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 As a highly conserved system , the activation of the Notch pathway has been implicated in the tumorigenesis of various hematologic diseases , including leukemias , lymphomas , and multiple myeloma . The Notch3 receptor is frequently expressed in T-cell acute lymphoblastic leukemia ( T-ALL ) . METHODS To explore its possibility as a therapeutic target for T-ALL , we investigated the effect of Notch3 silencing on Jurkat and SupT1 cells using a novel tumor-specific short hairpin RNA ( shRNA ) driven by survivin promoters . RESULTS We found that downregulated expression of Notch3 correlated with significant apoptosis and inhibition of proliferation . CONCLUSION These facts suggest that downregulating expression of Notch3 could attenuate the Notch signaling activity in T-ALL . All these results indicate that inhibition of Notch3 expression can result in potent antitumor activity in T-ALL .
    OUTPUT:

agent
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: BACKGROUND As a highly conserved system , the activation of the Notch pathway has been implicated in the tumorigenesis of various hematologic diseases , including leukemias , lymphomas , and multiple myeloma . The Notch3 receptor is frequently expressed in T-cell acute lymphoblastic leukemia ( T-ALL ) . METHODS To explore its possibility as a therapeutic target for T-ALL , we investigated the effect of Notch3 silencing on Jurkat and SupT1 cells using a novel tumor-specific short hairpin RNA ( shRNA ) driven by survivin promoters . RESULTS We found that downregulated expression of Notch3 correlated with significant apoptosis and inhibition of proliferation . CONCLUSION These facts suggest that downregulating expression of Notch3 could attenuate the Notch signaling activity in T-ALL . All these results indicate that inhibition of Notch3 expression can result in potent antitumor activity in T-ALL .
    OUTPUT:
