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.
    ###
    INPUT: We have used a combination of vitamin A ( all-trans-retinyl palmitate ) , 5-fluorouracil ( 5-FU ) and radiation to treat human head and neck squamous cell carcinoma ( HNSCC ) . This chemoradiotherapy is called " FAR therapy. " In this study we examined the effects of all-trans-retinoic acid ( ATRA ) , the active metabolite of vitamin A , and ATRA plus 5-FU on two HNSCC cell lines ( YCU-N861 and YCU-H891 ) to gain insight into the molecular mechanisms of FAR therapy . ATRA at 1 mM ( the order of concentration found in HNSCC tumors treated with FAR therapy ) inhibited cell proliferation and caused G1 cell cycle arrest in both cell lines . This was associated with a decrease in cyclin D1 , an increase in p27(Kip1) and a reduction in the hyperphosphorylated form of retinoblastoma protein ( pRB ) . With YCU-N861 cells , ATRA also caused a decrease in Bcl-2 and Bcl-X(L) and an increase in Bax . Both ATRA and 5-FU activated c-Jun N-terminal kinase ( JNK ) 1 and the combination of both agents resulted in additive or synergistic activation of JNK1 , and also enhanced the induction of apoptosis . The YCU-H891 cells , in which the epidermal growth factor receptor ( EGFR)-signal transducer and activator of transcription 3 ( Stat3 ) pathway is constitutively activated , were more resistant to treatments with ATRA , 5-FU and the combination of both agents than YCU-N861 cells . A dominant negative Stat3 construct strongly enhanced the cellular sensitivity of this cell line to 5-FU but not to ATRA . In addition there is evidence that activation of Stat3 is associated with cellular resistance to radiation in HNSCC . Therefore , the addition to FAR therapy of agents that inhibit activation of the Stat3 pathway may enhance the clinical response of patients with HNSCC to FAR therapy .
    OUTPUT:

agent
sustaining proliferative signaling;evading growth suppressors;resisting cell death
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: We have used a combination of vitamin A ( all-trans-retinyl palmitate ) , 5-fluorouracil ( 5-FU ) and radiation to treat human head and neck squamous cell carcinoma ( HNSCC ) . This chemoradiotherapy is called " FAR therapy. " In this study we examined the effects of all-trans-retinoic acid ( ATRA ) , the active metabolite of vitamin A , and ATRA plus 5-FU on two HNSCC cell lines ( YCU-N861 and YCU-H891 ) to gain insight into the molecular mechanisms of FAR therapy . ATRA at 1 mM ( the order of concentration found in HNSCC tumors treated with FAR therapy ) inhibited cell proliferation and caused G1 cell cycle arrest in both cell lines . This was associated with a decrease in cyclin D1 , an increase in p27(Kip1) and a reduction in the hyperphosphorylated form of retinoblastoma protein ( pRB ) . With YCU-N861 cells , ATRA also caused a decrease in Bcl-2 and Bcl-X(L) and an increase in Bax . Both ATRA and 5-FU activated c-Jun N-terminal kinase ( JNK ) 1 and the combination of both agents resulted in additive or synergistic activation of JNK1 , and also enhanced the induction of apoptosis . The YCU-H891 cells , in which the epidermal growth factor receptor ( EGFR)-signal transducer and activator of transcription 3 ( Stat3 ) pathway is constitutively activated , were more resistant to treatments with ATRA , 5-FU and the combination of both agents than YCU-N861 cells . A dominant negative Stat3 construct strongly enhanced the cellular sensitivity of this cell line to 5-FU but not to ATRA . In addition there is evidence that activation of Stat3 is associated with cellular resistance to radiation in HNSCC . Therefore , the addition to FAR therapy of agents that inhibit activation of the Stat3 pathway may enhance the clinical response of patients with HNSCC to FAR therapy .
    OUTPUT:
