Initial neoplastic events often occur due to genomic alterations, and it is now accepted that the progression from neoplastic initiation to malignancy happens, at least in part, due to the failure of immune surveillance. Cancer cells successfully escape immune recognition and elimination, and also create an immune suppressive microenvironment. Tumors use various mechanisms to escape recognition and support growth within this complex network by altering signaling pathways which could directly or indirectly modulate the activity of immune effector cells. Thus, recent therapeutic efforts were dedicated to immunotherapeutic applications and significant progress has been made in the areas of targeted and immunotherapies. However, durable clinical benefit has occurred only in a small subset of responding patients. It is currently hypothesized that a suppressive metabolic microenvironment also contributes to ineffective T cell function. It is assumed that tumor progression is characterized by a complex network of interactions among different cell types that cooperatively exploit metabolic reprogramming. As we start to recognize that cancer cells use different metabolism processes than normal cells, better understanding of the functional mechanisms of regulation and reprograming of the metabolic landscape in cancer cells is crucial. However, the exact role of metabolism in T cells and in the tumor microenvironment is not known. Identifying metabolic targets that mediate immunosuppression and are fundamental in sustaining tumor growth is of key importance to be able to increase efficacy of immunotherapies. In this Research Topic, we solicit high quality original research and review manuscripts that are focusing on research on metabolism and metabolic targets related to immunotherapies.
Initial neoplastic events often occur due to genomic alterations, and it is now accepted that the progression from neoplastic initiation to malignancy happens, at least in part, due to the failure of immune surveillance. Cancer cells successfully escape immune recognition and elimination, and also create an immune suppressive microenvironment. Tumors use various mechanisms to escape recognition and support growth within this complex network by altering signaling pathways which could directly or indirectly modulate the activity of immune effector cells. Thus, recent therapeutic efforts were dedicated to immunotherapeutic applications and significant progress has been made in the areas of targeted and immunotherapies. However, durable clinical benefit has occurred only in a small subset of responding patients. It is currently hypothesized that a suppressive metabolic microenvironment also contributes to ineffective T cell function. It is assumed that tumor progression is characterized by a complex network of interactions among different cell types that cooperatively exploit metabolic reprogramming. As we start to recognize that cancer cells use different metabolism processes than normal cells, better understanding of the functional mechanisms of regulation and reprograming of the metabolic landscape in cancer cells is crucial. However, the exact role of metabolism in T cells and in the tumor microenvironment is not known. Identifying metabolic targets that mediate immunosuppression and are fundamental in sustaining tumor growth is of key importance to be able to increase efficacy of immunotherapies. In this Research Topic, we solicit high quality original research and review manuscripts that are focusing on research on metabolism and metabolic targets related to immunotherapies.
