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: Evidence suggests that stem-like cells are responsible for initiation , maintenance and recurrence of solid tumors , including Glioblastoma Multiforme ( GBM ) . GBM is an intractable , highly lethal tumor of the central nervous system . Although epidermal growth factor receptor ( EGFR ) is highly expressed in many GBMs , anti-EGFR therapies have been unsuccessful as treatment . Few studies have examined EGFR activation in GBM stem cells ( GSCs ) to determine if patient-specific GSCs are amenable to anti-EGFR therapy pre-clinically . We hypothesized that EGFR activation in GSCs varied between patients and was an important determinant of responsiveness to anti-EGFR therapy . Cell cycle and apoptosis analysis was performed on tumor-spheres by immuncytochemistry in the presence and absence of the AG1478 . Second messenger pathways operative in these processes were elucidated by immunoblotting . EGFR activated AKT and inactivated GSK3beta in EGFR+/PTEN+ GSCs . AG1478 and erlotinib significantly decreased the total number of tumor-spheres that EGFR+/ PTEN+ GSCs generated and the rate of sphere formation . Inhibition of EGFR signaling by AG1478 increased GSC senescence and apoptosis , likely via inhibition of AKT and activation of GSK3beta . Sphere formation by EGFR-/ PTEN- GSCs was independent of EGF stimulation , but dependant on B27 growth supplement . Our data suggest that EGFR+/PTEN+ GSCs are susceptible to anti-EGFR therapy in vitro .
    OUTPUT:

agent
enabling replicative immortality;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.
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    INPUT: Evidence suggests that stem-like cells are responsible for initiation , maintenance and recurrence of solid tumors , including Glioblastoma Multiforme ( GBM ) . GBM is an intractable , highly lethal tumor of the central nervous system . Although epidermal growth factor receptor ( EGFR ) is highly expressed in many GBMs , anti-EGFR therapies have been unsuccessful as treatment . Few studies have examined EGFR activation in GBM stem cells ( GSCs ) to determine if patient-specific GSCs are amenable to anti-EGFR therapy pre-clinically . We hypothesized that EGFR activation in GSCs varied between patients and was an important determinant of responsiveness to anti-EGFR therapy . Cell cycle and apoptosis analysis was performed on tumor-spheres by immuncytochemistry in the presence and absence of the AG1478 . Second messenger pathways operative in these processes were elucidated by immunoblotting . EGFR activated AKT and inactivated GSK3beta in EGFR+/PTEN+ GSCs . AG1478 and erlotinib significantly decreased the total number of tumor-spheres that EGFR+/ PTEN+ GSCs generated and the rate of sphere formation . Inhibition of EGFR signaling by AG1478 increased GSC senescence and apoptosis , likely via inhibition of AKT and activation of GSK3beta . Sphere formation by EGFR-/ PTEN- GSCs was independent of EGF stimulation , but dependant on B27 growth supplement . Our data suggest that EGFR+/PTEN+ GSCs are susceptible to anti-EGFR therapy in vitro .
    OUTPUT:
