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: TP53 mutations compromising p53 transcriptional function occur in more than 50% of human cancers , including pancreatic adenocarcinoma , and render cancer cells more resistant to conventional therapy . In the last few years , many efforts have been addressed to identify p53-reactivating molecules able to restore the wild-type transcriptionally competent conformation of the mutated proteins . Here , we show that two of these compounds , CP-31398 and RITA , induce cell growth inhibition , apoptosis , and autophagy by activating p53/DNA binding and p53 phosphorylation ( Ser15 ) , without affecting the total p53 amount . These effects occur in both wild-type and mutant p53 pancreatic adenocarcinoma cell lines , whereas they are much less pronounced in normal human primary fibroblasts . Furthermore , CP-31398 and RITA regulate the axis SESN1-2/AMPK/mTOR by inducing AMPK phosphorylation on Thr172 , which has a crucial role in the autophagic response . The protective role of autophagy in cell growth inhibition by CP-31398 and RITA is supported by the finding that the AMPK inhibitor compound C or the autophagy inhibitors chloroquine or 3-methyladenine sensitize both pancreatic adenocarcinoma cell lines to the apoptotic response induced by p53-reactivating molecules . Our results demonstrate for the first time a survival role for autophagy induced by p53-reactivating molecules , supporting the development of an anti-cancer therapy based on autophagy inhibition associated to p53 activation .
    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: TP53 mutations compromising p53 transcriptional function occur in more than 50% of human cancers , including pancreatic adenocarcinoma , and render cancer cells more resistant to conventional therapy . In the last few years , many efforts have been addressed to identify p53-reactivating molecules able to restore the wild-type transcriptionally competent conformation of the mutated proteins . Here , we show that two of these compounds , CP-31398 and RITA , induce cell growth inhibition , apoptosis , and autophagy by activating p53/DNA binding and p53 phosphorylation ( Ser15 ) , without affecting the total p53 amount . These effects occur in both wild-type and mutant p53 pancreatic adenocarcinoma cell lines , whereas they are much less pronounced in normal human primary fibroblasts . Furthermore , CP-31398 and RITA regulate the axis SESN1-2/AMPK/mTOR by inducing AMPK phosphorylation on Thr172 , which has a crucial role in the autophagic response . The protective role of autophagy in cell growth inhibition by CP-31398 and RITA is supported by the finding that the AMPK inhibitor compound C or the autophagy inhibitors chloroquine or 3-methyladenine sensitize both pancreatic adenocarcinoma cell lines to the apoptotic response induced by p53-reactivating molecules . Our results demonstrate for the first time a survival role for autophagy induced by p53-reactivating molecules , supporting the development of an anti-cancer therapy based on autophagy inhibition associated to p53 activation .
    OUTPUT:
