RT Journal Article
SR Electronic
T1 Tumor-associated macrophages in multiple myeloma: advances in biology and therapy
JF Journal for ImmunoTherapy of Cancer
JO J Immunother Cancer
FD BMJ Publishing Group Ltd
SP e003975
DO 10.1136/jitc-2021-003975
VO 10
IS 4
A1 Jennifer Sun
A1 Chaelee Park
A1 Nicole Guenthner
A1 Shannon Gurley
A1 Luna Zhang
A1 Berit Lubben
A1 Ola Adebayo
A1 Hannah Bash
A1 Yixuan Chen
A1 Mina Maksimos
A1 Barbara Muz
A1 Abdel Kareem Azab
YR 2022
UL http://jitc.bmj.com/content/10/4/e003975.abstract
AB Multiple myeloma (MM) is a cancer of plasma cells in the bone marrow (BM) and represents the second most common hematological malignancy in the world. The MM tumor microenvironment (TME) within the BM niche consists of a wide range of elements which play important roles in supporting MM disease progression, survival, proliferation, angiogenesis, as well as drug resistance. Together, the TME fosters an immunosuppressive environment in which immune recognition and response are repressed. Macrophages are a central player in the immune system with diverse functions, and it has been long established that macrophages play a critical role in both inducing direct and indirect immune responses in cancer. Tumor-associated macrophages (TAMs) are a major population of cells in the tumor site. Rather than contributing to the immune response against tumor cells, TAMs in many cancers are found to exhibit protumor properties including supporting chemoresistance, tumor proliferation and survival, angiogenesis, immunosuppression, and metastasis. Targeting TAM represents a novel strategy for cancer immunotherapy, which has potential to indirectly stimulate cytotoxic T cell activation and recruitment, and synergize with checkpoint inhibitors and chemotherapies. In this review, we will provide an updated and comprehensive overview into the current knowledge on the roles of TAMs in MM, as well as the therapeutic targets that are being explored as macrophage-targeted immunotherapy, which may hold key to future therapeutics against MM.