Multiple Myeloma is a haematological malignancy caused by malignant transformation of B-lymphocytes, the white blood cells that normally produce antibodies, into pathological clonal plasma cells that accumulate mainly in the bone marrow and in other tissues and organs, such as the kidneys. Multiple Myeloma leads to substantial morbidity and mortality, characterized by end organ damage – renal impairment, hypercalcemia, lytic bony lesions, and anemia.
Multiple Myeloma has an estimated incidence rates of 1.5 per 100,000 and ~114,000 new cases diagnosed worldwide each year. There has been a marked increase in incident cases from 1990. The overall 5-year survival rate of Multiple Myeloma patients is 50.7%.
The ubiquitin-proteasome pathway represents the major pathway for intracellular protein degradation, a tightly regulated and complex process that plays a central role in regulating cellular function and maintaining homoeostasis in every eukaryotic cell. It has become evident that defects within this pathway are associated with a number of diseases, including cancer; thus, inhibition of this pathway should prevent malignant cells from proliferation. Indeed, proteasome inhibition has emerged as an important therapeutic strategy in Multiple Myeloma, and its First-in-class agent, bortezomib, has demonstrated great positive therapeutic efficacy and has contributed substantially to the observed improvement in survival in Multiple Myeloma patients over the past decade. However, despite its high efficiency, a large proportion of patients do not achieve sufficient clinical response.
Molecular biomarkers for prediction of drug responsiveness remain major challenge in Multiple Myeloma, in order to identify the responsive population, and consider alternative treatment options to those patients who do not respond.
PTM Biosciences is applying its Post Translational Modifications (PTM) profiling platform by analyzing bone marrow aspirate of Multiple Myeloma patients and generating diagnostic biomarkers that can predict the response of Multiple Myeloma patients to proteasome inhibition and serve as the basis for the development of novel treatments.