Multiple myeloma (MM) is the second most common hematologic malignancy, characterized by neoplastic proliferation of clonal plasma cells in the bone marrow. Standard treatment of MM eligible and ineligible for autologous stem cell transplantation primarily consists of traditional corticosteroids, alkylating agents and anthracyclines, as well as novel agents like proteasome inhibitors (PIs), immunomodulatory drugs (IMiDs), histone deacetylase inhibitors, monoclonal antibodies, and other emerging immunotherapeutic approaches. Whilst introduction of these novel agents has significantly improved the survival of patients, drug resistance remains a major challenge. For example, MM patients who have become refractory to first generation PIs and IMiDs have been found to be associated with poor outcomes.
Mechanistically, drug resistance in MM can be caused by genetic abnormalities, epigenetic alterations, dysregulation of apoptosis, senescence, autophagy, and other signaling pathways, as well as changes in membrane transporters and metabolism. Moreover, cancer stem cells, the microenvironment, and clonal evolution also contribute to drug resistance in MM. Improving our understanding of these causes of resistance will enable the identification of novel drug targets and treatment strategies to counteract this problem.
The aim of this collection is to collate research which sheds light on mechanisms of drug resistance in MM, as well as on how novel drugs and combinations can be utilized to overcome resistance and improve outcomes for patients.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Multiple myeloma (MM) is the second most common hematologic malignancy, characterized by neoplastic proliferation of clonal plasma cells in the bone marrow. Standard treatment of MM eligible and ineligible for autologous stem cell transplantation primarily consists of traditional corticosteroids, alkylating agents and anthracyclines, as well as novel agents like proteasome inhibitors (PIs), immunomodulatory drugs (IMiDs), histone deacetylase inhibitors, monoclonal antibodies, and other emerging immunotherapeutic approaches. Whilst introduction of these novel agents has significantly improved the survival of patients, drug resistance remains a major challenge. For example, MM patients who have become refractory to first generation PIs and IMiDs have been found to be associated with poor outcomes.
Mechanistically, drug resistance in MM can be caused by genetic abnormalities, epigenetic alterations, dysregulation of apoptosis, senescence, autophagy, and other signaling pathways, as well as changes in membrane transporters and metabolism. Moreover, cancer stem cells, the microenvironment, and clonal evolution also contribute to drug resistance in MM. Improving our understanding of these causes of resistance will enable the identification of novel drug targets and treatment strategies to counteract this problem.
The aim of this collection is to collate research which sheds light on mechanisms of drug resistance in MM, as well as on how novel drugs and combinations can be utilized to overcome resistance and improve outcomes for patients.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
