human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: Hepatocellular carcinoma ( HCC ) is the fifth most common cancer worldwide . Major risk factors of HCC include infection with hepatitis B or C viruses , alcohol and non-alcoholic fatty liver disease . HCC is difficult to diagnose at early stage , and has a very poor survival rate when diagnosed at a late stage . The majority of HCC-related deaths result from local invasion ( to cause liver failure ) or distant metastases . There is an urgent need to identify effective molecular targets for the treatment of the disease . As the target of an established class of therapeutic agent thiazolidinediones ( TZDs ) , peroxisome-proliferator-activated receptor Î³ ( PPARÎ³ ) has been widely studied for its role in the development of HCC . A substantial body of evidence based on in vitro and in vivo models indicates that the activation of PPARÎ³ is able to inhibit HCC cell proliferation and tumor growth through inducing cell cycle arrest and apoptosis via the regulation of a panel of downstream effector molecules . PPARÎ³ activation also induces an inhibitory effect on HCC metastasis . Meanwhile , there is new evidence suggesting that PPARÎ³ inhibition could also be anti-tumorigenic . In the present review , we summarize the available information on the role of PPARÎ³ in HCC development and spread , and discuss whether PPARÎ³ activation by TZDs could play a role in the treatment of HCC , summarizing both in vitro and in vivo . Considering the available data , PPARÎ³ seems to exert beneficial effects against HCC and may therefore represent as a therapeutic target .
    OUTPUT:

agent
resisting cell death;sustaining proliferative signaling;activating invasion and metastasis
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: Hepatocellular carcinoma ( HCC ) is the fifth most common cancer worldwide . Major risk factors of HCC include infection with hepatitis B or C viruses , alcohol and non-alcoholic fatty liver disease . HCC is difficult to diagnose at early stage , and has a very poor survival rate when diagnosed at a late stage . The majority of HCC-related deaths result from local invasion ( to cause liver failure ) or distant metastases . There is an urgent need to identify effective molecular targets for the treatment of the disease . As the target of an established class of therapeutic agent thiazolidinediones ( TZDs ) , peroxisome-proliferator-activated receptor Î³ ( PPARÎ³ ) has been widely studied for its role in the development of HCC . A substantial body of evidence based on in vitro and in vivo models indicates that the activation of PPARÎ³ is able to inhibit HCC cell proliferation and tumor growth through inducing cell cycle arrest and apoptosis via the regulation of a panel of downstream effector molecules . PPARÎ³ activation also induces an inhibitory effect on HCC metastasis . Meanwhile , there is new evidence suggesting that PPARÎ³ inhibition could also be anti-tumorigenic . In the present review , we summarize the available information on the role of PPARÎ³ in HCC development and spread , and discuss whether PPARÎ³ activation by TZDs could play a role in the treatment of HCC , summarizing both in vitro and in vivo . Considering the available data , PPARÎ³ seems to exert beneficial effects against HCC and may therefore represent as a therapeutic target .
    OUTPUT:
