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: Odontogenic tumors originate from the remains of migrating enamel epithelium after the completion of normal tooth genesis . These enamel epithelium remnants exhibit the ability to recapitulate the events that occur during tooth formation . Several lines of evidence suggest that aberrance in the signaling pathways similar to the ones that are used during tooth development , including the WNT pathway , might be the cause of odontogenic tumorigenesis and maintenance . In this study we demonstrated that WNT5A expression was intense in both the epithelial component of ameloblastomas , the most common epithelial odontogenic tumor , and in this tumor's likely precursor cell , the enamel epithelium located at the cervical loop of normal developing human tooth buds . Additionally , when WNT5A was overexpressed in enamel epithelium cells ( LS-8 ) , the clones expressing high levels of WNT5A ( S ) exhibited characteristics of tumorigenic cells , including growth factor independence , loss of anchorage dependence , loss of contact inhibition , and tumor formation in immunocompromised mice . Moreover , overexpression of WNT5A drastically increased LS-8 cell migration and actin reorganization when compared with controls . Suppression of endogenous WNT5A in LS-8 cells ( AS ) greatly impaired their migration and AS cells failed to form significant actin reorganization and membrane protrusion was rarely seen . Taken together , our data indicate that WNT5A signaling is important in modulating tumorigenic behaviors of enamel epithelium cells in ameloblastomas .
    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.
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    INPUT: Odontogenic tumors originate from the remains of migrating enamel epithelium after the completion of normal tooth genesis . These enamel epithelium remnants exhibit the ability to recapitulate the events that occur during tooth formation . Several lines of evidence suggest that aberrance in the signaling pathways similar to the ones that are used during tooth development , including the WNT pathway , might be the cause of odontogenic tumorigenesis and maintenance . In this study we demonstrated that WNT5A expression was intense in both the epithelial component of ameloblastomas , the most common epithelial odontogenic tumor , and in this tumor's likely precursor cell , the enamel epithelium located at the cervical loop of normal developing human tooth buds . Additionally , when WNT5A was overexpressed in enamel epithelium cells ( LS-8 ) , the clones expressing high levels of WNT5A ( S ) exhibited characteristics of tumorigenic cells , including growth factor independence , loss of anchorage dependence , loss of contact inhibition , and tumor formation in immunocompromised mice . Moreover , overexpression of WNT5A drastically increased LS-8 cell migration and actin reorganization when compared with controls . Suppression of endogenous WNT5A in LS-8 cells ( AS ) greatly impaired their migration and AS cells failed to form significant actin reorganization and membrane protrusion was rarely seen . Taken together , our data indicate that WNT5A signaling is important in modulating tumorigenic behaviors of enamel epithelium cells in ameloblastomas .
    OUTPUT:
