Genomics Inform.
2023 Sep;21(3):e31. 10.5808/gi.23011.
Identification of druggable genes for multiple myeloma based on genomic information
- Affiliations
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- 1Department of Clinical Pathology and Laboratory Medicine, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia
- 2Clinical Laboratory Installation, Dr. Sardjito Central General Hospital, Yogyakarta 55281, Indonesia
- 3Faculty of Pharmacy, Universitas Ahmad Dahlan, Yogyakarta 55164, Indonesia
- 4Research Centre for Pharmaceutical Ingredients and Traditional Medicine, National Research and Innovation Agency (BRIN), South Tangerang 15314, Indonesia
- 5Department of Pharmacy, University of Muhammadiyah Mataram, Mataram 83127, Indonesia
- 6Research Center for Vaccine and Drugs, National Research and Innovation Agency (BRIN), South Tangerang 15314, Indonesia
- KMID: 2547065
- DOI: http://doi.org/10.5808/gi.23011
Abstract
- Multiple myeloma (MM) is a hematological malignancy. It is widely believed that genetic factors play a significant role in the development of MM, as investigated in numerous studies. However, the application of genomic information for clinical purposes, including diagnostic and prognostic biomarkers, remains largely confined to research. In this study, we utilized genetic information from the Genomic-Driven Clinical Implementation for Multiple Myeloma database, which is dedicated to clinical trial studies on MM. This genetic information was sourced from the genome-wide association studies catalog database. We prioritized genes with the potential to cause MM based on established annotations, as well as biological risk genes for MM, as potential drug target candidates. The DrugBank database was employed to identify drug candidates targeting these genes. Our research led to the discovery of 14 MM biological risk genes and the identification of 10 drugs that target three of these genes. Notably, only one of these 10 drugs, panobinostat, has been approved for use in MM. The two most promising genes, calcium signal-modulating cyclophilin ligand (CAMLG) and histone deacetylase 2 (HDAC2), were targeted by four drugs (cyclosporine, belinostat, vorinostat, and romidepsin), all of which have clinical evidence supporting their use in the treatment of MM. Interestingly, five of the 10 drugs have been approved for other indications than MM, but they may also be effective in treating MM. Therefore, this study aimed to clarify the genomic variants involved in the pathogenesis of MM and highlight the potential benefits of these genomic variants in drug discovery.
