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 CDC4/FBXW7 , encoding a ubiquitin ligase , maps to 4q32 and has been implicated as a tumor suppressor gene and therapeutic target in many tumor types . Mutations in colonic adenomas , and the frequent losses on 4q described in gastric cancer prompt speculation about the role of CDC4/FBXW7 in gastric carcinogenesis . METHODS We assessed the role of CDC4/FBXW7 in gastric cancer , through loss of heterozygosity ( LOH ) and multiplex ligation-dependent probe amplification ( MLPA ) on 47 flow-sorted gastric carcinomas including early-onset gastric cancers ( EOGC ) and xenografted conventional gastric carcinomas . Ploidy analysis was carried out on 39 EOGCs and immunohistochemistry of CDC4/FBXW7 and its substrates c-myc , c-jun , Notch and cyclin E was performed on 204 gastric carcinomas using tissue microarrays ( TMAs ) . Sequence analysis of CDC4/FBXW7 was carried out on gastric carcinoma cell lines and xenografts . RESULTS Loss of heterozygosity of CDC4/FBXW7 occurred in 32% of EOGCs , and correlated with loss of expression in 26% . Loss of expression was frequent in both EOGC and conventional gastric cancers . No CDC4/FBXW7 mutations were found and loss of CDC4/FBXW7 did not correlate with ploidy status . There was a significant correlation between loss of CDC4/FBXW7 expression and upregulation of c-myc . CONCLUSION Loss of CDC4/FBXW7 appears to play a role in both EOGC and conventional gastric carcinogenesis , and c-myc overexpression is likely to be an important oncogenic consequence of CDC4/FBXW7 loss .
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agent
genomic instability and mutation
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 CDC4/FBXW7 , encoding a ubiquitin ligase , maps to 4q32 and has been implicated as a tumor suppressor gene and therapeutic target in many tumor types . Mutations in colonic adenomas , and the frequent losses on 4q described in gastric cancer prompt speculation about the role of CDC4/FBXW7 in gastric carcinogenesis . METHODS We assessed the role of CDC4/FBXW7 in gastric cancer , through loss of heterozygosity ( LOH ) and multiplex ligation-dependent probe amplification ( MLPA ) on 47 flow-sorted gastric carcinomas including early-onset gastric cancers ( EOGC ) and xenografted conventional gastric carcinomas . Ploidy analysis was carried out on 39 EOGCs and immunohistochemistry of CDC4/FBXW7 and its substrates c-myc , c-jun , Notch and cyclin E was performed on 204 gastric carcinomas using tissue microarrays ( TMAs ) . Sequence analysis of CDC4/FBXW7 was carried out on gastric carcinoma cell lines and xenografts . RESULTS Loss of heterozygosity of CDC4/FBXW7 occurred in 32% of EOGCs , and correlated with loss of expression in 26% . Loss of expression was frequent in both EOGC and conventional gastric cancers . No CDC4/FBXW7 mutations were found and loss of CDC4/FBXW7 did not correlate with ploidy status . There was a significant correlation between loss of CDC4/FBXW7 expression and upregulation of c-myc . CONCLUSION Loss of CDC4/FBXW7 appears to play a role in both EOGC and conventional gastric carcinogenesis , and c-myc overexpression is likely to be an important oncogenic consequence of CDC4/FBXW7 loss .
    OUTPUT:
