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: Platinum compounds are the foundation of chemotherapy regimens for non-small cell lung cancer ( NSCLC ) despite poor response rates and limited response duration . It has been reported that tumor expression of ERCC1 , a key component in nucleotide excision repair , may correlate with clinical response to platinum agents . We found that most primary lung tumor specimens demonstrated a stronger protein expression of poly ( ADP ribose ) polymerases 1 ( PARP1 ) than their normal counterparts . We therefore hypothesized that combining PARP inhibition with platinum compounds may be an approach to improve platinum-based therapy for NSCLC . Drug combination experiments revealed that two distinct PARP inhibitors , olaparib and veliparib not only potentiated the cell killing by cisplatin but also conferred cytotoxicity as a single agent specifically in ERCC1-low HCC827 and PC9 but not in ERCC1-high A549 and H157 lung cancer cells . Moreover , siRNA knockdown of ERCC1 in A549 and H157 cells increased their sensitivities to both cisplatin and olaparib in a synergistic manner in our model . Furthermore , mechanistic studies indicated that combined PARP inhibitor and cisplatin could lead to sustained DNA double strand breaks , prolonged G2/M cell cycle arrest with distinct activation of checkpoint kinase 1 signaling , and more pronounced apoptosis preferentially in lung cancer cells with low ERCC1 expression . Collectively , these data suggest that there is a synergistic relationship between PARP inhibition and low ERCC1 expression in NSCLC that could be exploited for novel therapeutic approaches in lung cancer therapy based on tumor ERCC1 expression .
    OUTPUT:

agent
evading growth suppressors;genomic instability and mutation;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: Platinum compounds are the foundation of chemotherapy regimens for non-small cell lung cancer ( NSCLC ) despite poor response rates and limited response duration . It has been reported that tumor expression of ERCC1 , a key component in nucleotide excision repair , may correlate with clinical response to platinum agents . We found that most primary lung tumor specimens demonstrated a stronger protein expression of poly ( ADP ribose ) polymerases 1 ( PARP1 ) than their normal counterparts . We therefore hypothesized that combining PARP inhibition with platinum compounds may be an approach to improve platinum-based therapy for NSCLC . Drug combination experiments revealed that two distinct PARP inhibitors , olaparib and veliparib not only potentiated the cell killing by cisplatin but also conferred cytotoxicity as a single agent specifically in ERCC1-low HCC827 and PC9 but not in ERCC1-high A549 and H157 lung cancer cells . Moreover , siRNA knockdown of ERCC1 in A549 and H157 cells increased their sensitivities to both cisplatin and olaparib in a synergistic manner in our model . Furthermore , mechanistic studies indicated that combined PARP inhibitor and cisplatin could lead to sustained DNA double strand breaks , prolonged G2/M cell cycle arrest with distinct activation of checkpoint kinase 1 signaling , and more pronounced apoptosis preferentially in lung cancer cells with low ERCC1 expression . Collectively , these data suggest that there is a synergistic relationship between PARP inhibition and low ERCC1 expression in NSCLC that could be exploited for novel therapeutic approaches in lung cancer therapy based on tumor ERCC1 expression .
    OUTPUT:
