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 The receptor tyrosine kinase family includes many transmembrane proteins with diverse physiological and pathophysiological functions . The involvement of tyrosine kinase signaling in promoting a more aggressive tumor phenotype within the context of chemotherapeutic evasion is gaining recognition . The Ron receptor is a tyrosine kinase receptor that has been implicated in the progression of breast cancer and evasion of tamoxifen therapy . RESULTS Here , we report that Ron expression is correlated with in situ , estrogen receptor alpha ( ERÎ±)-positive tumors , and is higher in breast tumors following neoadjuvant tamoxifen therapy . We also demonstrate that the majority of mammary tumors isolated from transgenic mice with mammary specific-Ron overexpression ( MMTV-Ron mice ) , exhibit appreciable ER expression . Moreover , genetic-ablation of ERÎ± , in the context of Ron overexpression , leads to delayed mammary tumor initiation and growth , but also results in an increased metastasis . CONCLUSIONS Ron receptor overexpression is associated with ERÎ±-positive human and murine breast tumors . In addition , loss of ERÎ± on a Ron overexpressing background in mice leads to the development of breast tumors which grow slower but which exhibit more metastasis and suggests that targeting of ERÎ± , as in the case of tamoxifen therapy , may reduce the growth of Ron overexpressing breast cancers but may cause these tumors to be more metastatic .
    OUTPUT:

agent
sustaining proliferative signaling;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 The receptor tyrosine kinase family includes many transmembrane proteins with diverse physiological and pathophysiological functions . The involvement of tyrosine kinase signaling in promoting a more aggressive tumor phenotype within the context of chemotherapeutic evasion is gaining recognition . The Ron receptor is a tyrosine kinase receptor that has been implicated in the progression of breast cancer and evasion of tamoxifen therapy . RESULTS Here , we report that Ron expression is correlated with in situ , estrogen receptor alpha ( ERÎ±)-positive tumors , and is higher in breast tumors following neoadjuvant tamoxifen therapy . We also demonstrate that the majority of mammary tumors isolated from transgenic mice with mammary specific-Ron overexpression ( MMTV-Ron mice ) , exhibit appreciable ER expression . Moreover , genetic-ablation of ERÎ± , in the context of Ron overexpression , leads to delayed mammary tumor initiation and growth , but also results in an increased metastasis . CONCLUSIONS Ron receptor overexpression is associated with ERÎ±-positive human and murine breast tumors . In addition , loss of ERÎ± on a Ron overexpressing background in mice leads to the development of breast tumors which grow slower but which exhibit more metastasis and suggests that targeting of ERÎ± , as in the case of tamoxifen therapy , may reduce the growth of Ron overexpressing breast cancers but may cause these tumors to be more metastatic .
    OUTPUT:
