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: BACKGROUND Though an increased efficacy of carmustine and temozolomide ( TMZ ) has been demonstrated by inactivation of O(6)-methylguanine-DNA methyltransferase ( MGMT ) with O(6)-benzyl-guanine ( BG ) in human pancreatic tumors refractive to alkylating agents , the regulatory mechanisms have not been explored . METHODS The effects of TMZ and BG on apoptosis , cell growth , the mitotic index , cell cycle distribution , and protein expression were studied by TUNEL , cell counting , flow cytometry , and Western blot analysis , respectively . RESULTS The wt-p53 human pancreatic tumor cell line Capan-2 and p53-efficient mouse embryonic fibroblasts ( MEFs ) were more responsive to treatment with TMZ + BG than mutant p53 Capan-1 and p53-null MEFs . S phase delay with a subsequent G2/M arrest was observed in Capans in response to BG + TMZ . The G1-to-S transition delay in Capan-2 was associated with p53-dependent apoptosis and was distinctly different from the presumed mismatch repair ( MMR ) killing operative during the G2/M arrest . The effect of p53 on BG + TMZ toxicity was supported by a marked change in apoptosis when p53 function was restored/inactivated . There was an early induction of MMR proteins in p53-efficient lines . CONCLUSION p53 provokes a classic proapoptotic response by delaying G1-to-S progression , but it may also facilitate cell killing by enhancing MMR-related cell cycle arrest and cell death .
    OUTPUT:

agent
evading growth suppressors;sustaining proliferative signaling;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: BACKGROUND Though an increased efficacy of carmustine and temozolomide ( TMZ ) has been demonstrated by inactivation of O(6)-methylguanine-DNA methyltransferase ( MGMT ) with O(6)-benzyl-guanine ( BG ) in human pancreatic tumors refractive to alkylating agents , the regulatory mechanisms have not been explored . METHODS The effects of TMZ and BG on apoptosis , cell growth , the mitotic index , cell cycle distribution , and protein expression were studied by TUNEL , cell counting , flow cytometry , and Western blot analysis , respectively . RESULTS The wt-p53 human pancreatic tumor cell line Capan-2 and p53-efficient mouse embryonic fibroblasts ( MEFs ) were more responsive to treatment with TMZ + BG than mutant p53 Capan-1 and p53-null MEFs . S phase delay with a subsequent G2/M arrest was observed in Capans in response to BG + TMZ . The G1-to-S transition delay in Capan-2 was associated with p53-dependent apoptosis and was distinctly different from the presumed mismatch repair ( MMR ) killing operative during the G2/M arrest . The effect of p53 on BG + TMZ toxicity was supported by a marked change in apoptosis when p53 function was restored/inactivated . There was an early induction of MMR proteins in p53-efficient lines . CONCLUSION p53 provokes a classic proapoptotic response by delaying G1-to-S progression , but it may also facilitate cell killing by enhancing MMR-related cell cycle arrest and cell death .
    OUTPUT:
