Tumour-associated macrophages and cancer

- TAM infiltration is linked to a poorer prognosis and resistance to therapy in several cancer types.
- Challenges are faced due to lack of TAM specific markers.
- Next generation sequencing methods have improved TAM characterisation.
- Inhibition of TAM recruitment represents an attractive target for anti-tumour therapy.
- Combining TAM inhibition with standard therapy has shown promise in early results.

Our understanding of the complex roles and functions of tumour-associated myeloid cells has improved vastly over the last few years. Alternatively activated macrophages, TAMs, are an abundant part of solid and haematological malignancies and have been linked with progression, metastasis and resistance to therapy. Still, characterisation and TAM targeting is hindered by a lack of TAM specific markers, but advances in next generation technologies are rapidly increasing our understanding of the sheer diversity of myeloid differentiation and phenotypic regulation. These technologies help to shed light on the heterogeneous phenotypic states of myeloid cells within the tumour. Alternative approaches to influence the myeloid compartment within cancers surround inhibition of myeloid recruitment or 're-education' of the plastic TAM phenotype. Our knowledge continuously grows on how even 'established' therapies might influence the myeloid compartment within tumours. Now the promising results from elegant pre-clinical studies at first translate into the clinic and use combination therapies with myeloid inhibitors and standard chemotherapy.