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: Senescence , an inherent tumor suppressive mechanism , is a critical determinant for chemotherapy . In the present study , we show that the monocarboxylate transporter 2 ( MCT2 ) protein was tumor-selectively expressed in human colorectal malignancies and knockdown of MCT2 induces mitochondrial dysfunction , cell-cycle arrest , and senescence without additional cellular stress in colorectal cancer cell lines . Moreover , the reactive oxygen species ( ROS ) scavenger , N-acetylcysteine , blocked MCT2 knockdown-induced growth arrest and cellular senescence , indicating a pivotal role of ROS in this pathway . Dramatic induction of mitochondrial superoxide generation and decrease in ATP production was observed , indicating that mitochondrial dysfunction is the major mechanism underlying MCT2 knockdown-induced ROS generation . Senescence-associated DNA damage was also evident from the increase in promyelocytic leukemia bodies , Î³H2AX foci , and SAHF . Conversely , overexpression of MCT2 prevented doxorubicin-induced ROS accumulation ( P = 0.0002 ) and cell growth inhibition ( P = 0.001 ) . MCT2 knockdown suppressed KRAS mutant colorectal tumor growth in vivo . In addition , MCT2 knockdown and cytostatic drug combination further enhanced the antitumor effect . These findings support the use of MCT2 as a promising target for inhibition of colorectal cancer .
    OUTPUT:

agent
enabling replicative immortality;sustaining proliferative signaling;tumor promoting inflammation;genomic instability and mutation
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: Senescence , an inherent tumor suppressive mechanism , is a critical determinant for chemotherapy . In the present study , we show that the monocarboxylate transporter 2 ( MCT2 ) protein was tumor-selectively expressed in human colorectal malignancies and knockdown of MCT2 induces mitochondrial dysfunction , cell-cycle arrest , and senescence without additional cellular stress in colorectal cancer cell lines . Moreover , the reactive oxygen species ( ROS ) scavenger , N-acetylcysteine , blocked MCT2 knockdown-induced growth arrest and cellular senescence , indicating a pivotal role of ROS in this pathway . Dramatic induction of mitochondrial superoxide generation and decrease in ATP production was observed , indicating that mitochondrial dysfunction is the major mechanism underlying MCT2 knockdown-induced ROS generation . Senescence-associated DNA damage was also evident from the increase in promyelocytic leukemia bodies , Î³H2AX foci , and SAHF . Conversely , overexpression of MCT2 prevented doxorubicin-induced ROS accumulation ( P = 0.0002 ) and cell growth inhibition ( P = 0.001 ) . MCT2 knockdown suppressed KRAS mutant colorectal tumor growth in vivo . In addition , MCT2 knockdown and cytostatic drug combination further enhanced the antitumor effect . These findings support the use of MCT2 as a promising target for inhibition of colorectal cancer .
    OUTPUT:
