New diagnostic strategy for multiple myeloma: A review

Abstract

Multiple myeloma (MM) is the second most prevalent hematological malignancy and is distinguished by the aberrant proliferation of monoclonal plasma cells inside the bone marrow and production of M-protein. This condition frequently results in bone deterioration, acute kidney damage, anemia, and hypercalcemia. However, the clinical manifestations and accompanying symptoms of MM vary and may change as the condition evolves. Therefore, diagnosis of MM is difficult. At present, the confirmation of MM diagnosis necessitates the use of bone marrow biopsy, a procedure that is both invasive and challenging for assessing dynamic alterations in the disease. The integration of laboratory testing technologies with imaging technology has the potential to enhance the diagnostic effectiveness and provide a thorough evaluation of disease progression and prognosis in patients with MM. All the examination methods have advantages and disadvantages. Therefore, diagnosis is determined by the application of clinical characteristics, serological tests, and imaging investigations.

Role of Non-Coding RNAs in Diagnosis, Prediction and Prognosis of Multiple Myeloma

“…In addition, this test allows the performing of immunophenotyping and cytogenetics. The use of imaging methods makes it possible to detect lytic bone lesions, determine the size of the neoplastic infiltration or adequately perform differentiation and staging [ 14 ]. The following criteria must be met to make a final diagnosis of MM: the presence of at least 10% clonal plasma cells on bone marrow examination or biopsy-confirmed plasmocytoma and the presence of at least one myeloma-defining event (MDE).…”

“…Moreover, 45% of patients have trisomies involving chromosomes 3, 5, 7, 9, 11, 15, 19 and/or 21. The following secondary genetic changes are observed: monosomy of chromosomes 13, 14, 17 (15-50% of patients with MM), translocations involving the MYC gene: t (8,14); t (8,11)-in 15% of patients and in 10-40% of them-deletions including the genes: CDKN2C and FAM46C (1p), CD27 (12p), RB1 and DIS3 (13p), TRAF3 (14p), TP53 (17p). Moreover, in some patients (6-25%) mutations of the BRAF, KRAS and NRAS genes are observed, the products of which are involved in the MAPK signaling pathway, thus stimulating cell proliferation and survival [5].…”