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: Î³-Tocotrienol and sesamin are phytochemicals that display potent anticancer activity . Since sesamin inhibits the metabolic degradation of tocotrienols , studies were conducted to determine if combined treatment with sesamin potentiates the antiproliferative effects of Î³-tocotrienol on neoplastic mouse ( +SA ) and human ( MCF-7 and MDA-MB-231 ) mammary cancer cells . Results showed that treatment with Î³-tocotrienol or sesamin alone induced a significant dose-responsive growth inhibition , whereas combination treatment with these agents synergistically inhibited the growth of +SA , MCF-7 and MDA-MB-231 mammary cancer cells , while similar treatment doses were found to have little or no effect on normal ( mouse CL-S1 and human MCF-10A ) mammary epithelial cell growth or viability . However , sesamin synergistic enhancement of Î³-tocotrienol-induced anticancer effects was not found to be mediated from a reduction in Î³-tocotrienol metabolism . Rather , combined treatment with subeffective doses of Î³-tocotrienol and sesamin was found to induce G1 cell cycle arrest , and a corresponding decrease in cyclin D1 , CDK2 , CDK4 , CDK6 , phospho-Rb , and E2F1 levels , and increase in p27 and p16 levels . Additional studies showed that the antiproliferative effect of combination treatment did not initiate apoptosis or result in a decrease in mammary cancer cell viability . Taken together , these findings indicate that the synergistic antiproliferative action of combined Î³-tocotrienol and sesamin treatment in mouse and human mammary cancer cells is cytostatic , not cytotoxic , and results from G1 cell cycle arrest .
    OUTPUT:

agent
evading growth suppressors;sustaining proliferative signaling;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.
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    INPUT: Î³-Tocotrienol and sesamin are phytochemicals that display potent anticancer activity . Since sesamin inhibits the metabolic degradation of tocotrienols , studies were conducted to determine if combined treatment with sesamin potentiates the antiproliferative effects of Î³-tocotrienol on neoplastic mouse ( +SA ) and human ( MCF-7 and MDA-MB-231 ) mammary cancer cells . Results showed that treatment with Î³-tocotrienol or sesamin alone induced a significant dose-responsive growth inhibition , whereas combination treatment with these agents synergistically inhibited the growth of +SA , MCF-7 and MDA-MB-231 mammary cancer cells , while similar treatment doses were found to have little or no effect on normal ( mouse CL-S1 and human MCF-10A ) mammary epithelial cell growth or viability . However , sesamin synergistic enhancement of Î³-tocotrienol-induced anticancer effects was not found to be mediated from a reduction in Î³-tocotrienol metabolism . Rather , combined treatment with subeffective doses of Î³-tocotrienol and sesamin was found to induce G1 cell cycle arrest , and a corresponding decrease in cyclin D1 , CDK2 , CDK4 , CDK6 , phospho-Rb , and E2F1 levels , and increase in p27 and p16 levels . Additional studies showed that the antiproliferative effect of combination treatment did not initiate apoptosis or result in a decrease in mammary cancer cell viability . Taken together , these findings indicate that the synergistic antiproliferative action of combined Î³-tocotrienol and sesamin treatment in mouse and human mammary cancer cells is cytostatic , not cytotoxic , and results from G1 cell cycle arrest .
    OUTPUT:
