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: Proton radiotherapy has gained more favor among oncologists as a treatment option for localized and deep-seated tumors . In addition , protons are a major constituent of the space radiation astronauts receive during space flights . The potential for these exposures to lead to , or enhance cancer risk has not been well studied . Our objective is to study the biological effects of low energy protons on epithelial cells and its propensity to enhance transforming growth factor beta 1 ( TGFÎ²1)-mediated epithelial-mesenchymal transition ( EMT ) , a process occurring during tumor progression and critical for invasion and metastasis . Non-transformed mink lung epithelial cells ( Mv1Lu ) and hTERT- immortalized human esophageal epithelial cells ( EPC ) were used in this study . EMT was identified by alterations in cell morphology , EMT-related gene expression changes determined using real-time PCR , and EMT changes in specific cellular markers detected by immunostaining and western blotting . Although TGFÎ²1 treatment alone is able to induce EMT in both Mv1Lu and EPC cells , low energy protons ( 5 MeV ) at doses as low as 0.1 Gy can enhance TGFÎ²1 induced EMT . Protons alone can also induce a mild induction of EMT . SD208 , a potent TGFÎ² Receptor 1 ( TGFÎ²R1 ) kinase inhibitor , can efficiently block TGFÎ²1/Smad signaling and attenuate EMT induction . We suggest a model for EMT after proton irradiation in normal and cancerous tissue based on our results that showed that low and high doses of protons can sensitize normal human epithelial cells to mesenchymal transition , more prominently in the presence of TGFÎ²1 , but also in the absence of TGFÎ²1 .
    OUTPUT:

agent
activating invasion and metastasis
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: Proton radiotherapy has gained more favor among oncologists as a treatment option for localized and deep-seated tumors . In addition , protons are a major constituent of the space radiation astronauts receive during space flights . The potential for these exposures to lead to , or enhance cancer risk has not been well studied . Our objective is to study the biological effects of low energy protons on epithelial cells and its propensity to enhance transforming growth factor beta 1 ( TGFÎ²1)-mediated epithelial-mesenchymal transition ( EMT ) , a process occurring during tumor progression and critical for invasion and metastasis . Non-transformed mink lung epithelial cells ( Mv1Lu ) and hTERT- immortalized human esophageal epithelial cells ( EPC ) were used in this study . EMT was identified by alterations in cell morphology , EMT-related gene expression changes determined using real-time PCR , and EMT changes in specific cellular markers detected by immunostaining and western blotting . Although TGFÎ²1 treatment alone is able to induce EMT in both Mv1Lu and EPC cells , low energy protons ( 5 MeV ) at doses as low as 0.1 Gy can enhance TGFÎ²1 induced EMT . Protons alone can also induce a mild induction of EMT . SD208 , a potent TGFÎ² Receptor 1 ( TGFÎ²R1 ) kinase inhibitor , can efficiently block TGFÎ²1/Smad signaling and attenuate EMT induction . We suggest a model for EMT after proton irradiation in normal and cancerous tissue based on our results that showed that low and high doses of protons can sensitize normal human epithelial cells to mesenchymal transition , more prominently in the presence of TGFÎ²1 , but also in the absence of TGFÎ²1 .
    OUTPUT:
