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: AIM To elucidate the roles of receptor tyrosine kinases RET and VEGFR2 and the RAF/MEK/ERK signaling cascade in cancer treatment with sorafenib . METHODS The cell lines A549 , HeLa , and HepG2 were tested . The enzyme activity was examined under cell-free conditions using 384-well microplate assays . Cell proliferation was evaluated using the Invitrogen Alarmar Blue assay . Gene expression was analyzed using the Invitrogen SYBR Green expression assays with a sequence detection system . Protein expression analysis was performed using Western blotting . RESULTS Sorafenib potently suppressed the activities of cRAF , VEGFR2 , and RET with IC(50) values of 20.9 , 4 and 0.4 nmol/L , respectively . Sorafenib inhibited cRAF , VEGFR2 , and RET via non-ATP-competitive , ATP-competitive and mixed-type modes , respectively . In contrast , sorafenib exerted only moderate cytotoxic effects on the proliferation of the 3 cell lines . The IC(50) values for inhibition of A549 , HeLa , and HepG2 cells were 8572 , 4163 , and 8338 nmol/L , respectively . In the 3 cell lines , sorafenib suppressed the cell proliferation mainly by blocking the MEK/ERK downstream pathway at the posttranscriptional level , which in turn regulated related gene expression via a feed-back mechanism . CONCLUSION This study provides novel evidence that protein kinases RET and VEGFR2 play crucial roles in cancer treatment with sorafenib .
    OUTPUT:

agent
sustaining proliferative signaling
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: AIM To elucidate the roles of receptor tyrosine kinases RET and VEGFR2 and the RAF/MEK/ERK signaling cascade in cancer treatment with sorafenib . METHODS The cell lines A549 , HeLa , and HepG2 were tested . The enzyme activity was examined under cell-free conditions using 384-well microplate assays . Cell proliferation was evaluated using the Invitrogen Alarmar Blue assay . Gene expression was analyzed using the Invitrogen SYBR Green expression assays with a sequence detection system . Protein expression analysis was performed using Western blotting . RESULTS Sorafenib potently suppressed the activities of cRAF , VEGFR2 , and RET with IC(50) values of 20.9 , 4 and 0.4 nmol/L , respectively . Sorafenib inhibited cRAF , VEGFR2 , and RET via non-ATP-competitive , ATP-competitive and mixed-type modes , respectively . In contrast , sorafenib exerted only moderate cytotoxic effects on the proliferation of the 3 cell lines . The IC(50) values for inhibition of A549 , HeLa , and HepG2 cells were 8572 , 4163 , and 8338 nmol/L , respectively . In the 3 cell lines , sorafenib suppressed the cell proliferation mainly by blocking the MEK/ERK downstream pathway at the posttranscriptional level , which in turn regulated related gene expression via a feed-back mechanism . CONCLUSION This study provides novel evidence that protein kinases RET and VEGFR2 play crucial roles in cancer treatment with sorafenib .
    OUTPUT:
