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: Epidermal growth factor receptor ( EGFR ) and human epidermal growth factor receptor 2 ( HER2 ) amplification occurs in over 30% of esophageal carcinomas . Combination therapies with EGFR and HER2-targeting agents and cytotoxic agents are considered a potential therapeutic option for esophageal cancer . We evaluated the antitumor effects of lapatinib , a dual tyrosine kinase inhibitor which simultaneously inhibits EGFR and HER2 , 5-fluorouracil ( 5-Fu ) alone and in combination on esophageal cancer cells . The antiproliferative activity of lapatinib , 5-Fu and lapatinib plus 5-Fu was measured by MTT assay and the combination index ( CI ) values were calculated . Additionally , cell cycle distribution of lapatinib alone and the combination with 5-Fu were detected by flow cytometry analysis . AnnexinV-FITC and propidium iodide stain were used for analyzing the apoptotic cells after cells were treated with either agent alone or in combination . The EGFR and HER2 activated signaling pathways were monitored by western blotting . The combination of lapatinib and 5-Fu synergistically inhibited cell proliferation and exhibited an enhanced proapoptotic effect on esophageal cancer cells . The potentiation effect of combined treatment was associated with downregulation of EGFR and HER2 signaling pathways because data from western blot analysis showed that lapatinib in combination with 5-Fu markedly reduced the phosphorylation of EGFR and HER2 , and inhibited the activation of downstream signaling molecules , such as AKT and ERK . A significant G1 arrest was also observed in cell cycle analysis after exposing cells to lapatinib , however , combination with 5-Fu did not enhance G1 arrest . These results indicate that the combination of the lapatinib and 5-Fu is a promising treatment option for esophageal carcinoma with HER2 amplification .
    OUTPUT:

agent
resisting cell death;sustaining proliferative signaling
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: Epidermal growth factor receptor ( EGFR ) and human epidermal growth factor receptor 2 ( HER2 ) amplification occurs in over 30% of esophageal carcinomas . Combination therapies with EGFR and HER2-targeting agents and cytotoxic agents are considered a potential therapeutic option for esophageal cancer . We evaluated the antitumor effects of lapatinib , a dual tyrosine kinase inhibitor which simultaneously inhibits EGFR and HER2 , 5-fluorouracil ( 5-Fu ) alone and in combination on esophageal cancer cells . The antiproliferative activity of lapatinib , 5-Fu and lapatinib plus 5-Fu was measured by MTT assay and the combination index ( CI ) values were calculated . Additionally , cell cycle distribution of lapatinib alone and the combination with 5-Fu were detected by flow cytometry analysis . AnnexinV-FITC and propidium iodide stain were used for analyzing the apoptotic cells after cells were treated with either agent alone or in combination . The EGFR and HER2 activated signaling pathways were monitored by western blotting . The combination of lapatinib and 5-Fu synergistically inhibited cell proliferation and exhibited an enhanced proapoptotic effect on esophageal cancer cells . The potentiation effect of combined treatment was associated with downregulation of EGFR and HER2 signaling pathways because data from western blot analysis showed that lapatinib in combination with 5-Fu markedly reduced the phosphorylation of EGFR and HER2 , and inhibited the activation of downstream signaling molecules , such as AKT and ERK . A significant G1 arrest was also observed in cell cycle analysis after exposing cells to lapatinib , however , combination with 5-Fu did not enhance G1 arrest . These results indicate that the combination of the lapatinib and 5-Fu is a promising treatment option for esophageal carcinoma with HER2 amplification .
    OUTPUT:
