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: Our study was to elucidate the mechanisms whereby BMS-345541 ( BMS , a specific IκB kinase β inhibitor ) inhibits the repair of DNA double-strand breaks ( DSBs ) and evaluate whether BMS can sensitize MCF-7 breast cancer cells ( MCF-7 cells ) to ionizing radiation ( IR ) in an apoptosis-independent manner . In this study , MCF-7 cells were exposed to IR in vitro and in vivo with or without pretreatment of BMS . The effects of BMS on the repair of IR-induced DSBs by homologous recombination ( HR ) and non-homologous end-joining ( NHEJ ) were analyzed by the DR-GFP and EJ5-GFP reporter assays and IR-induced γ-H2AX , 53BP1 , Brca1 and Rad51 foci assays . The mechanisms by which BMS inhibits HR were examined by microarray analysis and quantitative reverse transcription PCR . The effects of BMS on the sensitivity of MCF-7 cells to IR were determined by MTT and clonogenic assays in vitro and tumor growth inhibition in vivo in a xenograft mouse model . The results showed that BMS selectively inhibited HR repair of DSBs in MCF-7 cells , most likely by down-regulation of several genes that participate in HR . This resulted in a significant increase in the DNA damage response that sensitizes MCF-7 cells to IR-induced cell death in an apoptosis-independent manner . Furthermore , BMS treatment sensitized MCF-7 xenograft tumors to radiation therapy in vivo in an association with a significant delay in the repair of IR-induced DSBs . These data suggest that BMS is a novel HR inhibitor that has the potential to be used as a radiosensitizer to increase the responsiveness of cancer to radiotherapy .
    OUTPUT:

agent
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: Our study was to elucidate the mechanisms whereby BMS-345541 ( BMS , a specific IκB kinase β inhibitor ) inhibits the repair of DNA double-strand breaks ( DSBs ) and evaluate whether BMS can sensitize MCF-7 breast cancer cells ( MCF-7 cells ) to ionizing radiation ( IR ) in an apoptosis-independent manner . In this study , MCF-7 cells were exposed to IR in vitro and in vivo with or without pretreatment of BMS . The effects of BMS on the repair of IR-induced DSBs by homologous recombination ( HR ) and non-homologous end-joining ( NHEJ ) were analyzed by the DR-GFP and EJ5-GFP reporter assays and IR-induced γ-H2AX , 53BP1 , Brca1 and Rad51 foci assays . The mechanisms by which BMS inhibits HR were examined by microarray analysis and quantitative reverse transcription PCR . The effects of BMS on the sensitivity of MCF-7 cells to IR were determined by MTT and clonogenic assays in vitro and tumor growth inhibition in vivo in a xenograft mouse model . The results showed that BMS selectively inhibited HR repair of DSBs in MCF-7 cells , most likely by down-regulation of several genes that participate in HR . This resulted in a significant increase in the DNA damage response that sensitizes MCF-7 cells to IR-induced cell death in an apoptosis-independent manner . Furthermore , BMS treatment sensitized MCF-7 xenograft tumors to radiation therapy in vivo in an association with a significant delay in the repair of IR-induced DSBs . These data suggest that BMS is a novel HR inhibitor that has the potential to be used as a radiosensitizer to increase the responsiveness of cancer to radiotherapy .
    OUTPUT:
