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Challagundla 3, Subash C. Jonnalagadda 4, Tulin Budak-Alpdogan 2 and Manoj K. Pandey 1, *  \nCitation: Elbezanti, W.O.; Challagundla, K.B.; Jonnalagadda, S.C.; Budak-Alpdogan, T.; Pandey, M.K. Past, Present, and a Glance into the Future of Multiple Myeloma Treatment. Pharmaceuticals 2023, 16, 415. [https://doi.org/10.3390/](https://doi.org/10.3390/)[ ](https://doi.org/10.3390/)ph16030415  \nAcademic Editor: Akinobu Ota  \nReceived: 31 December 2022  \nRevised: 28 February 2023  \nAccepted: 2 March 2023  \nPublished: 8 March 2023  \nCopyright: © 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \n1 Department of Biomedical Sciences, Cooper Medical School of Rowan University, 401S Broadway, Camden, NJ 08103, USA  \n2 Department of Hematology, MD Anderson Cancer Center at Cooper, Cooper Health System, Camden, NJ 08103, USA  \n3 Department of Biochemistry and Molecular Biology, The Fred and Pamela Buffett Cancer Center, The Child Health Research Institute, University of Nebraska Medical Center, Omaha, NE 68198, USA  \n4 Department of Chemistry and Biochemistry, Rowan University, Glassboro, NJ 08028, USA  \n* [Correspondence: pandey@rowan.edu](Correspondence: pandey@rowan.edu); Tel.: +1-856-956-2751  \nAbstract: Multiple myeloma (MM) is a challenging hematological cancer which typically grows in bone marrow. MM accounts for 10% of hematological malignancies and 1.8% of cancers. The recent treatment strategies have significantly improved progression-free survival for MM patients in the last decade; however, a relapse for most MM patients is inevitable. In this review we discuss current treatment, important pathways for proliferation, survival, immune suppression, and resistance that could be targeted for future treatments.  \nKeywords: multiple myeloma; B-cell malignancy; bone marrow microenvironment; drug resistance; proteasome inhibitors; immunotherapies  \n1. The Pathogenesis of Multiple Myeloma  \nMultiple myeloma (MM) is a mature B-cell neoplasm that is characterized by uncontrolled growth of plasma cells (PCs) in bone marrow (BM) which leads to excessive secretion of antibodies. The progression of MM is a multistep process that starts with anasymptomatic premalignant condition known as monoclonal gammopathy of undetermined significance (MGUS), in which BM produces abnormal PCs and secretes M protein instead of normal antibodies [1] . With the increase in oncogenic mutations, MGUS evolves into smoldering MM (SMM), which is characterized by a higher serum level of M protein and a higher percentage of clonal PCs. About 50% of patients with SMM show a constant increase of M protein and develop MM [2] . While both MGUS and SMM are asymptomatic, complications of accumulated proteins may start to affect the kidneys [3] . Almost 20–40% of MM patients have renal disease by the time of diagnosis [4] .  \nThe complexity of MM is attributed to the clinical and biological heterogeneity of the disease that further genetically evolves during its progression [5] . MM cells have a wide range of genetic changes including point mutations, insertions, deletions, multiploidy, and chromosomal translocations [6] . For example, trisomic MM and patients with t(11;14) are considered standard-risk patients. On the other hand, MM patients with t(4;14), t(14;16), t(14;20), p53 mutation, gain 1q, or del(17p) are considered to be high-risk [7,8] . Moreover, the bone marrow microenvironment (BMM) plays an important role in disease development, progression, and resistance [9] . All these factors enhance different signaling pathways that contribute t","cbCaihvZcMHiJUFo","https://ap.wps.com/l/cbCaihvZcMHiJUFo","pdf",3537537,27,"English","# Abstract\n# The Pathogenesis of Multiple Myeloma\n## Disease stages (MGUS to smoldering MM)\n## Clinical complications and heterogeneity\n## Genetic risk groups\n# Signaling pathways and resistance mechanisms\n## PI3K/AKT/mTOR, NF-κB, JAK2/STAT3\n## Cytokines and microenvironmental factors\n# Bone marrow microenvironment (niches)\n## Immune, vascular, and endosteal niches\n# Major signaling pathways in MM","[{\"question\":\"What is the biological basis of multiple myeloma progression?\",\"answer\":\"Multiple myeloma is characterized by uncontrolled growth of plasma cells in the bone marrow. Progression begins from an asymptomatic premalignant condition (MGUS) and evolves through smoldering multiple myeloma, eventually leading to clinically evident disease.\"},{\"question\":\"Why is relapse considered inevitable in multiple myeloma?\",\"answer\":\"Although treatment strategies have improved progression-free survival, relapse is described as inevitable for most patients. The review links relapse to complex mechanisms including resistance and pathway activation that support survival despite therapy.\"},{\"question\":\"Which major signaling pathways are discussed as targets for future treatments?\",\"answer\":\"The review highlights pathways such as PI3K/AKT/mTOR, NF-κB, and JAK2/STAT3, along with additional signaling networks influenced by cell adhesion within the bone marrow microenvironment. These pathways contribute to proliferation, survival, immune suppression, and resistance.\"}]","Past, Present, and a Glance into the Future of Multiple Myeloma Treatment | PDF",1790249516,68]