BACKGROUND/AIMS: Colorectal adenoma and cancer are known to be associated with obesity. Leptin, an adipocyte-derived hormone that plays a crucial role in obesity has been suggested as a growth factor in colon cancer. However, the association between adenoma and leptin remains controversial. We evaluated the leptin expression in human colorectal adenoma and its correlation to clinicopathologic factors. METHODS: Leptin expression was assessed by immunohistochemistry in 91 samples of colorectal adenoma larger than 5 mm, which were removed by endoscopic polypectomy. All patients underwent colonoscopy for cancer screening at Seoul Paik Hospital from 2007 to 2008 and we only included the patients less than 50 years of age. Leptin expression and its relationship with clinicopathologic features were analyzed. RESULTS: Eighty samples were available for the interpretation of leptin expression and showed positive in 42 (52.5%) cases and negative in 38 (47.5%) cases. As body mass index (BMI) increased based on World Health Organization (WHO) classification the positivity of leptin expression also increased (p(trend)=0.02). In leptin positive group, the correlation of leptin expression with adenoma size and histological showed positive tendency without statistical significance. CONCLUSIONS: Leptin expression of colorectal adenoma was associated with BMI. The question of whether leptin contributes to colorectal adenoma development is unresolved and will require additional studies.
Adenoma/complications/metabolism/*pathology ; Adult ; Body Mass Index ; Colonoscopy ; Colorectal Neoplasms/complications/metabolism/*pathology ; Female ; Humans ; Leptin/*metabolism ; Male ; Middle Aged ; Obesity/complications

Granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil trafficking and is highly expressed in multiple tumors. Myeloid derived suppressor cells (MDSCs) promote neoplastic progression through multiple mechanisms by immune suppression. Despite the findings of G-CSF function in colon cancer progression, the precise mechanism of G-CSF on MDSCs regulation and its blockade effects on tumor growth remains a worthy area of investigation. In this study we observed an overexpression of G-CSF in a mouse colitis-associated cancer (CAC) model, which was consistent with the accumulation of MDSCs in mouse colon tissues. Further in vitro studies demonstrated that G-CSF could promote MDSCs survival and activation through signal transducer and activator of transcription 3 (STAT3) signaling pathway. Moreover, compared with isotype control, anti-G-CSF mAb treatment demonstrated reduced MDSC accumulation, which led to a marked decrease in neoplasm size and number in mice. Our results indicated that G-CSF is a critical regulating molecule in the migration, proliferation and function maintenance of MDSCs, which could be a potential therapeutic target for colitis-associated cancer.
Animals ; Carcinogenesis ; Colitis ; complications ; Colorectal Neoplasms ; complications ; drug therapy ; immunology ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Granulocyte Colony-Stimulating Factor ; genetics ; metabolism ; Immunotherapy ; Mice ; Molecular Targeted Therapy ; Myeloid Cells ; immunology ; metabolism ; pathology