Neoplastic Proliferation Of Plasma Cells Research Articles

Clinical use of proteasome inhibitors in the treatment of multiple myeloma.

Multiple myeloma (MM) is an incurable hematological malignancy characterized by the clonal proliferation of neoplastic plasma cells. The use of proteasome inhibitors in the treatment of MM has led to significant improvements in outcomes. This article reviews data on the use of the two approved proteasome inhibitors (bortezomib and carlfilzomib), as well as newer agents under development. Emphasis is placed on the clinical use of proteasome inhibitors, including management of side effects and combination with other agents.

A Comparison of Outcomes in the First-Line Treatment of Multiple Myeloma Presenting with Single Versus Multiple Monoclonal Paraproteins

Background: Multiple myeloma (MM) is characterized by the neoplastic proliferation of plasma cells that most often produce a single monoclonal immunoglobulin (M-protein). In approximately 2% of cases however, two or more distinct M-proteins of different immunoglobulin isotype are noted at diagnosis. The International Myeloma Working Group (IMWG) does not provide specific guidelines for determination of treatment response for MM with multiple M-proteins (MMP) and evidence comparing response and treatment outcomes of patients (pts) with MMP to those with a single M-protein (SMP) is lacking. The current tacit convention for assessing treatment response is to sum all M-proteins to get an aggregate M-protein value to compare to subsequent aggregate M-proteins over time. This approach has not been formally validated; it is unknown whether pts with MMP have a different natural history of the disease or response to treatment. We therefore conducted a retrospective analysis comparing clinical outcomes of 1st-line therapy of patients with MMP vs SMP.Methods: A retrospective cohort study of MM pts undergoing first-line therapy was performed by interrogation of the clinical database at the Weill Cornell Medical College / New York Presbyterian Hospital. Subjects diagnosed with active MM who received first-line treatment were included. MMP status was assigned to any patient (pt) with two or more distinct bands appearing on a serum protein electrophoresis with different isotypes on serum immunofixation prior to receiving any therapy. Baseline pt characteristics, therapy received, treatment, and survival outcomes were collected and compared. For pts with MMP, response was determined by following the change in sum of all M-proteins and following the sum as a SMP when applying IMWG criteria.Results: 170 pts were identified in the period of 2005-2014 and included in the analysis: 159 pts (93.5%) with SMP and 11 (6.5%) with MMP. Pts with MMP were older (median age 72 vs 62, P = 0.01) with a lower degree of bone marrow plasmacytosis (median 19% vs 45%, P = .003), with a trend towards a higher rate of extramedullary presentation (18.2% vs 4.5%, P = 0.051). Staging by ISS and Durie-Salmon, presence of adverse cytogenetics, sex, lactate dehydrogenase, C-reactive protein, baseline hemoglobin, and serum creatinine were similar in the two groups. The M-protein isotype distribution for SMP and MMP are shown below in Table 1, with no clear pattern emerging for the SMP group. Pts with SMP were more likely to have been treated with thalidomide (32% vs 0 pts, P = .025) and less with alkylating agents (8.8 vs 27.2%, p = 0.49), however were equally likely to have received treatment with lenalidomide, bortezomib, or autologous stem cell transplant. Overall response to therapy appeared deeper in SMP vs MMP (Table 2) but was not statistically different (P = 0.053). Median PFS was similar for SMP and MMP at 148 vs 135 weeks, respectively (log rank P = 0.87). Overall survival was also unaffected by the presence of MMP: median OS for SMP and MMP was 411 and 423 weeks, (log rank P = .42). A logistic regression model showed higher age (OR 1.15, 95% CI 1.04,1.28) and lower percent plasmacytosis (OR 0.92, 95% CI 0.87, 0.98) to be associated with the presence of MMP at diagnosis.Discussion: The presence of more than one distinct M-spike isotype at diagnosis of active MM was not associated with adverse treatment or survival outcomes. The current convention of following the sum of all M-proteins in these pts is valid. The IMWG criteria should be amended to formally clarify this method of determination of response in pts with MMP.Table 1:Multiple M-protein isotypesM-Protein IsotypesN = 170 (%)IgG-kappa60 (35.3)IgG-lambda33 (19.4)IgA-kappa16 (9.4)IgA-lambda16 (9.4)Free kappa24 (14.1)Free lambda9 (5.3)IgD-lambda1 (0.6)IgG lambda and IgG kappa2 (1.1%)IgG kappa and IgA kappa2 (1.1%)IgA kappa and IgG lambda2 (1.1%)IgG kappa and free mu heavy chains1 (0.6%)IgG lambda and IgA lambda1 (0.6%)IgG kappa and IgG lambda and IgM kappa1 (0.6%)Biclonal IgG kappa, monoclonal IgA kappa1 (0.6%)IgG kappa, IgM kappa, and IgA kappa1 (0.6%)Table 2:Overall response for SMP vs MMPIMWG ResponseSG(N = 159)PG(N = 11)POverall Response RateN = 155N = 11.053PD32SD140PR385VGPR633CR30SCR381 DisclosuresMark:Celgene: Membership on an entity’s Board of Directors or advisory committees, Research Funding, Speakers Bureau; Millennium: Membership on an entity’s Board of Directors or advisory committees, Speakers Bureau; Onyx: Research Funding, Speakers Bureau. Niesvizky:Celgene: Membership on an entity’s Board of Directors or advisory committees, Research Funding, Speakers Bureau; Millennium: Membership on an entity’s Board of Directors or advisory committees, Research Funding, Speakers Bureau; Onyx: Membership on an entity’s Board of Directors or advisory committees, Research Funding, Speakers Bureau.

