Dr Takanori Kitamura
Background and research interest.
Tumour metastasis has been a leading cause of cancer death, indicating that current immunotherapy and chemotherapy have had limited success in treating the disease. It is thus necessary to find novel approaches to suppress the expansion of metastatic tumors to prolong patient’s survival.
Data from mouse models including ours suggest that tumour-infiltrating myeloid cells, such as tumour-associated macrophages (TAMs) and neutrophils (TANs) promote metastatic processes in several tumor types such as breast, colon, and lung cancer. TAMs and TANs are also reported to protect cancer cells from immune rejection by CD8+ T and NK cells and to restrict efficacy of cytotoxic drugs at the primary sites.
These data suggest that keeping out and/or suppressing these pro-metastatic stromal cells is an attractive strategy to restrict metastatic tumour growth by withdrawal of environmental supports and by increasing efficiency of current therapeutic modalities for metastatic diseases. We are thus interested in the cooperative actions of these cells for metastatic tumor growth and effects on cytotoxic cells and drugs at the secondary sites.
Our goal is to find effective and tumour specific targets to suppress pro-metastatic functions of stromal cells, in particular myeloid cells. The following three projects are ongoing or planned.
- Interaction between TAMs and other types of immune cells at the metastasis site.
- Improvement of efficacy of chemo- and immunotherapies for metastatic diseases by blocking TAM/TAN functions via chemokine receptor inhibition.
- Identification of tumor-type specific or common environments that regulates TAM/TAN functions.
Dr Dahlia Doughty Shenton, Postdoctoral Fellow