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: Like all cancers , breast cancer is considered to result in part from the accumulation of multiple genetic alterations leading to oncogene overexpression and tumor suppressor loss . More recently , CpG island hypermethylation is known to be associated with gene silencing in cancer , and these silenced genes can be reactivated by 5-aza-2'-deoxycytidine ( 5-Aza-CdR ) . Retionoic acid receptor beta 2 gene is a tumor suppressor gene and the chemopreventive effects of retinoids are due to induction of RAR beta 2 . In this study , the effect of 5-Aza-CdR RAR beta 2 restoration was investigated in the MRK-nu-1 human female breast cancer cell line . Changes of the RAR beta 2 methylation status were assessed by methylation-specific PCR . Reverse transcription PCR was used to evaluate RARb beta 2 restoration . Cell cycling and growth inhibition were studied using flow cytometric analysis of DNA content and CellTiter 96 AQueous non-radioactive cell proliferation assay , respectively. 5-Aza-CdR treatment resulted in complete demethylation of the RAR beta 2 gene . RAR beta 2 restoration was accompanied by cell cycle arrest ( increase in the G0/G1- and decrease in the S- and G2/M-phases ) and time-dependent growth inhibition . In conclusion , RAR beta 2 can be activated in vitro by 5-Aza-CdR , which may be one of the mechanisms for the tumor cell growth inhibition by 5-Aza-CdR .
    OUTPUT:

agent
evading growth suppressors
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: Like all cancers , breast cancer is considered to result in part from the accumulation of multiple genetic alterations leading to oncogene overexpression and tumor suppressor loss . More recently , CpG island hypermethylation is known to be associated with gene silencing in cancer , and these silenced genes can be reactivated by 5-aza-2'-deoxycytidine ( 5-Aza-CdR ) . Retionoic acid receptor beta 2 gene is a tumor suppressor gene and the chemopreventive effects of retinoids are due to induction of RAR beta 2 . In this study , the effect of 5-Aza-CdR RAR beta 2 restoration was investigated in the MRK-nu-1 human female breast cancer cell line . Changes of the RAR beta 2 methylation status were assessed by methylation-specific PCR . Reverse transcription PCR was used to evaluate RARb beta 2 restoration . Cell cycling and growth inhibition were studied using flow cytometric analysis of DNA content and CellTiter 96 AQueous non-radioactive cell proliferation assay , respectively. 5-Aza-CdR treatment resulted in complete demethylation of the RAR beta 2 gene . RAR beta 2 restoration was accompanied by cell cycle arrest ( increase in the G0/G1- and decrease in the S- and G2/M-phases ) and time-dependent growth inhibition . In conclusion , RAR beta 2 can be activated in vitro by 5-Aza-CdR , which may be one of the mechanisms for the tumor cell growth inhibition by 5-Aza-CdR .
    OUTPUT:
