Cell adhesion molecule (CAM) is a diverse protein family with vital functions in fundamental cell biological processes including, but not limited to, cell structural scaffold, cell behaviors (binding, migration, and invasion), and cell signaling crosstalk between cells and their microenvironment. There are 4 major groups of CAMs: integrins, immunoglobulin superfamily cell adhesion molecules, cadherins, and selectins. It has long been recognized that some CAMs are aberrantly expressed in multiple myeloma (MM), a plasma cell cancer that is still incurable. Many of those CAMs are considered as biomarkers for MM diagnosis and patient stratification. Growing evidence illustrates the functions of specific CAM members in myelomagenesis, MM bone marrow niche integration, MM immune-microenvironment regulation, and treatment responses. As our knowledge of CAMs grows, CAM-targeted therapies in MM have been developed and examined preclinically and clinically with the entry of some into standard practice already. Rapid and efficient translation into effective therapies from bench to bedside and the potential for synergism with evolving knowledge in immune-oncology calls our attention to cell adhesion molecules in multiple myeloma.
This Research Topic aims to summarize our knowledge of CAMs and how CAMs influence the immune microenvironment in MM. We will obtain perspectives from physicians, pathologists, bioinformatics specialists, and basic researchers for comprehensive discussions of the topic. Of note, the clinical success of monoclonal antibodies against CD38, an adhesion molecule, endorses the strategy of targeting key CAMs for MM treatment. CAMs that are expressed on MM cells such as SDC1(CD138) or aberrantly expressed such as NCAM1(CD56), have been selected for the development of chimeric antigen receptor (CAR) gene-modified T cell therapy (CAR-T). In addition, emerging findings from basic research in the past decades reveal the roles of CAMs in MM pathogenesis (e.g., CXCR4), chemo-resistance (e.g., ICAM1), and relapse after treatment (e.g. ALCAM). In this Research Topic, key findings of MM CAMs will be reviewed, milestone advances will be outlined, and frontiers of the field will be discussed.
We welcome any types of manuscripts, including Original Research, Review articles, Clinical Trials, and Case Reports of adhesion molecules’ study in multiple myeloma focusing on, but not limited to, the following themes:
- The role of adhesion molecules in myelomagenesis
- The role of adhesion molecules in myeloma bone marrow homing and extramedullary metastasis
- The role of adhesion molecules in myeloma drug-resistance
- The role of adhesion molecules in myeloma tumor microenvironment, in particular, myeloma immune-microenvironment
- Adhesion molecules targeted therapy in multiple myeloma
- The role of adhesion molecules in myeloma associated bone disease or other myeloma associated complications
Topic editor F.J. Reu owns Bristol Myers Squibb stock from previous employment and declares this as potential competing interest with regards to the Research Topic Subject.
Cell adhesion molecule (CAM) is a diverse protein family with vital functions in fundamental cell biological processes including, but not limited to, cell structural scaffold, cell behaviors (binding, migration, and invasion), and cell signaling crosstalk between cells and their microenvironment. There are 4 major groups of CAMs: integrins, immunoglobulin superfamily cell adhesion molecules, cadherins, and selectins. It has long been recognized that some CAMs are aberrantly expressed in multiple myeloma (MM), a plasma cell cancer that is still incurable. Many of those CAMs are considered as biomarkers for MM diagnosis and patient stratification. Growing evidence illustrates the functions of specific CAM members in myelomagenesis, MM bone marrow niche integration, MM immune-microenvironment regulation, and treatment responses. As our knowledge of CAMs grows, CAM-targeted therapies in MM have been developed and examined preclinically and clinically with the entry of some into standard practice already. Rapid and efficient translation into effective therapies from bench to bedside and the potential for synergism with evolving knowledge in immune-oncology calls our attention to cell adhesion molecules in multiple myeloma.
This Research Topic aims to summarize our knowledge of CAMs and how CAMs influence the immune microenvironment in MM. We will obtain perspectives from physicians, pathologists, bioinformatics specialists, and basic researchers for comprehensive discussions of the topic. Of note, the clinical success of monoclonal antibodies against CD38, an adhesion molecule, endorses the strategy of targeting key CAMs for MM treatment. CAMs that are expressed on MM cells such as SDC1(CD138) or aberrantly expressed such as NCAM1(CD56), have been selected for the development of chimeric antigen receptor (CAR) gene-modified T cell therapy (CAR-T). In addition, emerging findings from basic research in the past decades reveal the roles of CAMs in MM pathogenesis (e.g., CXCR4), chemo-resistance (e.g., ICAM1), and relapse after treatment (e.g. ALCAM). In this Research Topic, key findings of MM CAMs will be reviewed, milestone advances will be outlined, and frontiers of the field will be discussed.
We welcome any types of manuscripts, including Original Research, Review articles, Clinical Trials, and Case Reports of adhesion molecules’ study in multiple myeloma focusing on, but not limited to, the following themes:
- The role of adhesion molecules in myelomagenesis
- The role of adhesion molecules in myeloma bone marrow homing and extramedullary metastasis
- The role of adhesion molecules in myeloma drug-resistance
- The role of adhesion molecules in myeloma tumor microenvironment, in particular, myeloma immune-microenvironment
- Adhesion molecules targeted therapy in multiple myeloma
- The role of adhesion molecules in myeloma associated bone disease or other myeloma associated complications
Topic editor F.J. Reu owns Bristol Myers Squibb stock from previous employment and declares this as potential competing interest with regards to the Research Topic Subject.