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: Adults and children with high-risk CRLF2-rearranged acute lymphoblastic leukemia ( ALL ) respond poorly to current cytotoxic chemotherapy and suffer unacceptably high rates of relapse , supporting the need to use alternative therapies . CRLF2 encodes the thymic stromal lymphopoietin ( TSLP ) receptor , which activates cell signaling in normal lymphocytes on binding its ligand , TSLP . We hypothesized that aberrant cell signaling occurs in CRLF2-rearranged ALL and can be targeted by signal transduction inhibitors of this pathway . In a large number of primary CRLF2-rearranged ALL samples , we observed increased basal levels of pJAK2 , pSTAT5 , and pS6 . We thus characterized the biochemical sequelae of CRLF2 and JAK alterations in CRLF2-rearranged ALL primary patient samples via analysis of TSLP-mediated signal transduction . TSLP stimulation of these leukemias further induced robust JAK/STAT and PI3K/mTOR pathway signaling . JAK inhibition abrogated phosphorylation of JAK/STAT and , surprisingly , of PI3K/mTOR pathway members , suggesting an interconnection between these signaling networks and providing a rationale for testing JAK inhibitors in clinical trials . The PI3K/mTOR pathway inhibitors rapamycin , PI103 , and PP242 also inhibited activated signal transduction and translational machinery proteins of the PI3K/mTOR pathway , suggesting that signal transduction inhibitors targeting this pathway also may have therapeutic relevance for patients with CRLF2-rearranged ALL and merit further preclinical testing .
    OUTPUT:

agent
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: Adults and children with high-risk CRLF2-rearranged acute lymphoblastic leukemia ( ALL ) respond poorly to current cytotoxic chemotherapy and suffer unacceptably high rates of relapse , supporting the need to use alternative therapies . CRLF2 encodes the thymic stromal lymphopoietin ( TSLP ) receptor , which activates cell signaling in normal lymphocytes on binding its ligand , TSLP . We hypothesized that aberrant cell signaling occurs in CRLF2-rearranged ALL and can be targeted by signal transduction inhibitors of this pathway . In a large number of primary CRLF2-rearranged ALL samples , we observed increased basal levels of pJAK2 , pSTAT5 , and pS6 . We thus characterized the biochemical sequelae of CRLF2 and JAK alterations in CRLF2-rearranged ALL primary patient samples via analysis of TSLP-mediated signal transduction . TSLP stimulation of these leukemias further induced robust JAK/STAT and PI3K/mTOR pathway signaling . JAK inhibition abrogated phosphorylation of JAK/STAT and , surprisingly , of PI3K/mTOR pathway members , suggesting an interconnection between these signaling networks and providing a rationale for testing JAK inhibitors in clinical trials . The PI3K/mTOR pathway inhibitors rapamycin , PI103 , and PP242 also inhibited activated signal transduction and translational machinery proteins of the PI3K/mTOR pathway , suggesting that signal transduction inhibitors targeting this pathway also may have therapeutic relevance for patients with CRLF2-rearranged ALL and merit further preclinical testing .
    OUTPUT:
