Understanding the molecular mechanisms behind the pathogenesis of GU defects is important for genetic counseling and the implementation of therapeutic interventions. The present study suggests that chromosomal region 2p15 and OTX1 are involved in GU tract development, but further detailed studies are needed to identify a causal relationship. SB203580 colorectal carcinoma is the third most common cancer worldwide and the fourth most common cause of death. In 2008 alone, approximately 1.23 million new cases of colorectal cancer were diagnosed around the world, and 608,000 people died from the disease. The standard treatment for this cancer is surgical, but outcomes are far from satisfactory, with up to 50% of patients suffering recurrence or death within 5 years of surgery. Targeting telomerase in colon carcinoma may provide an effective alternative or complement to surgical treatment. Telomerase, a ribonucleoprotein complex containing an internal RNA template and a catalytic protein with telomere-specific reverse transcriptase activity, extends telomeres at the end of eukaryotic chromosomes, thus preventing cell senescence and death. Telomerase appears to play a key role in tumor growth and proliferation: expression and activity of the enzyme are abnormally elevated in most cancers, and down-regulating the enzyme inhibits growth and proliferation. While hTR is constitutively present in normal and tumor cells, hTERT is the rate-limiting component of the telomerase complex, and its expression correlates with telomerase activity. In normal somatic tissues, hTERT activity is repressed, but both hTERT expression and telomerase activity are elevated in most human tumors. Several studies indicate that telomerase may be key to immortalizing cells as a necessary step in oncogenesis, making hTERT a potentially useful clinical biomarker and target for anticancer research. In colorectal cancer, up to 85% of cells contain active telomerase, whereas only about 5% of normal colorectal cells contain active enzyme. Therefore targeting the expression or activity of telomerase may provide a novel therapy for colorectal cancer. Given that no highly selective telomerase inhibitors are available for treating any cancer, we focused on gene therapy approaches. Gene therapy is expected to play a key role in nextgeneration cancer therapy in conjunction with conventional treatments such as surgery, chemotherapy, and radiotherapy. One gene therapy is RNA interference, which can down-regulate the expression of specific genes, allowing the functions of the genes to be analyzed or blocked for therapeutic purposes. In the present study, we designed a novel hTERT small interfering RNA and expressed the corresponding short hairpin RNA in human colorectal cells in vitro and in nude mice. We found that knocking down hTERT expression inhibited human colon carcinoma cell growth, raising the possibility of gene therapy approaches that target hTERT.