Immune cell promotion of metastasis
By T. Kitamura, Binzhi Qian, J. Pollard. Nature reviews. Immunology, 2015
1,090 citations recorded by the source corpus.
Metastatic disease is the major cause of death from cancer, and immunotherapy and chemotherapy have had limited success in reversing its progression. Data from mouse models suggest that the recruitment of immunosuppressive cells to tumours protects metastatic cancer cells from surveillance by killer cells, which nullifies the effects of immunotherapy and thus establishes metastasis. Furthermore, in most cases, tumour-infiltrating immune cells differentiate into cells that promote each step of the metastatic cascade and thus are novel targets for therapy. In this Review, we describe how tumour-infiltrating immune cells contribute to the metastatic cascade and we discuss potential therapeutic strategies to target these cells.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/93bcb0a7b41afdbec6ca01b943330507b198b002
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
In Oncology
Citations in the corpus
- Roles of the immune system in cancer: from tumor initiation to metastatic progression (2018, background): “3; Noy and Pollard 2014; Kitamura et al. 2015; Gonzalez et al. 2018).”
- EMERGING BIOLOGICAL PRINCIPLES OF METASTASIS (2017, neutral): “Myeloid cells have also been identified as important contributors to the formation of a favorable metastatic microenvironment (Kitamura et al., 2015), where a unique population of metastasisassociated macrophages may be responsible for not only provoking, but also sustaining metastatic growth, perha”
- Tumor-Associated Macrophages and Neutrophils in Tumor Microenvironment (2016, background): “CCL2, CXCL12, CSF-1, SDF-1, complements, and SEMA3A for macrophage recruitment [30, 106].”
- The Cancer Stem Cell Niche: How Essential is the Niche in Regulating Stemness of Tumor Cells? (2015, neutral): “These MetSCs produce CCL2 and attract CCR2+ inflammatory monocytes that become metastatic-associated macrophages and support metastatic growth (Kitamura et al., 2015).”