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: Autophagy is activated in response to cellular stressors and mediates lysosomal degradation and recycling of cytoplasmic material and organelles as a temporary cell survival mechanism . Defective autophagy is implicated in human pathology , as disruption of protein and organelle homeostasis enables disease-promoting mechanisms such as toxic protein aggregation , oxidative stress , genomic damage , and inflammation . We previously showed that autophagy-defective immortalized mouse mammary epithelial cells are susceptible to metabolic stress , DNA damage , and genomic instability . We now report that autophagy deficiency is associated with endoplasmic reticulum ( ER ) and oxidative stress , and with deregulation of p62-mediated keratin homeostasis in mammary cells , allograft tumors , and mammary tissues from genetically engineered mice . In human breast tumors , high phospho(Ser73)-K8 levels are inversely correlated with Beclin 1 expression . Thus , autophagy preserves cellular fitness by limiting ER and oxidative stress , a function potentially important in autophagy-mediated suppression of mammary tumorigenesis . Furthermore , autophagy regulates keratin homeostasis in the mammary gland via a p62-dependent mechanism . High phospho(Ser73)-K8 expression may be a marker of autophagy functional status in breast tumors and , as such , could have therapeutic implications for breast cancer patients .
    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: Autophagy is activated in response to cellular stressors and mediates lysosomal degradation and recycling of cytoplasmic material and organelles as a temporary cell survival mechanism . Defective autophagy is implicated in human pathology , as disruption of protein and organelle homeostasis enables disease-promoting mechanisms such as toxic protein aggregation , oxidative stress , genomic damage , and inflammation . We previously showed that autophagy-defective immortalized mouse mammary epithelial cells are susceptible to metabolic stress , DNA damage , and genomic instability . We now report that autophagy deficiency is associated with endoplasmic reticulum ( ER ) and oxidative stress , and with deregulation of p62-mediated keratin homeostasis in mammary cells , allograft tumors , and mammary tissues from genetically engineered mice . In human breast tumors , high phospho(Ser73)-K8 levels are inversely correlated with Beclin 1 expression . Thus , autophagy preserves cellular fitness by limiting ER and oxidative stress , a function potentially important in autophagy-mediated suppression of mammary tumorigenesis . Furthermore , autophagy regulates keratin homeostasis in the mammary gland via a p62-dependent mechanism . High phospho(Ser73)-K8 expression may be a marker of autophagy functional status in breast tumors and , as such , could have therapeutic implications for breast cancer patients .
    OUTPUT:
