Update on Risk Stratification Model of Smoldering Multiple Myeloma: A Systematic Review

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5512-5512
Author(s):  
Saad Ullah Malik ◽  
Ahmad Abu-Hashyeh ◽  
Muhammad Sardar ◽  
Mohammad M Alhousani ◽  
Emilia Cindy Leigh ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Plasma Cells ◽  
Cell Maturation ◽  
B Cell Maturation ◽  
Smoldering Multiple Myeloma ◽  
Pet Ct ◽  
M Proteins ◽  
Pet Ct Scan ◽  
Bence Jones Proteins

Background: Smoldering multiple myeloma (SMM) was stratified into risk classes based on several models including Mayo clinic and Spanish myeloma working group models. After the revision of diagnostic criteria for multiple myeloma (MM) in 2014, the ultra-high risk SMM patients (>80% clonal plasma cells at two years) were re-classified as active MM patients. Thus, predictors of progression in patients currently diagnosed as SMM are unknown and reassessment of existing models is required. We aim to identify the risk factors associated with progression in SMM patients classified according to updated guidelines. Methods We performed a literature search following PRISMA guidelines and used following bibliographic databases: MEDLINE (Ovid and PubMed), EMBASE, The Cochrane Library and Cochrane Central Register of Controlled Trials (CENTRAL), as well as annual meetings abstracts from inception till 1st,August 2019. We used MeSH and Emtree terms as well as performed open search for "smoldering multiple myeloma", "smoldering myeloma", and "asymptomatic multiple myeloma". Two independent reviewers screened the literature. We used snowballing technique to screen abstracts and reference within articles to include titles. Cochrane collaboration tool was used to asses risk of bias among included studies Results Our search retrieved 419 titles. After going through the titles and abstracts 38 articles were selected for full text review. Final review led to inclusion of 11 articles. Levels of serum M proteins, percentage of bone marrow plasma cells (BMPCs), serum free light chain ratio (FLCr) and PET/CT scan findings of whole body were most consistently and reliably indicated the progression of SMM to MM (Table 1). New studies are suggesting that B-cell maturation levels (BCMA), evolving M-proteins (eMP) and evolving hemoglobin levels (eHb) are also an accurate measure of SMM progression and should be incorporated in the risk stratification models. A study by Gonsalves WI et al. also suggested that levels of circulating clonal plasma cells with a cutoff of 150 was an important prognostic marker in their study. Immunoparesis status and role of Bence Jones proteins in reliably predicting the progression of SMM was debatable because they were significant in univariate analysis but were not significant in multivariate analysis (Table 1). Conclusion Serum M protein levels (2 g/dL), percentage of BMPCs (20%), serum FLCr (20) and PET/CT scan were reliable in predicting the prognosis of smoldering MM. New techniques like B-cell maturation levels(74.4 ng/mL), evolving M-proteins and evolving hemoglobin levels can play a significant role in proposing future risk predictive models of SMM. Role of immunoparesis and Bence Jones proteins is debatable. Table 1 Disclosures Anwer: Seattle Genetics: Membership on an entity's Board of Directors or advisory committees; In-Cyte: Speakers Bureau.

Initial Presentation Of Multiple Myeloma As Intraparenchymal Brain Mass

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5402-5402
Author(s):  
Ishan Malhotra ◽  
Abhinav B. Chandra ◽  
Yiwu Huang
Keyword(s):  
Central Nervous System ◽  
Multiple Myeloma ◽  
Nervous System ◽  
Ct Scan ◽  
Plasma Cells ◽  
Light Chains ◽  
Left Lateral Ventricle ◽  
Pet Ct ◽  
M Spike ◽  
Pet Ct Scan

Abstract Case presentation 38 year old African female presented with complaints of severe headache which had started couple of weeks prior to presentation and was progressively becoming worse. Patient underwent a CT scan of the head which revealed a 3.2 X 3.3 X 3.7 cm lobulated hyperdense periventricular mass in the left temporoparietal area with surrounding vasogenic edema with mass effect on the adjacent left lateral ventricle and 0.6 cm midline shift to the right with uncal herniation and effacement of left cerebral peduncle with dilatation of left temporal horn. MRI of the brain revealed a 3.1 X 2.6 X 3.6 cm lobulated mass in left lateral ventricle trigone. Radiologically, differential diagnoses included intraventricular meningioma, lymphoma, choroid plexus papilloma or metastasis. Patient underwent left craniotomy for tumor resection. Patient had an uneventful post-operative recovery and the resected tumor was high grade malignant neoplasm with plasmablastic features and immunohistochemical stains revealed that the tumor cells were positive for CD138, CD30, MUM-1, Bcl-2, vimentin and lambda light chains and were negative for kappa light chains, CD3, CD20, PAX-5, CD79a, GFAP, cytokeratin, AE1/AE3, synaptophysin, chromogranin, EMA, S-100, Melan-A, CD45, CD56 and EBV(EBER-ISH). Ki-67 was about 80%. Serum protein electrophoresis (SPEP) was sent that showed an M-spike of 3.3 g/dl that was IgG lambda. A bone marrow biopsy showed 100 % infiltration with plasma cells. Patient underwent a CT chest/abdomen/pelvis and a PET/CT scan which revealed multiple scattered subcutaneous masses throughout the body and an asymptomatic mass near spinal cord at C1. Patient was treated with VTD-PACE regimen (bortezomib, thalidomide, decadron, cisplatin, liposomal doxorubicin, cyclophosphamide, and etoposide). She received two cycles of VTD-PACE chemotherapy regimen with excellent response to the treatment. Her M-spike protein which prior to treatment was 3.3 g/dl disappeared after second cycle of chemotherapy and her subcutaneous lesion also dramatically improved on repeat PET/CT scan. The C1 dural lesion also had significant improvement after the chemotherapy. Her IgG also decreased from 5070 mg/dl to 791 mg/dl. She was referred for autologus stem cell transplant. She was subsequently started on weekly cyclophosphamide, bortezomib and decadron. Discussion Malignancies of plasma cells comprise 1% of malignant neoplasms which includes multiple myeloma, solitary plasmacytomas (including solitary bone plasmacytoma and extramedullary plasmacytomas) and immunoglobulin deposition syndromes. Central nervous system (CNS) involvement of multiple myeloma itself is not a common entity. Fassas et al. published data of 18 cases over a course of 10 years. Gozzetti et al. published their data of 50 patients in 2012. Of these 50 patients, 76% had osteo-dural or primary dural multiple myeloma (OD-DMM) and 24% had central nervous system myelomatosis. They found that patients treated with novel agents had better outcome than patients treated with conventional drugs. Cases with initial presentation of intracranial plasmacytomas are even rarer. Patients with CNS myeloma have poor prognosis with median survival being around 4- 5 months. Our patient had excellent response with two cycles of VTD-PACE regimen with negative M-spike, normalization of IgG and decrease in size of subcutaneous nodules and C1 spinal lesion. She has survived for 5 months without autologus transplant and is currently on weekly cyclophosphamide, bortezomib and decadron. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Immunotherapeutic strategies targeting B cell maturation antigen in multiple myeloma

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Yi Fang ◽  
Jian Hou
Keyword(s):  
Multiple Myeloma ◽  
B Cell ◽  
Plasma Cells ◽  
Residual Disease ◽  
Hematologic Malignancy ◽  
Therapeutic Strategies ◽  
Cell Maturation ◽  
B Cell Maturation ◽  
Clone Evolution ◽  
B Cell Maturation Antigen

AbstractMultiple myeloma (MM) is the second most common hematologic malignancy, and is characterized by the clonal expansion of malignant plasma cells. Despite the recent improvement in patient outcome due to the use of novel therapeutic agents and stem cell transplantation, all patients eventually relapse due to clone evolution. B cell maturation antigen (BCMA) is highly expressed in and specific for MM cells, and has been implicated in the pathogenesis as well as treatment development for MM. In this review, we will summarize representative anti-BCMA immune therapeutic strategies, including BCMA-targeted vaccines, anti-BCMA antibodies and BCMA-targeted CAR cells. Combination of different immunotherapeutic strategies of targeting BCMA, multi-target immune therapeutic strategies, and adding immune modulatory agents to normalize anti-MM immune system in minimal residual disease (MRD) negative patients, will also be discussed.

scholarly journals B-Cell Maturation Antigen (BCMA) As a Target for New Drug Development in Relapsed and/or Refractory Multiple Myeloma

2020 ◽  
Author(s):  
Hanley N. Abramson
Keyword(s):  
Multiple Myeloma ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
B Cell ◽  
Plasma Cells ◽  
Cell Types ◽  
Cell Maturation ◽  
New Drug ◽  
B Cell Maturation ◽  
B Cell Maturation Antigen

During the past two decades there has been a major shift in the choice of agents to treat multiple myeloma, whether newly diagnosed or in the relapsed/refractory stage. The introduction of new drug classes, such as proteasome inhibitors, immunomodulators, and anti-CD38 and anti-SLAMF7 monoclonal antibodies, coupled with autologous stem cell transplantation, have approximately doubled the disease’s five-year survival rate. However, this positive news is tempered by the realization that these measures are not curative and patients eventually relapse and/or become resistant to the drug’s effects. Thus, there is a need to discover newer myeloma-driving molecular markers and develop innovative drugs designed to precisely regulate the actions of such putative targets. B cell maturation antigen (BCMA), which is found almost exclusively on the surfaces of malignant plasma cells to the exclusion of other cell types, including their normal counterparts, has emerged as a specific target of interest in this regard. Immunotherapeutic agents have been at the forefront of research designed to block BCMA activity. These agents encompass monoclonal antibodies, such as the drug conjugate belantamab mafodotin; bispecific T-cell engager strategies exemplified by AMG 420; and chimeric antigen receptor (CAR) T-cell therapeutics that include idecabtagene vicleucel (bb2121) and JNJ-68284528.

Belantamab mafodotin in the treatment of relapsed or refractory multiple myeloma

2020 ◽  
Vol 16 (34) ◽  
pp. 2783-2798 ◽  
Author(s):  
Semira Sheikh ◽  
Eyal Lebel ◽  
Suzanne Trudel
Keyword(s):  
Multiple Myeloma ◽  
B Cell ◽  
Plasma Cells ◽  
Safety Data ◽  
Unmet Need ◽  
Cell Maturation ◽  
Antibody Drug Conjugate ◽  
Refractory Multiple Myeloma ◽  
B Cell Maturation ◽  
B Cell Maturation Antigen

Multiple myeloma remains an incurable disease, with a large proportion of patients in the relapsed/refractory setting often unable to achieve durable responses. Novel, well-tolerated and highly effective therapies in this patient population represent an unmet need. Preclinical studies have shown that B-cell maturation antigen is nearly exclusively expressed on normal and malignant plasma cells, thereby identifying it as a highly selective target for immunotherapeutic approaches. Belantamab mafodotin (GSK2857916, belamaf) is a first-in-class antibody–drug conjugate directed at B-cell maturation antigen and has shown promising activity in clinical trials. In this review, we provide an overview of belantamab mafodotin as a compound and present the available clinical efficacy and safety data in the treatment of relapsed/refractory multiple myeloma.

scholarly journals Expression of Myeloma Cell and Soluble B-Cell Maturation Antigen (BCMA) in Relapsed and Refractory Multiple Myeloma Patients Treated with GSK2857916 in BMA117159

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 1977-1977 ◽  
Author(s):  
E.J. Dettman ◽  
Fabio Rigat ◽  
Josh Albert ◽  
Ruth Barnard ◽  
Mary Birchler ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Plasma Cells ◽  
Cell Maturation ◽  
Employment Equity ◽  
B Cell Maturation ◽  
Post Infusion ◽  
Equity Ownership ◽  
Expansion Cohort ◽  
B Cell Maturation Antigen

Abstract Introduction: B-cell maturation antigen (BCMA) is a cell surface receptor that is widely expressed on multiple myeloma (MM) cells. GSK2857916 is a humanized Fc enhanced IgG1 anti-BCMA antibody conjugated to the microtubule inhibitor monomethyl auristatin-F (MMAF). Safety and clinical efficacy of a Q3W GSK2857916 dosing schedule were assessed in relapsed/refractory MM subjects in the first time in human trial BMA117159. In the dose escalation phase, 38 subjects were treated with doses from 0.03 mg/kg up to 4.60 mg/kg, followed by an expansion cohort of 35 subjects at a dose of 3.40 mg/kg where an overall response rate (ORR) of 60% (21/35; 95% CI 42.1-76.1) by IMWG criteria was demonstrated (Trudel, et al. Blood 2017). Several novel biomarkers were followed during the BMA117159 study, including: the level of BCMA expression on MM cells and circulating soluble BCMA (sBCMA). Methods: The expression of BCMA on MM cells was measured in subjects enrolled in BMA117159 at baseline in formalin-fixed paraffin-embedded bone marrow aspirate samples using a BCMA Immunohistochemistry (IHC) assay and a dual color IHC assay with BCMA and CD138 (plasma cell marker). The antibody to detect BCMA (J6M0) uses the same CDR regions as GSK2857916. BCMA staining was quantified as a percentage positive of all cells, percentage of plasma cells as determined by morphology, or in CD138+ cells (for the dual color IHC assay). Soluble BCMA was measured in serum samples collected at pre- and post-infusion at cycle 1 using immunoassays to determine the levels of free and GSK2857916-bound sBCMA. All measurements were performed at central laboratories. Results: Among the subjects enrolled in BMA117159, the baseline BCMA expression was found specifically in plasma cells using BCMA IHC, with a median of 100% plasma cells expressing BCMA across all subjects, compared to a median of 5% of all bone marrow cells expressing BCMA. In the dose expansion cohort, no differences by response group were noted in BCMA staining with both responders (PR or better) and non-responders having 100% BCMA positivity in plasma cells. Comparable results were observed using a dual staining IHC assay for BCMA and CD138, where 95% of CD138+ cells expressed BCMA in non-responders compared with 88% in responders. Examination of circulating sBCMA in BMA117159 subjects revealed high sBCMA levels, with a baseline median concentration of free sBCMA of 58 ng/mL across all doses (n = 68; range 4 ng/mL to >1000 ng/mL). Among patients enrolled in the expansion phase, the median baseline sBCMA concentrations were higher in non-responders compared to responders (81 ng/mL, n = 12; compared to 43 ng/mL, n = 19). However, high baseline sBCMA levels were also found in responders with levels up to 262 ng/mL. To examine whether sBCMA may act as a surrogate for BCMA expression in tumor cells, the relationship between these measures was examined; however, no strong associations were observed between baseline sBCMA and BCMA IHC staining (Spearman rho = 0.27). The binding of GSK2857916 to sBCMA can be measured by comparing the post-infusion levels of free sBCMA measured 60 minutes after the start of infusion to those found at pre-infusion. It was found that the reduction in free sBCMA appeared to be related to the dose level administered, and doses above 1.92 mg/kg consistently achieved a greater than 90% reduction of free sBMCA. Conclusions: These preliminary data indicate that tumor cells from MM patients participating in BMA117159 consistently expressed the BCMA receptor at baseline, and the levels of expression did not appear to be associated with response to treatment. At higher dose levels, it was found that GSK2857916 bound a large fraction of sBCMA, and responses to GSK2857916 were observed in 60% of dose expansion subjects with either low or high baseline sBCMA. However, at present, the sample sizes are limited, and further investigations in future studies are necessary to understand the value of these biomarkers for treatment decisions. Study is funded by GlaxoSmithKline (NCT02064387); drug linker technology is licensed from Seattle Genetics; monoclonal antibody is produced using POTELLIGENT® Technology licensed from BioWa. Disclosures Dettman: GlaxoSmithKline: Employment, Equity Ownership. Rigat:GlaxoSmithKline: Employment, Equity Ownership. Albert:GlaxoSmithKline: Employment, Equity Ownership. Barnard:GlaxoSmithKline: Employment, Equity Ownership. Birchler:GlaxoSmithKline: Employment, Equity Ownership. Deghenhardt:GlaxoSmithKline: Employment, Equity Ownership. DeWall:GlaxoSmithKline: Employment, Equity Ownership. Gaye:GlaxoSmithKline: Employment, Equity Ownership. He:GlaxoSmithKline: Employment, Equity Ownership. Liu:GlaxoSmithKline: Employment, Equity Ownership. Opalinska:GlaxoSmithKline: Employment, Equity Ownership.

PET-CT Has Major Diagnostic Value in the Evaluation of Smoldering Multiple Myeloma

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3382-3382 ◽  
Author(s):  
Brittany L. Dykstra ◽  
Shaji Kumar ◽  
Angela Dispenzieri ◽  
Martha Q. Lacy ◽  
Francis Buadi ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Ct Scan ◽  
Conflicts Of Interest ◽  
Significant Risk ◽  
Smoldering Multiple Myeloma ◽  
Increased Risk ◽  
Pet Ct ◽  
Rate Of Progression ◽  
Risk Of Progression ◽  
Pet Ct Scan

