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Dysregulated metabolism is a long-described phenomenon of all cancers. In particular, the “Warburg Effect” is the preferred use of anaerobic glycolysis for nutrient production and proliferation in all tumor cells. Metabolic changes have been studied in multiple myeloma (MM) and it was shown that MM cells depend on glucose and glutamine metabolism. Higher levels of certain metabolites were also found in myeloma patients but were lost when patients achieved remission. Alterations in bone marrow (BM) metabolism was found to be an early feature of both monoclonal gammopathy of undetermined significance (MGUS) and MM. Furthermore, targeting glutamine metabolism was found to sensitize cells to Bcl-2 inhibition with venetoclax, and both Lactate Dehydrogenase A (LDHA) and Hypoxia-inducible factor 1-alpha (HIF1α) were found to be targets for drug resistance (eg. bortezomib) under hypoxic conditions in the BM.
Therefore, there is a strong rationale for further analysis of metabolomics in MM. In a study published in PLOS One, Normann Steiner from the Medical University of Innesbruck, and colleagues, examined the metabolomic profile of MGUS patients (pts), newly diagnosed MM pts, and relapsed and refractory (RR) MM pts, and found marked differences between these subsets and healthy controls.
Differences in the metabolomic profile were identified between MGUS and MM patients compared to healthy controls. The different metabolites identified highlight proteins that could be targeted in myeloma and include the IDO1 enzyme and proteins involved in the glutaminolysis pathway (such as glutamine synthase [GS], cellular glutamine transporter [GLUTs], or oncogenes that regulate this pathway), as well as several others, although further investigations are required to fully establish the link between these metabolites and disease progression. With improved methodologies to identify smaller differences, metabolic profiling may also impact diagnostics and help monitor disease progression.
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