. In multivariate analyses, only differentiation and TNM stages were found to be independent predictors of PFS. In conclusion, compared with LSCC and rectal cancer, RSCC has larger tumor size, poor differentiation, advanced TNM stage and shorter survival. The shorter survival in RSCC might be attributed to the advanced tumor stage caused by its inherent position feature of proximal colon rather than genetic difference.

Highlights

  • Colorectal cancer (CRC) is the third most commonly diagnosed cancer globally, accounting for 10.0% of all new cancer cases

  • The mutational profiles (KRAS, mismatch repair (MMR), CpG island methylator phenotype (CIMP)) of Left-Sided Colon Cancer (LSCC) and rectal cancer were similar, but were different from that of Right-Sided Colon Cancer (RSCC). This result was attributed to their differing origins: RSCC originated from midgut, while Left-sided Colorectal Cancer (LCRC) originated from hindgut[3]

  • The difference among RSCC, LSCC and rectal cancer patients has been remaining a serious debate for a long time

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Summary

Introduction

Colorectal cancer (CRC) is the third most commonly diagnosed cancer globally, accounting for 10.0% of all new cancer cases. It is reported that rectal cancer is different from colon cancer in aetiology, genetics, anatomy, clinical manifestation, biological feature, treatment response and clinical outcomes[3,4,5,6]. The mutational profiles (KRAS, MMR, CIMP) of LSCC and rectal cancer were similar, but were different from that of RSCC. This result was attributed to their differing origins: RSCC originated from midgut, while LCRC originated from hindgut[3]. Several studies reported that gene mutation and protein expression of P53 differed significantly between RSCC and LSCRC26, 28, 29, but others showed that no significant association was identified between p53 protein expression and tumor site[30]. Our previous study showed that topoisomerase II alpha (TOPIIα) expression was related with T stage, N stage, recurrence and prognosis[33]

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