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: Previously we have found deregulation of collagen metabolism in human pancreatitis and pancreatic cancer tissues . Insulin-like growth factor-I ( IGF-I ) is known to stimulate collagen biosynthesis through interaction with IGF-I receptor . IGF-I binding proteins ( BPs ) regulate the activity of IGF-I . We investigated whether serum and tissue IGF-I and IGF-BPs as well as tissue IGF-I receptor expression may reflect disturbances of collagen metabolism in patients with pancreatitis and pancreatic cancer . In pancreatitis tissue , a significant increase in IGF-I and IGFBP-3 content was accompanied by a distinct increase in IGF-I receptor expression , compared to control pancreas tissue . In contrast , serum from patients with pancreatitis did not show significant increases in IGF-I and IGFBP-3 levels , however , significant increases in IGFBP-1 level ( 2.5 fold ) . Moreover , a distinct decrease in radioactive IGF-binding to the BPs , compared to control serum , was found . Pancreatic cancer tissue and serum of patients with pancreatic cancer showed significant increases in IGF-I , IGFBP-3 and IGFBP-1 content , accompanied by dramatic increases in IGF-I tissue receptor expression , compared to controls . In serum of patients with pancreatic cancer distinct increases in radioactive IGF-binding to 46 kDa BP , compared to control serum , were observed . The data suggest that disturbances in tissue collagen metabolism during pancreatic diseases may result from deregulation of IGF-I homeostasis and that elevated serum levels of IGF-I , IGFBP-3 and IGFBP-1 may serve as markers of pancreatic cancer .
    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.
    ###
    INPUT: Previously we have found deregulation of collagen metabolism in human pancreatitis and pancreatic cancer tissues . Insulin-like growth factor-I ( IGF-I ) is known to stimulate collagen biosynthesis through interaction with IGF-I receptor . IGF-I binding proteins ( BPs ) regulate the activity of IGF-I . We investigated whether serum and tissue IGF-I and IGF-BPs as well as tissue IGF-I receptor expression may reflect disturbances of collagen metabolism in patients with pancreatitis and pancreatic cancer . In pancreatitis tissue , a significant increase in IGF-I and IGFBP-3 content was accompanied by a distinct increase in IGF-I receptor expression , compared to control pancreas tissue . In contrast , serum from patients with pancreatitis did not show significant increases in IGF-I and IGFBP-3 levels , however , significant increases in IGFBP-1 level ( 2.5 fold ) . Moreover , a distinct decrease in radioactive IGF-binding to the BPs , compared to control serum , was found . Pancreatic cancer tissue and serum of patients with pancreatic cancer showed significant increases in IGF-I , IGFBP-3 and IGFBP-1 content , accompanied by dramatic increases in IGF-I tissue receptor expression , compared to controls . In serum of patients with pancreatic cancer distinct increases in radioactive IGF-binding to 46 kDa BP , compared to control serum , were observed . The data suggest that disturbances in tissue collagen metabolism during pancreatic diseases may result from deregulation of IGF-I homeostasis and that elevated serum levels of IGF-I , IGFBP-3 and IGFBP-1 may serve as markers of pancreatic cancer .
    OUTPUT:
