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

作　　者：Yue Yuan Jian Zhang Qin Zhou 

机构地区：[1]The Division of Molecular Nephrology and the Creative Training Center for Undergraduates,the M.O.E.Key Laboratory of Laboratory Medical Diagnostics,the College of Laboratory Medicine,Chongqing Medical University,Chongqing 400016,China [2]State Key Laboratory of Developmental Biology,Institute of Genetics and Developmental Biology,Chinese Academy of Sciences,Beijing 100101,China

出　　处：《Journal of Genetics and Genomics》2016年第2期99-102,共4页遗传学报（英文版）

基　　金：financially supported through grants from National Natural Science Foundation of China(Nos.31471359;31271563 and 81572076);the Ministry of Science and Technology of China(Nos.2011CB944002 and2013CB945000);the Chinese Academy of Sciences(No.XDA01010108)

摘　　要：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）.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）.

关 键 词：cell HCC Overexpression of Jak1 Activating Mutants in Hepatocytes Is Insufficient to Generate Hepatocellular Carcinoma in Zebrafish JAK 

分 类 号：R735.7[医药卫生—肿瘤]