Abstract Background: The goal of this study was to determine the predictive value of (18) F-fluorodeoxyglucose positron emission tomography-computed tomography (PET-CT) in patients with suspected smoldering multiple myeloma (SMM), specifically to determine if a positive PET-CT was associated with a significant risk of progression to multiple myeloma (MM) within 2 years. Methods: We identified all patients with a diagnosis of SMM from January 2000 to March 2014 who had undergone a PET-CT scan as part of their clinical evaluation utilizing the Mayo Clinic Data Discovery and Query Database and a review of available medical records. The PET-CT findings, results of other diagnostic tests, and clinical course were then abstracted. A positive PET-CT was defined as radiologist interpretation of increased uptake in one or more focal areas. The primary endpoint was progression to active MM within the first 2 years following a positive PET-CT result among patients who were observed without therapy. Secondary endpoints included the proportion of patients in whom the diagnosis of active MM was made solely based on the findings of the PET-CT, the probability of progression within 2 years in patients with a negative PET-CT who were observed, and estimating differences in probability of progression based on presence or absence of underlying osteolysis in patients with a positive PET-CT. Results: 198 patients (100 male and 98 female) were identified with a suspected diagnosis of SMM in whom a PET-CT scan had been performed as part of the diagnostic evaluation. The median age was 69, range 35-92. The PET-CT was positive (defined as one or more focal lesions with increased uptake) in 82 patients, and negative in 116 patients. Of the 82 patients with a positive PET-CT, 49 were diagnosed and treated as MM, while 33 were considered to still have SMM and observed. Of the 49 patients diagnosed as MM, 12 (24%) were upstaged to the diagnosis of active disease solely based on the findings of the PET-CT; in the remaining 37 patients other MM defining events were also identified on other laboratory tests conducted during the same visit. Similarly, of the 116 patients with a negative PET-CT, 17 (15%) were diagnosed and treated as MM based on other laboratory parameters, while 99 were considered to have SMM and observed. Thus, 33 patients with a positive PET-CT and 99 patients with a negative PET-CT were observed without therapy; the rate of progression to MM within 2 years was then compared between these 2 groups. Nineteen of 33 patients (56%) with a positive PET-CT and observed as SMM progressed to active myeloma within 2 years; in contrast 27 of 99 patients (28%) with a negative PET-CT observed as SMM progressed within 2 years, P=0.0034. We then restricted the analysis to patients in whom the PET-CT was done within 90 days of diagnosis of SMM. The rate of progression within 2 years in this subset was 74% (14 of 19 patients) among those with a positive PET-CT versus 27% (12 of 44 patients) with a negative PET-CT, p=0.0015 (see Figure). Among these patients, the relative risk of progression with a positive PET-CT was 2.7 (95% CI 1.6-4.7). The median time to progression with positive PET-CT was 16 months versus 55 months with negative PET-CT, P=0.0001. Among the 19 patients with a positive PET-CT observed as SMM, the rate of progression was 77% (10 of 13 patients) among those with evidence of underlying osteolysis, and 66% (4 of 6 patients) among those without evidence of osteolysis. Conclusions: Patients with a positive PET-CT scan and underlying osteolysis when observed without therapy have a high risk (77%) of progression to MM within 2 years. This is probably an underestimate of the true risk since it excludes patients with presumably higher grade lesions on PET-CT were initiated on therapy based solely on the PET-CT finding (n=12 in this cohort). Our findings validate the recent IMWG recommendation that patients with a positive PET-CT and underlying osteolysis should be considered as active myeloma. Patients with a positive PET-CT and no underlying osteolysis are also at increased risk of progression, 66% within 2 years. Figure 1 Figure 1. Figure 2 Figure 2. Disclosures No relevant conflicts of interest to declare.

scholarly journals B-Cell Maturation Antigen (BCMA) as a Target for New Drug Development in Relapsed and/or Refractory Multiple Myeloma

2020 ◽  
Vol 21 (15) ◽  
pp. 5192 ◽  
Author(s):  
Hanley N. Abramson
Keyword(s):  
Multiple Myeloma ◽  
Monoclonal Antibodies ◽  
T Cell ◽  
B Cell ◽  
Plasma Cells ◽  
Cell Types ◽  
Cell Maturation ◽  
New Drug ◽  
B Cell Maturation ◽  
B Cell Maturation Antigen

During the past two decades there has been a major shift in the choice of agents to treat multiple myeloma, whether newly diagnosed or in the relapsed/refractory stage. The introduction of new drug classes, such as proteasome inhibitors, immunomodulators, and anti-CD38 and anti-SLAMF7 monoclonal antibodies, coupled with autologous stem cell transplantation, has approximately doubled the disease’s five-year survival rate. However, this positive news is tempered by the realization that these measures are not curative and patients eventually relapse and/or become resistant to the drug’s effects. Thus, there is a need to discover newer myeloma-driving molecular markers and develop innovative drugs designed to precisely regulate the actions of such putative targets. B cell maturation antigen (BCMA), which is found almost exclusively on the surfaces of malignant plasma cells to the exclusion of other cell types, including their normal counterparts, has emerged as a specific target of interest in this regard. Immunotherapeutic agents have been at the forefront of research designed to block BCMA activity. These agents encompass monoclonal antibodies, such as the drug conjugate belantamab mafodotin; bispecific T-cell engager strategies exemplified by AMG 420; and chimeric antigen receptor (CAR) T-cell therapeutics that include idecabtagene vicleucel (bb2121) and JNJ-68284528.

scholarly journals Chimeric antigen receptor T-cell therapies for multiple myeloma

Blood ◽  
2017 ◽  
Vol 130 (24) ◽  
pp. 2594-2602 ◽  
Author(s):  
Lekha Mikkilineni ◽  
James N. Kochenderfer
Keyword(s):  
Multiple Myeloma ◽  
T Cells ◽  
T Cell ◽  
B Cell ◽  
Plasma Cells ◽  
Cell Maturation ◽  
Cell Therapies ◽  
B Cell Maturation ◽  
Car T ◽  
B Cell Maturation Antigen

Abstract Multiple myeloma (MM) is a nearly always incurable malignancy of plasma cells, so new approaches to treatment are needed. T-cell therapies are a promising approach for treating MM, with a mechanism of action different than those of standard MM treatments. Chimeric antigen receptors (CARs) are fusion proteins incorporating antigen-recognition domains and T-cell signaling domains. T cells genetically engineered to express CARs can specifically recognize antigens. Success of CAR-T cells (CAR-Ts) against leukemia and lymphoma has encouraged development of CAR-T therapies for MM. Target antigens for CARs must be expressed on malignant cells, but expression on normal cells must be absent or limited. B-cell maturation antigen is expressed by normal and malignant plasma cells. CAR-Ts targeting B-cell maturation antigen have demonstrated significant antimyeloma activity in early clinical trials. Toxicities in these trials, including cytokine release syndrome, have been similar to toxicities observed in CAR-T trials for leukemia. Targeting postulated CD19+ myeloma stem cells with anti-CD19 CAR-Ts is a novel approach to MM therapy. MM antigens including CD138, CD38, signaling lymphocyte–activating molecule 7, and κ light chain are under investigation as CAR targets. MM is genetically and phenotypically heterogeneous, so targeting of >1 antigen might often be required for effective treatment of MM with CAR-Ts. Integration of CAR-Ts with other myeloma therapies is an important area of future research. CAR-T therapies for MM are at an early stage of development but have great promise to improve MM treatment.

The Role of B-Cell Maturation Antigen in the Biology and Management of, and as a Potential Therapeutic Target in, Multiple Myeloma

2017 ◽  
Vol 13 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Eric Sanchez ◽  
Emily J. Smith ◽  
Moryel A. Yashar ◽  
Saurabh Patil ◽  
Mingjie Li ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
B Cell ◽  
Therapeutic Target ◽  
Cell Maturation ◽  
Potential Therapeutic Target ◽  
B Cell Maturation ◽  
B Cell Maturation Antigen

scholarly journals The Role of 18F-FDG-PET/CT Scan in the Management of Multiple Myeloma

2020 ◽  
Vol 5 (2) ◽  
pp. 119-123
Author(s):  
Shirin Haghighat
Keyword(s):  
Multiple Myeloma ◽  
Ct Scan ◽  
Fdg Pet ◽  
Bone Involvement ◽  
Whole Body ◽  
Newly Diagnosed ◽  
Pet Ct ◽  
Fdg Pet Ct ◽  
Pet Ct Scan

Bone lesion is a myeloma-defining event which is reported in 80% of multiple myeloma patients. Imaging of bone is essential in the evaluation of pattern and extent of bone involvement. Recently, whole body X ray (WBXR) has been replaced by more accurate imaging such as whole bode MRI and FDG-PET/CT scan. This review article provides the advantages and role of PET/CT scan in the diagnosis and management of multiple myeloma patients. Generally, PET/CT in diagnosis of bone involvement of newly diagnosed myeloma patients is more sensitive than WBXR. The prognostic value of PET/CT in newly diagnosed patients has been described as well. Different studies have demonstrated that several PET parameters such as the number of focal lesions (FL), SUVmax and extramedullary disease(EMD) may affect the outcome of multiple myeloma patients. Interstingely, the main role of PET/CT in myeloma patients is treatment response monitoring and to some extent assessment of MRD. PET/CT appears to be superior than MRI in evaluation of response due to its ability in differentiating active lesion from negative one.

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