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: Stable ectopic expression of Flt3 receptor tyrosine kinase is usually performed in interleukin 3 ( IL-3)-dependent murine cell lines like Ba/F3 , resulting in loss of IL-3 dependence . Such high-level Flt3 expression has to date not been reported in human acute myeloid leukemia ( AML ) cell lines , despite the fact that oncogenic Flt3 aberrancies are frequent in AML patients . We show here that ectopic Flt3 expression in different human cancer cell lines might reduce proliferation and induce apoptotic cell death , involving Bax/Bcl2 modulation . Selective depletion of Flt3-expressing cells occurred in human AML cell lines transduced with retroviral Flt3 constructs , shown here using the HL-60 leukemic cell line . Flt3 expression was investigated in two cellular model systems , the SAOS-2 osteosarcoma cell line and the human embryonic kidney HEK293 cell line , and proliferation was reduced in both systems . HEK293 cells underwent apoptosis upon ectopic Flt3 expression and cell death could be rescued by overexpression of Bcl-2 . Furthermore , we observed that the Flt3-induced inhibition of proliferation in HL-60 cells appeared to be Bax-dependent . Our results thus suggest that excessive Flt3 expression has growth-suppressive properties in several human cancer cell lines .
    OUTPUT:

agent
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: Stable ectopic expression of Flt3 receptor tyrosine kinase is usually performed in interleukin 3 ( IL-3)-dependent murine cell lines like Ba/F3 , resulting in loss of IL-3 dependence . Such high-level Flt3 expression has to date not been reported in human acute myeloid leukemia ( AML ) cell lines , despite the fact that oncogenic Flt3 aberrancies are frequent in AML patients . We show here that ectopic Flt3 expression in different human cancer cell lines might reduce proliferation and induce apoptotic cell death , involving Bax/Bcl2 modulation . Selective depletion of Flt3-expressing cells occurred in human AML cell lines transduced with retroviral Flt3 constructs , shown here using the HL-60 leukemic cell line . Flt3 expression was investigated in two cellular model systems , the SAOS-2 osteosarcoma cell line and the human embryonic kidney HEK293 cell line , and proliferation was reduced in both systems . HEK293 cells underwent apoptosis upon ectopic Flt3 expression and cell death could be rescued by overexpression of Bcl-2 . Furthermore , we observed that the Flt3-induced inhibition of proliferation in HL-60 cells appeared to be Bax-dependent . Our results thus suggest that excessive Flt3 expression has growth-suppressive properties in several human cancer cell lines .
    OUTPUT:
