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: Multiple myeloma is characterized by the clonal expansion of malignant plasma cells ( multiple myeloma cells [ MMCs] ) , in the bone marrow . Osteolytic bone lesions are detected in 80% of patients because of increased osteoclastic bone resorption and reduced osteoblastic bone formation . MMCs are found closely associated with sites of increased bone resorption . Osteoclasts strongly support MMC survival in vitro . To further elucidate the mechanisms involved in osteoclast/MMC interaction , we have identified 552 genes overexpressed in osteoclasts compared with other bone marrow cell subpopulations . Osteoclasts express specifically genes coding for 4 CCR2-targeting chemokines and genes coding for MMC growth factors . An anti-CCR2 monoclonal antibody blocked osteoclast chemoattractant activity for MMC , and CCR2 chemokines are also MMC growth factors , promoting mitogen-activated protein kinase activation in MMC . An anti-insulin growth factor-1 receptor monoclonal antibody completely blocked the osteoclast-induced survival of MMC suppressing both osteoclast and MMC survival . Specific a proliferation-inducing ligand or IL-6 inhibitors partially blocked osteoclast-induced MMC survival . These data may explain why newly diagnosed patients whose MMC express high levels of CCR2 present numerous bone lesions . This study displays additional mechanisms involved in osteoclast/MMC interaction and suggests using CCR2 and/or insulin growth factor-1 targeting strategies to block this interaction and prevent drug resistance .
    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: Multiple myeloma is characterized by the clonal expansion of malignant plasma cells ( multiple myeloma cells [ MMCs] ) , in the bone marrow . Osteolytic bone lesions are detected in 80% of patients because of increased osteoclastic bone resorption and reduced osteoblastic bone formation . MMCs are found closely associated with sites of increased bone resorption . Osteoclasts strongly support MMC survival in vitro . To further elucidate the mechanisms involved in osteoclast/MMC interaction , we have identified 552 genes overexpressed in osteoclasts compared with other bone marrow cell subpopulations . Osteoclasts express specifically genes coding for 4 CCR2-targeting chemokines and genes coding for MMC growth factors . An anti-CCR2 monoclonal antibody blocked osteoclast chemoattractant activity for MMC , and CCR2 chemokines are also MMC growth factors , promoting mitogen-activated protein kinase activation in MMC . An anti-insulin growth factor-1 receptor monoclonal antibody completely blocked the osteoclast-induced survival of MMC suppressing both osteoclast and MMC survival . Specific a proliferation-inducing ligand or IL-6 inhibitors partially blocked osteoclast-induced MMC survival . These data may explain why newly diagnosed patients whose MMC express high levels of CCR2 present numerous bone lesions . This study displays additional mechanisms involved in osteoclast/MMC interaction and suggests using CCR2 and/or insulin growth factor-1 targeting strategies to block this interaction and prevent drug resistance .
    OUTPUT:
