Being able to monitor the levels of malignant progenitor cells in Multiple Myeloma, as opposed to the plasma cell burden or clinical symptoms alone, will be an important move forward in the management of this disease. The expression of cancer testis antigen MAGE C1 has been previously linked to the malignant stem cell at all stages of this disease, while BAGE2 expression has been clearly associated with the progression to a more advanced disease stage and thus clonal evolution. We investigated the use of a multiplex QRTPCR approach to monitor the co-expression of these transcripts in the peripheral blood as an alternative monitoring methodology. We compared the levels of MAGEC1 and BAGE2 mRNA in the PBMC population to serum M protein and serum beta 2 microglobulin levels at 3-monthly intervals over a 2-year period for 12 patients on chemotherapy regimens. The analysis indicated that the novel QRTPCR analysis of MAGE C1 expression in the less invasive peripheral blood sample type was extremely relevant as a potential minimal residual disease-monitoring tool. Expression of this cancer testis antigen was detectable in all patients throughout treatment, with comparable increases and decreases to serum M protein and/or serum beta 2 microglobulin, but with the advantage of being able to detect disease at a lower level and potentially signal relapse prior to a full clinical relapse. Expression of BAGE2 was only observed in a few patients, but its expression was clearly associated with a worsening clinical profile. As with MAGEC1, the detection of this transcript occurred at least 3 months prior to clinical changes in some patients, indicating its potential use in early medical intervention.

Citation Format: Karen Shires, Kirsty Wienand. MAGEC1 and BAGE2 mRNA expression can be used to monitor chemotherapy treatment responses in multiple myeloma patients and pre-empt clinical relapse [abstract]. In: Proceedings of the AACR International Conference: New Frontiers in Cancer Research; 2017 Jan 18-22; Cape Town, South Africa. Philadelphia (PA): AACR; Cancer Res 2017;77(22 Suppl):Abstract nr B18.