![]() ![]() Myeloid suppressor lines inhibit T cell responses by an NO-dependent mechanism. Immune suppression by neutrophils and granulocytic myeloid-derived suppressor cells: similarities and differences. Tumour-mediated upregulation of chemoattractants and recruitment of myeloid cells predetermines lung metastasis. Hiratsuka, S., Watanabe, A., Aburatani, H. MMP9 induction by vascular endothelial growth factor receptor-1 is involved in lung-specific metastasis. Inhibition of the Kit ligand/c-Kit axis attenuates metastasis in a mouse model mimicking local breast cancer relapse after radiotherapy. Hypoxia-induced lysyl oxidase is a critical mediator of bone marrow cell recruitment to form the premetastatic niche. VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche. A preclinical mouse model of invasive lobular breast cancer metastasis. Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis. Ultraviolet-radiation-induced inflammation promotes angiotropism and metastasis in melanoma. Granulocyte-colony stimulating factor promotes lung metastasis through mobilization of Ly6G+Ly6C+ granulocytes. Tumor entrained neutrophils inhibit seeding in the premetastatic lung. ![]() ![]() Usefulness of the neutrophil-to-lymphocyte ratio in predicting short- and long-term mortality in breast cancer patients. Usefulness of pretreatment neutrophil to lymphocyte ratio in predicting disease-specific survival in breast cancer patients. The tumour-induced systemic environment as a critical regulator of cancer progression and metastasis. Microenvironmental regulation of tumor progression and metastasis. Our data indicate that targeting this novel cancer-cell-initiated domino effect within the immune system-the γδ T cell/IL-17/neutrophil axis-represents a new strategy to inhibit metastatic disease. Moreover, the absence of γδ T cells or neutrophils profoundly reduces pulmonary and lymph node metastases without influencing primary tumour progression. Neutralization of IL-17 or G-CSF and absence of γδ T cells prevents neutrophil accumulation and downregulates the T-cell-suppressive phenotype of neutrophils. Tumour-induced neutrophils acquire the ability to suppress cytotoxic T lymphocytes carrying the CD8 antigen, which limit the establishment of metastases. We mechanistically demonstrate that interleukin (IL)-1β elicits IL-17 expression from gamma delta (γδ) T cells, resulting in systemic, granulocyte colony-stimulating factor (G-CSF)-dependent expansion and polarization of neutrophils in mice bearing mammary tumours. Here we show that tumours maximize their chance of metastasizing by evoking a systemic inflammatory cascade in mouse models of spontaneous breast cancer metastasis. However, the precise contribution of tumour-induced systemic inflammation to metastasis and the mechanisms regulating systemic inflammation are poorly understood. Within this local microenvironment and in distant organs, immune cells and their mediators are known to facilitate metastasis formation 1, 2. The different steps of the metastatic cascade rely on reciprocal interactions between cancer cells and their microenvironment. Metastatic disease remains the primary cause of death for patients with breast cancer. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |