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: Many reports have emphasized the role of gastrin as a growth factor for normal gastrointestinal mucosa and gastrointestinal cancers . Recent studies have pointed out that this peptide acts also as a growth factor for the pancreatic cancer cell line AR42J . This effect is mediated by gastrin [ cholecystokinin ( CCK)-B ] receptors . In the present study , we investigated gastrin ( CCK-B ) receptor expression in the azaserine-induced rat pancreatic carcinoma DSL-6 , comparing it to normal rat pancreas , and we also characterized CCK receptor subtypes in this tumor . The results showed that there is extensive gastrin binding to the DSL-6 pancreatic carcinoma . No evidence of specific gastrin binding to normal pancreas was found . Analysis of the ability of gastrin-17-I to inhibit 125I-gastrin-I binding demonstrated that gastrin bound to a single class of receptors with a Kd of 0.21 +/- 0.04 nM and a binding capacity of 184 +/- 29 fmol/mg protein. 125I-Gastrin-I binding was inhibited by the specific CCK-B receptor antagonist L365,260 approximately 40 times more effectively than by the specific CCK-A receptor antagonist L364,718 . Analysis of the ability of cholecystokinin octapeptide ( CCK-8 ) to inhibit 125I-Bolton-Hunter-CCK-8 binding revealed two CCK binding sites , i.e. , a high affinity site and a low affinity site . The observed binding affinities of CCK-8 were then introduced into the computer analysis of the dose-inhibition curve of the ability of gastrin-17-I to inhibit binding of 125I-Bolton-Hunter-CCK-8 , which was significantly better fit by a three-site model than by a two-site model . The three sites meet the criteria for CCK-B , high affinity CCK-A , and low affinity CCK-A receptors . The binding capacity of CCK-B receptors constitutes 34% of the total high affinity CCK binding sites . This study demonstrated that DSL-6 pancreatic carcinoma expresses three subtypes of CCK receptors . Gastrin ( CCK-B ) receptors , which were not detected in normal rat pancreas , constitute about one third of the total high affinity CCK receptors . We suggest that novel expression of gastrin ( CCK-B ) receptors may be generated by gene mutation or amplification during carcinogenesis and may play an important role in promoting tumor growth .
    OUTPUT:

agent
sustaining proliferative signaling
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: Many reports have emphasized the role of gastrin as a growth factor for normal gastrointestinal mucosa and gastrointestinal cancers . Recent studies have pointed out that this peptide acts also as a growth factor for the pancreatic cancer cell line AR42J . This effect is mediated by gastrin [ cholecystokinin ( CCK)-B ] receptors . In the present study , we investigated gastrin ( CCK-B ) receptor expression in the azaserine-induced rat pancreatic carcinoma DSL-6 , comparing it to normal rat pancreas , and we also characterized CCK receptor subtypes in this tumor . The results showed that there is extensive gastrin binding to the DSL-6 pancreatic carcinoma . No evidence of specific gastrin binding to normal pancreas was found . Analysis of the ability of gastrin-17-I to inhibit 125I-gastrin-I binding demonstrated that gastrin bound to a single class of receptors with a Kd of 0.21 +/- 0.04 nM and a binding capacity of 184 +/- 29 fmol/mg protein. 125I-Gastrin-I binding was inhibited by the specific CCK-B receptor antagonist L365,260 approximately 40 times more effectively than by the specific CCK-A receptor antagonist L364,718 . Analysis of the ability of cholecystokinin octapeptide ( CCK-8 ) to inhibit 125I-Bolton-Hunter-CCK-8 binding revealed two CCK binding sites , i.e. , a high affinity site and a low affinity site . The observed binding affinities of CCK-8 were then introduced into the computer analysis of the dose-inhibition curve of the ability of gastrin-17-I to inhibit binding of 125I-Bolton-Hunter-CCK-8 , which was significantly better fit by a three-site model than by a two-site model . The three sites meet the criteria for CCK-B , high affinity CCK-A , and low affinity CCK-A receptors . The binding capacity of CCK-B receptors constitutes 34% of the total high affinity CCK binding sites . This study demonstrated that DSL-6 pancreatic carcinoma expresses three subtypes of CCK receptors . Gastrin ( CCK-B ) receptors , which were not detected in normal rat pancreas , constitute about one third of the total high affinity CCK receptors . We suggest that novel expression of gastrin ( CCK-B ) receptors may be generated by gene mutation or amplification during carcinogenesis and may play an important role in promoting tumor growth .
    OUTPUT:
