Metabolic Effects of Recurrent Genetic Aberrations in Multiple Myeloma.
Timon A BloedjesGuus de WildeJeroen E J GuikemaPublished in: Cancers (2021)
Oncogene activation and malignant transformation exerts energetic, biosynthetic and redox demands on cancer cells due to increased proliferation, cell growth and tumor microenvironment adaptation. As such, altered metabolism is a hallmark of cancer, which is characterized by the reprogramming of multiple metabolic pathways. Multiple myeloma (MM) is a genetically heterogeneous disease that arises from terminally differentiated B cells. MM is characterized by reciprocal chromosomal translocations that often involve the immunoglobulin loci and a restricted set of partner loci, and complex chromosomal rearrangements that are associated with disease progression. Recurrent chromosomal aberrations in MM result in the aberrant expression of MYC, cyclin D1, FGFR3/MMSET and MAF/MAFB. In recent years, the intricate mechanisms that drive cancer cell metabolism and the many metabolic functions of the aforementioned MM-associated oncogenes have been investigated. Here, we discuss the metabolic consequences of recurrent chromosomal translocations in MM and provide a framework for the identification of metabolic changes that characterize MM cells.
Keyphrases
- copy number
- multiple myeloma
- genome wide
- cell cycle arrest
- induced apoptosis
- gene expression
- dna methylation
- cell death
- squamous cell carcinoma
- transcription factor
- human immunodeficiency virus
- oxidative stress
- cell proliferation
- hepatitis c virus
- young adults
- hiv infected
- squamous cell
- endoplasmic reticulum stress
- single molecule
- childhood cancer
- men who have sex with men
- antiretroviral therapy