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: Aberrant expression and polymorphism of fibroblast growth factor receptor 4 ( FGFR4 ) has been linked to tumor progression and anticancer drug resistance . We describe here a novel mechanism of tumor progression by matrix degradation involving epithelial-to-mesenchymal transition in response to membrane-type 1 matrix metalloproteinase ( MT1-MMP , MMP-14 ) induction at the edge of tumors expressing the FGFR4-R388 risk variant . Both FGFR4 and MT1-MMP were upregulated in tissue biopsies from several human cancer types including breast adenocarcinomas , where they were partially coexpressed at the tumor/stroma border and tumor invasion front . The strongest overall coexpression was found in prostate carcinoma . Studies with cultured prostate carcinoma cell lines showed that the FGFR4-R388 variant , which has previously been associated with poor cancer prognosis , increased MT1-MMP-dependent collagen invasion . In this experimental model , knockdown of FGFR4-R388 or MT1-MMP by RNA interference blocked tumor cell invasion and growth in collagen . This was coupled with impaired phosphorylation of FGFR substrate 2 and Src , upregulation of E-cadherin , and suppression of cadherin-11 and N-cadherin . These in vitro results were substantiated by reduced MT1-MMP content and in vivo growth of prostate carcinoma cells after the FGFR4-R388 gene silencing . In contrast , knockdown of the alternative FGFR4-G388 allele enhanced MT1-MMP and invasive tumor cell growth in vivo and within three-dimensional collagen . These results will help to explain the reported association of the FGFR4-R388 variant with the progression and poor prognosis of certain types of tumors .
    OUTPUT:

agent
activating invasion and metastasis;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: Aberrant expression and polymorphism of fibroblast growth factor receptor 4 ( FGFR4 ) has been linked to tumor progression and anticancer drug resistance . We describe here a novel mechanism of tumor progression by matrix degradation involving epithelial-to-mesenchymal transition in response to membrane-type 1 matrix metalloproteinase ( MT1-MMP , MMP-14 ) induction at the edge of tumors expressing the FGFR4-R388 risk variant . Both FGFR4 and MT1-MMP were upregulated in tissue biopsies from several human cancer types including breast adenocarcinomas , where they were partially coexpressed at the tumor/stroma border and tumor invasion front . The strongest overall coexpression was found in prostate carcinoma . Studies with cultured prostate carcinoma cell lines showed that the FGFR4-R388 variant , which has previously been associated with poor cancer prognosis , increased MT1-MMP-dependent collagen invasion . In this experimental model , knockdown of FGFR4-R388 or MT1-MMP by RNA interference blocked tumor cell invasion and growth in collagen . This was coupled with impaired phosphorylation of FGFR substrate 2 and Src , upregulation of E-cadherin , and suppression of cadherin-11 and N-cadherin . These in vitro results were substantiated by reduced MT1-MMP content and in vivo growth of prostate carcinoma cells after the FGFR4-R388 gene silencing . In contrast , knockdown of the alternative FGFR4-G388 allele enhanced MT1-MMP and invasive tumor cell growth in vivo and within three-dimensional collagen . These results will help to explain the reported association of the FGFR4-R388 variant with the progression and poor prognosis of certain types of tumors .
    OUTPUT:
