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.
    ###
    INPUT: A distinct group of breast cancers , called " basal " or " triple-negative " ( TN ) cancers express both basal cytokeratins and the epidermal growth factor receptor , but fail to express estrogen receptors , progesterone receptors or HER2 and have stem-like or mesenchymal features . They are particularly aggressive , are frequently chemo-resistant , with p53 mutation , up-regulation of IL-6 and Stat3 . Because TN cells are particularly sensitive to the anti-diabetic agent metformin , we hypothesized that it may target JAK2/Stat3 signaling . The effects of metformin upon Stat3 expression and activation were examined in four human TN cell lines . Metformin's effects were also studied in sublines with forced over-expression of constitutively active ( CA ) Stat3 , as well as lines with stable knockdown of Stat3 . Metformin inhibited Stat3 activation ( P-Stat3 ) at Tyr705 and Ser727 and downstream signaling in each of the four parental cell lines . CA-Stat3 transfection attenuated , whereas Stat3 knockdown enhanced , the effects of metformin upon growth inhibition and apoptosis induction . A Stat3 specific inhibitor acted synergistically with metformin in reducing cell growth and inducing apoptosis . An mTOR inhibitor showed no significant interaction with metformin . In summary , Stat3 is a critical regulator of metformin action in TN cancer cells , providing the potential for enhancing metformin's efficacy in the clinical setting .
    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.
    ###
    INPUT: A distinct group of breast cancers , called " basal " or " triple-negative " ( TN ) cancers express both basal cytokeratins and the epidermal growth factor receptor , but fail to express estrogen receptors , progesterone receptors or HER2 and have stem-like or mesenchymal features . They are particularly aggressive , are frequently chemo-resistant , with p53 mutation , up-regulation of IL-6 and Stat3 . Because TN cells are particularly sensitive to the anti-diabetic agent metformin , we hypothesized that it may target JAK2/Stat3 signaling . The effects of metformin upon Stat3 expression and activation were examined in four human TN cell lines . Metformin's effects were also studied in sublines with forced over-expression of constitutively active ( CA ) Stat3 , as well as lines with stable knockdown of Stat3 . Metformin inhibited Stat3 activation ( P-Stat3 ) at Tyr705 and Ser727 and downstream signaling in each of the four parental cell lines . CA-Stat3 transfection attenuated , whereas Stat3 knockdown enhanced , the effects of metformin upon growth inhibition and apoptosis induction . A Stat3 specific inhibitor acted synergistically with metformin in reducing cell growth and inducing apoptosis . An mTOR inhibitor showed no significant interaction with metformin . In summary , Stat3 is a critical regulator of metformin action in TN cancer cells , providing the potential for enhancing metformin's efficacy in the clinical setting .
    OUTPUT:
