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: BACKGROUND Chemokines are involved in multiple aspects of pathogenesis and cellular trafficking in tumorigenesis . In this study , we report that the latest member of the C-X-C-type chemokines , CXCL17 ( DMC/VCC-1 ) , recruits immature myeloid-derived cells and enhances early tumor progression . METHODOLOGY/PRINCIPAL FINDINGS CXCL17 was preferentially expressed in some aggressive types of gastrointestinal , breast , and lung cancer cells . CXCL17 expression did not impart NIH3T3 cells with oncogenic potential in vitro , but CXCL17-expressing NIH3T3 cells could form vasculature-rich tumors in immunodeficient mice . Our data showed that CXCL17-expressing tumor cells increased immature CD11b(+)Gr1(+) myeloid-derived cells at tumor sites in mice and promoted CD31(+) tumor angiogenesis . Extensive chemotactic assays proved that CXCL17-responding cells were CD11b(+)Gr1(high)F4/80(-) cells ( â 90% ) with a neutrophil-like morphology in vitro . Although CXCL17 expression could not increase the number of CD11b(+)Gr1(+) cells in tumor-burdened SCID mice or promote metastases of low metastatic colon cancer cells , the existence of CXCL17-responding myeloid-derived cells caused a striking enhancement of xenograft tumor formation . CONCLUSIONS/SIGNIFICANCE These results suggest that aberrant expression of CXCL17 in tumor cells recruits immature myeloid-derived cells and promotes tumor progression through angiogenesis .
    OUTPUT:

agent
inducing angiogenesis;activating invasion and metastasis
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: BACKGROUND Chemokines are involved in multiple aspects of pathogenesis and cellular trafficking in tumorigenesis . In this study , we report that the latest member of the C-X-C-type chemokines , CXCL17 ( DMC/VCC-1 ) , recruits immature myeloid-derived cells and enhances early tumor progression . METHODOLOGY/PRINCIPAL FINDINGS CXCL17 was preferentially expressed in some aggressive types of gastrointestinal , breast , and lung cancer cells . CXCL17 expression did not impart NIH3T3 cells with oncogenic potential in vitro , but CXCL17-expressing NIH3T3 cells could form vasculature-rich tumors in immunodeficient mice . Our data showed that CXCL17-expressing tumor cells increased immature CD11b(+)Gr1(+) myeloid-derived cells at tumor sites in mice and promoted CD31(+) tumor angiogenesis . Extensive chemotactic assays proved that CXCL17-responding cells were CD11b(+)Gr1(high)F4/80(-) cells ( â 90% ) with a neutrophil-like morphology in vitro . Although CXCL17 expression could not increase the number of CD11b(+)Gr1(+) cells in tumor-burdened SCID mice or promote metastases of low metastatic colon cancer cells , the existence of CXCL17-responding myeloid-derived cells caused a striking enhancement of xenograft tumor formation . CONCLUSIONS/SIGNIFICANCE These results suggest that aberrant expression of CXCL17 in tumor cells recruits immature myeloid-derived cells and promotes tumor progression through angiogenesis .
    OUTPUT:
