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: In an attempt to find a strategy to modulate the proliferation of vascular endothelial cells , we examined whether constitutive activation of proto-oncogen protein p21 ( Ras ) induced the reentry of confluent human umbilical vascular endothelial cells ( HUVECs ) into the S phase . When an adenovirus construct expressing a constitutively active Ras mutant ( Ad/RasG12V ) was infected into HUVECs , their morphology changed strikingly and they appeared to be transformed . However , Ad/RasG12V-infected HUVECs did not enter the S phase , as determined by assessing 3H-thymidine incorporation . In accordance with the above results , the expression of cyclin A both at the transcript and protein levels did not increase in Ad/RasG12V-infected HUVECs relative to that in control cells , although the expression of cyclin D1 was induced in Ad/RasG12V-infected cells . Interestingly , the expression of the cyclin-dependent kinase ( CDK ) inhibitor p21cip1 was remarkably increased while that of p27kip1 did not decrease in Ad/RasG12V-infected HUVECs . Furthermore , CDK2 activity was not induced in Ad/RasG12V-infected HUVECs . These results suggested that the constitutive activation of Ras promoted the reentry of confluent HUVECs in the G0 phase into the G1 phase , but not into the S phase . The results also indicated that the constitutive activation of Ras might have induced the persistent expression of p21cip1 and p27kip1 , and that this induction of p21cip1 and p27kip1 expression possibly caused the cell cycle arrest at the G1 phase .
    OUTPUT:

agent
sustaining proliferative signaling;evading growth suppressors
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: In an attempt to find a strategy to modulate the proliferation of vascular endothelial cells , we examined whether constitutive activation of proto-oncogen protein p21 ( Ras ) induced the reentry of confluent human umbilical vascular endothelial cells ( HUVECs ) into the S phase . When an adenovirus construct expressing a constitutively active Ras mutant ( Ad/RasG12V ) was infected into HUVECs , their morphology changed strikingly and they appeared to be transformed . However , Ad/RasG12V-infected HUVECs did not enter the S phase , as determined by assessing 3H-thymidine incorporation . In accordance with the above results , the expression of cyclin A both at the transcript and protein levels did not increase in Ad/RasG12V-infected HUVECs relative to that in control cells , although the expression of cyclin D1 was induced in Ad/RasG12V-infected cells . Interestingly , the expression of the cyclin-dependent kinase ( CDK ) inhibitor p21cip1 was remarkably increased while that of p27kip1 did not decrease in Ad/RasG12V-infected HUVECs . Furthermore , CDK2 activity was not induced in Ad/RasG12V-infected HUVECs . These results suggested that the constitutive activation of Ras promoted the reentry of confluent HUVECs in the G0 phase into the G1 phase , but not into the S phase . The results also indicated that the constitutive activation of Ras might have induced the persistent expression of p21cip1 and p27kip1 , and that this induction of p21cip1 and p27kip1 expression possibly caused the cell cycle arrest at the G1 phase .
    OUTPUT:
