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: Peroxisome proliferator-activated receptor-Î³ ( PPARÎ³ ) is an anti-inflammatory molecule . To study its biologic function in myeloid cells , dominant-negative PPARÎ³ ( dnPPARÎ³ ) was overexpressed in a myeloid-specific bitransgenic mouse model . In this bitransgenic system , overexpression of the dnPPARÎ³-Flag fusion protein in myeloid-lineage cells abnormally elevated frequencies and total numbers of IL-7RÎ±(-)Lin(-)c-Kit(+)Sca-1(-) , Lin(-)/Scal(+)/c-Kit(+) , common myeloid , and granulocyte-monocyte progenitor populations in the BM. dnPPARÎ³ overexpression led to up-regulation of IL-1Î² , IL-6 , and TNFÎ± in the blood plasma . As a result , CD11b(+)Ly6G(+) cells were systemically increased in association with activation of Stat3 , NF-ÎºB , Erk1/2 , and p38 molecules . Myeloid-derived suppressor cells ( MDSCs ) inhibited the proliferation and lymphokine production of wild-type CD4+ T cells in vitro . CD4+ T cells from doxycycline-treated bitransgenic mice displayed reduced proliferation and lymphokine release . Both CD4+ and CD8+ T-cell populations were decreased in doxycycline-treated bitransgenic mice . Multiple forms of carcinoma and sarcoma in the lung , liver , spleen , and lymph nodes were observed in doxycycline-treated bitransgenic mice . BM transplantation revealed that a myeloid-autonomous defect was responsible for MDSC expansion , immunosuppression , and tumorigenesis in these mice . These studies suggest that anti-inflammatory PPARÎ³ in myeloid-lineage cells plays a key role in controlling pro-inflammatory cytokine synthesis , MDSC expansion , immunosuppression , and the development of cancer .
    OUTPUT:

agent
sustaining proliferative signaling;tumor promoting inflammation
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: Peroxisome proliferator-activated receptor-Î³ ( PPARÎ³ ) is an anti-inflammatory molecule . To study its biologic function in myeloid cells , dominant-negative PPARÎ³ ( dnPPARÎ³ ) was overexpressed in a myeloid-specific bitransgenic mouse model . In this bitransgenic system , overexpression of the dnPPARÎ³-Flag fusion protein in myeloid-lineage cells abnormally elevated frequencies and total numbers of IL-7RÎ±(-)Lin(-)c-Kit(+)Sca-1(-) , Lin(-)/Scal(+)/c-Kit(+) , common myeloid , and granulocyte-monocyte progenitor populations in the BM. dnPPARÎ³ overexpression led to up-regulation of IL-1Î² , IL-6 , and TNFÎ± in the blood plasma . As a result , CD11b(+)Ly6G(+) cells were systemically increased in association with activation of Stat3 , NF-ÎºB , Erk1/2 , and p38 molecules . Myeloid-derived suppressor cells ( MDSCs ) inhibited the proliferation and lymphokine production of wild-type CD4+ T cells in vitro . CD4+ T cells from doxycycline-treated bitransgenic mice displayed reduced proliferation and lymphokine release . Both CD4+ and CD8+ T-cell populations were decreased in doxycycline-treated bitransgenic mice . Multiple forms of carcinoma and sarcoma in the lung , liver , spleen , and lymph nodes were observed in doxycycline-treated bitransgenic mice . BM transplantation revealed that a myeloid-autonomous defect was responsible for MDSC expansion , immunosuppression , and tumorigenesis in these mice . These studies suggest that anti-inflammatory PPARÎ³ in myeloid-lineage cells plays a key role in controlling pro-inflammatory cytokine synthesis , MDSC expansion , immunosuppression , and the development of cancer .
    OUTPUT:
