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.
    ###
    INPUT: The androgen receptor ( AR ) plays a central role in prostate cancer progression to the castration-resistant ( CR ) lethal state . L-Dopa decarboxylase ( DDC ) is an AR coactivator that increases in expression with disease progression and is coexpressed with the receptor in prostate adenocarcinoma cells , where it may enhance AR activity . Here , we hypothesize that the DDC enzymatic inhibitor , carbidopa , can suppress DDC-coactivation of AR and retard prostate tumor growth . Treating LNCaP prostate cancer cells with carbidopa in transcriptional assays suppressed the enhanced AR transactivation seen with DDC overexpression and decreased prostate-specific antigen ( PSA ) mRNA levels . Carbidopa dose-dependently inhibited cell growth and decreased survival in LNCaP cell proliferation and apoptosis assays . The inhibitory effect of carbidopa on DDC-coactivation of AR and cell growth/survival was also observed in PC3 prostate cancer cells ( stably expressing AR ) . In vivo studies demonstrated that serum PSA velocity and tumor growth rates elevated â¼2-fold in LNCaP xenografts , inducibly overexpressing DDC , were reverted to control levels with carbidopa administration . In castrated mice , treating LNCaP tumors , expressing endogenous DDC , with carbidopa delayed progression to the CR state from 6 to 10 weeks , while serum PSA and tumor growth decreased 4.3-fold and 5.4-fold , respectively . Our study is a first time demonstration that carbidopa can abrogate DDC-coactivation of AR in prostate cancer cells and tumors , decrease serum PSA , reduce tumor growth and delay CR progression . Since carbidopa is clinically approved , it may be readily used as a novel therapeutic strategy to suppress aberrant AR activity and delay prostate cancer progression .
    OUTPUT:

agent
resisting cell death;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 androgen receptor ( AR ) plays a central role in prostate cancer progression to the castration-resistant ( CR ) lethal state . L-Dopa decarboxylase ( DDC ) is an AR coactivator that increases in expression with disease progression and is coexpressed with the receptor in prostate adenocarcinoma cells , where it may enhance AR activity . Here , we hypothesize that the DDC enzymatic inhibitor , carbidopa , can suppress DDC-coactivation of AR and retard prostate tumor growth . Treating LNCaP prostate cancer cells with carbidopa in transcriptional assays suppressed the enhanced AR transactivation seen with DDC overexpression and decreased prostate-specific antigen ( PSA ) mRNA levels . Carbidopa dose-dependently inhibited cell growth and decreased survival in LNCaP cell proliferation and apoptosis assays . The inhibitory effect of carbidopa on DDC-coactivation of AR and cell growth/survival was also observed in PC3 prostate cancer cells ( stably expressing AR ) . In vivo studies demonstrated that serum PSA velocity and tumor growth rates elevated â¼2-fold in LNCaP xenografts , inducibly overexpressing DDC , were reverted to control levels with carbidopa administration . In castrated mice , treating LNCaP tumors , expressing endogenous DDC , with carbidopa delayed progression to the CR state from 6 to 10 weeks , while serum PSA and tumor growth decreased 4.3-fold and 5.4-fold , respectively . Our study is a first time demonstration that carbidopa can abrogate DDC-coactivation of AR in prostate cancer cells and tumors , decrease serum PSA , reduce tumor growth and delay CR progression . Since carbidopa is clinically approved , it may be readily used as a novel therapeutic strategy to suppress aberrant AR activity and delay prostate cancer progression .
    OUTPUT:
