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: The insulin-like growth factor ( IGF ) pathway represents one of the most studied molecular regulatory networks in oncology . Clinical trials investigating the therapeutic value of anti-IGF1 receptor ( IGF1R ) therapies in cancer , including prostate cancer , are ongoing . However , the multiple functions of the IGF network in the prostate are not entirely known . To elucidate the effects of IGF and insulin ( INS ) on prostate cells , we stimulated prostate cancer ( PC3 , DU145 , LNCaP , DUCaP ) and noncancerous prostate cells ( EP156T , RWPE-1 ) and observed differing responses : whereas cancer cells responded to IGF and INS exposure by way of enhanced cell proliferation and glucose consumption , basal to luminal differentiation was induced in noncancerous cells . The same diverse responses were observed when the growth factor receptors IGF1R or INSR were overexpressed . Down-regulation of IGF1R or INSR isoform A ( INSRA ) also inhibited only proliferation of cancer cells . The proliferative response induced by the INSR in cancer cells was mediated solely by the INSRA . Moreover we observed that the receptors of the IGF network mutually influence their expression and exert redundant functions , thus underscoring the functional molecular network formed by IGF , INS , IGF1R , and INSR . Collectively we found that both IGF1R and INSRA have oncogenic effects in prostate cancer , but the IGF network also has important physiological functions in the noncancerous prostate . These data provide new insights into the biology of the IGF network in the prostate , thereby facilitating the design and interpretation of clinical studies investigating IGF1R targeting agents .
    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: The insulin-like growth factor ( IGF ) pathway represents one of the most studied molecular regulatory networks in oncology . Clinical trials investigating the therapeutic value of anti-IGF1 receptor ( IGF1R ) therapies in cancer , including prostate cancer , are ongoing . However , the multiple functions of the IGF network in the prostate are not entirely known . To elucidate the effects of IGF and insulin ( INS ) on prostate cells , we stimulated prostate cancer ( PC3 , DU145 , LNCaP , DUCaP ) and noncancerous prostate cells ( EP156T , RWPE-1 ) and observed differing responses : whereas cancer cells responded to IGF and INS exposure by way of enhanced cell proliferation and glucose consumption , basal to luminal differentiation was induced in noncancerous cells . The same diverse responses were observed when the growth factor receptors IGF1R or INSR were overexpressed . Down-regulation of IGF1R or INSR isoform A ( INSRA ) also inhibited only proliferation of cancer cells . The proliferative response induced by the INSR in cancer cells was mediated solely by the INSRA . Moreover we observed that the receptors of the IGF network mutually influence their expression and exert redundant functions , thus underscoring the functional molecular network formed by IGF , INS , IGF1R , and INSR . Collectively we found that both IGF1R and INSRA have oncogenic effects in prostate cancer , but the IGF network also has important physiological functions in the noncancerous prostate . These data provide new insights into the biology of the IGF network in the prostate , thereby facilitating the design and interpretation of clinical studies investigating IGF1R targeting agents .
    OUTPUT:
