Relationsip between PTEN and VEGF Expression and Clinicopathological Characteristics in HCC

To investigate the expressions and significance of the tumor suppressor gene phosphatase and tensin homlog deleted on chromosome ten protein （PTEN） and vascular endothelial growth factor （VEGF） in hepatocellular carcinoma （HCC）, and to analyze the relationship between their expressions and the tumor＇s invasion and their pericarcinomatous tissues, the correlation of their expressions with the tumor＇s clinicopathological characteristics and invasion potential were studied. Our study showed that the expression level of PTEN in HCC was remarkably lower than that in pericarcinomatous liver tissues, while the expressions of both VEGF and MVD were higher than that in pericarcinomatous liver tissues. Correlation analysis revealed that the expression of PTEN was negatively related to the progression of the pathological differentiation and invasion of tumor, whereas the expressions of VEGF and MVD were positively related. Moreover, there was a negative relationship between the expression of PTEN and the expressions of VEGF and MVD, and a positive one between VEGF and MVD. The expressions of PTEN and VEGF may reveal the degree of differentiation and the invasive potential of HCC tissues. The mechanism by which the lack of PTEN expression probably induces abnormal hyperexpression of VEGF may play an important role in the invasion and metastasis of HCC.

Overexpression of Jak1 Activating Mutants in Hepatocytes Is Insufficient to Generate Hepatocellular Carcinoma in Zebrafish

Hepatocellular carcinoma （HCC）, a major subtype of liver cancers, is a prevalent human malignancy worldwide. In men, HCC is the fifth frequently diagnosed cancer but the second most common cause of cancer death. In women, it ranks seventh in cancer diagnosis and sixth in cancer-related death （Jemal et al., 2011）. Unlike some other cancers, such as breast cancer and colon cancer, the molecular etiology of HCC re- mains largely unknown. Infection of hepatitis virus is considered as a major risk factor in the development of liver cancers （Parkin, 2006）. Currently, there are limited options to treat HCC except for chemotherapy. Elucidating molecular mechanism of hepatocyte transformation will help develop new treatments for cancer. The widely accepted multi-step progression of carcinogenesis consists of genetic alterations which regulate cell proliferation, apoptosis and so on （Vogelstein and Kinzler, 1993）. Moreover, abnormal activation of signaling pathways has been proposed as an oncogenic driver for cancer development. For example, Kras activation occurs in 7% of human liver cancer patients. Activated Kras is sufficient to induce robust liver tumorigenesis in transgenic animal models （Nguyen et al., 2011）.