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: Gastrin stimulates the growth of pancreatic cancer cells through the activation of the cholecystokinin-B receptor ( CCK-BR ) , which has been found to be overexpressed in pancreatic cancer . In this study , we proposed that the CCK-BR drives growth of pancreatic cancer ; hence , interruption of CCK-BR activity could potentially be an ideal target for cancer therapeutics . The effect of CCK-BR downregulation in the human pancreatic adenocarcinoma cells was examined by utilizing specific CCK-BR-targeted RNA interference reagents . The CCK-BR receptor expression was both transiently and stably downregulated by transfection with selective CCK-BR small-interfering RNA or short-hairpin RNA , respectively , and the effects on cell growth and apoptosis were assessed . CCK-BR downregulation resulted in reduced cancer cell proliferation , decreased DNA synthesis , and cell cycle arrest as demonstrated by an inhibition of G(1) to S phase progression . Furthermore , CCK-BR downregulation increased caspase-3 activity , TUNEL-positive cells , and decreased X-linked inhibitor of apoptosis protein expression , suggesting apoptotic activity . Pancreatic cancer cell mobility was decreased when the CCK-BR was downregulated , as assessed by a migration assay . These results show the importance of the CCK-BR in regulation of growth and apoptosis in pancreatic cancer . Strategies to decrease the CCK-BR expression and activity may be beneficial for the development of new methods to improve the treatment for patients with pancreatic cancer .
    OUTPUT:

agent
evading growth suppressors;sustaining proliferative signaling;resisting cell death;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: Gastrin stimulates the growth of pancreatic cancer cells through the activation of the cholecystokinin-B receptor ( CCK-BR ) , which has been found to be overexpressed in pancreatic cancer . In this study , we proposed that the CCK-BR drives growth of pancreatic cancer ; hence , interruption of CCK-BR activity could potentially be an ideal target for cancer therapeutics . The effect of CCK-BR downregulation in the human pancreatic adenocarcinoma cells was examined by utilizing specific CCK-BR-targeted RNA interference reagents . The CCK-BR receptor expression was both transiently and stably downregulated by transfection with selective CCK-BR small-interfering RNA or short-hairpin RNA , respectively , and the effects on cell growth and apoptosis were assessed . CCK-BR downregulation resulted in reduced cancer cell proliferation , decreased DNA synthesis , and cell cycle arrest as demonstrated by an inhibition of G(1) to S phase progression . Furthermore , CCK-BR downregulation increased caspase-3 activity , TUNEL-positive cells , and decreased X-linked inhibitor of apoptosis protein expression , suggesting apoptotic activity . Pancreatic cancer cell mobility was decreased when the CCK-BR was downregulated , as assessed by a migration assay . These results show the importance of the CCK-BR in regulation of growth and apoptosis in pancreatic cancer . Strategies to decrease the CCK-BR expression and activity may be beneficial for the development of new methods to improve the treatment for patients with pancreatic cancer .
    OUTPUT:
