Estrogen is involved in suppression of colorectal cancer development and exerts its function via estrogen receptors alpha, beta and their splicing variants. Whether the recently indentified ER-alpha splicing variants, ER-alpha36 and ER-alpha46, play a role in colorectal cancer development is unknown. In this study, we quantified the mRNA copy numbers of wild type ER-alpha (ER-alpha66), ER-alpha46 and ER-alpha36 in 35 colorectal cancers and their matched normal colorectal tissues by quantitative real-time PCR assay, and correlated their mRNA levels with the clinicopathological properties of the tumors. We found that ER-alpha66, ER-alpha46 and ER-alpha36 mRNAs were coexpressed in all colorectal cancers and their matched normal tissues. The decreased mRNA levels of ER-alpha36 and ER-alpha46 whereas no difference of ER-alpha66 mRNA was observed in colorectal cancers compared to their matched normal tissues. Moreover, change in the expression of ER-alpha36 mRNA level was correlated with Dukes' stage of the tumor and the lymph node metastasis. ER-alpha36 mRNA was decreased significantly in Dukes' C+D compared to Dukes' A+B stage tumors (P=0.017), and the expression of ER-alpha36 mRNA in N(1)/N(2) was lower than that in N(0) lymph node metastasis (P=0.049). So ER-alpha36 and ER-alpha46 might be implicated in the development and progression of colorectal cancers.