CD166 Identifies Multiple Myeloma Cells That Preferentially Home to the Bone Marrow Microenvironment and Promote Disease Progression and Bone Lytic Disease

Multiple myeloma (MM) is an incurable malignancy characterized by the proliferation of neoplastic plasma cells in the bone marrow (BM) and by multiple lytic lesions throughout the skeleton. We previously reported that CD166 is a functional molecule on normal hematopoietic stem cells that plays a critical role in HSC homing to the BM and engraftment (Blood. 2014; 124(4):519-29.), suggesting that CD166 is involved in trafficking and lodgment of HSC. CD166, which is a member of the immunoglobulin superfamily capable of mediating both homophilic and heterophilic (CD6) interactions, has been shown to enhance metastasis and invasion in several tumors including breast cancer and melanoma. However, whether CD166 is involved in MM and whether it plays a role in MM progression or the bone lytic disease has not been addressed. H929-GFP MM cells were injected intravenously into NSG mice and GFP cells were recovered from the BM 14hr later. While only 29.9%±1.4% of total H929-GFP cells were CD166+, the frequency of CD166+ cells contained in BM-homed H929-GFP cells was significantly higher (80.0%±2.5%, n=9, p<0.01). Knocking-down (KD) CD166 expression on H929-GFP cells with shRNA reduced the homing of MM cells to the BM. The number of BM-homed GFP cells was significantly decreased for CD166KD cells (5658±904, n=6) compared to mock cells (8551±848, n=6; p<0.05). To examine the potential role of CD166 in osteolytic lesions, we used a novel Ex Vivo Organ Culture Assay (EVOCA) in which MM cells are co-cultured over calvariae from 10d-old pups for 7 days creating an in vitro 3D system for the interaction of MM cells with the bone microenvironment. EVOCA data from two MM cells lines, H929 and OPM2 as well as from three primary MM patients’ CD138+ BM cells demonstrated that bone osteolytic lesions were significantly reduced when CD166 was absent on either MM cells (sorted CD166- fraction) or osteoblast lineage cells (calvariae from CD166-/- mice). Osteolytic lesions can be caused by decreased osteoblastogenesis or increased osteoclastogenesis. Co-culturing BM stromal cells (BMSC) from WT or CD166-/- mice with mock or CD166KD H929 cells in osteoblastogenic media revealed that loss of CD166 on either MM cells or BMSC released the inhibition of mRNA expression of RUNX2, a critical transcriptional factor for early osteoblast differentiation, suggesting that interactions through CD166 suppresses osteoblastogenesis. Gene analysis of calvariae co-cultured with mock or CD166KD H929 cells revealed that the ratios of mRNA levels of RANKL to that of OPG, an important inhibitor of osteoclastogenesis, were elevated in cultures containing a CD166+ component suggesting that CD166 enhances osteoclastogenesis. Furthermore, co-cultures of BM monocytes (BMM) from WT or CD166-/- mice with mock or CD166KD H929 cells in the presence of RANKL and MCSF confirmed that the absence of CD166 on either BMM or MM cells results in significantly reduced osteoclast differentiation as evidenced by TRAP staining. Given that Akt signaling is regulated by CD166 and that Akt pathway is important in osteoclast differentiation, we examined whether or not the Akt pathway is involved in CD166-induced osteoclastogenesis in MM. Western blot analysis of BMM from WT or CD166-/- mice starved then stimulated with either mock or CD166 KD H929 cells revealed that phospho-Akt was significantly down-regulated in the absence of CD166 on either BMM or MM cells indicating that CD166 can activate the Akt pathway and promote MM-induced osteoclast differentiation. Finally, we compared in NSG mice the progression of MM initiated with control, mock or CD166KD H929-GFP cells (n=7-13/group, 2 independent experiments). Compared to control and mock groups, NSG mice transplanted with CD166KD cells showed delayed disease progression and prolonged survival as evidenced by serum levels of human IgA (kappa) and Kaplan-Meier survival curves (p<0.05), respectively. Meanwhile, the inhibition of osteocalcin mRNA expression in calvariae of NSG mice was significantly reduced in the presence of CD166KD cells compared to that with control or mock cells, suggesting again that expression of CD166 on MM cells inhibits osteoblastogenesis. These results suggest that CD166 directs MM cell homing and retention in the BM and promotes MM disease progression and propose that CD166 may induce osteoclastogenesis in MM through the Akt pathway. CD166 may serve as a therapeutic target in the treatment of MM. DisclosuresNo relevant conflicts of interest to declare.

Prognostic Implications of Oligoclonal Bands in Patients with Multiple Myeloma:Its Development per Se did Not Confer the Prologation of Survival

Background: Multiple myeloma (MM) is characterised by the production of monoclonal immunoglobulin (Ig) and clonal proliferation of neoplastic plasma cells in bone marrow. The emergence of oligoclonal bands (OB) in serum and/or urine immunofixation electrophoresis (IFE) that is different to that observed at diagnosis has been reported with varying frequency in patients with stem cell transplantation (SCT) or favourable response to chemotherapy, although its prognostic relevance remains unclear. Here, we retrospectively analysed clinical records and results serial serum and/or urine IFE to determine the frequency, clinical characteristics and prognostic impact of OB that developed after treatment. We also analysed the effects of OB on the results of free light chain (FLC) assay that may affect the stringent CR (sCR) criteria proposed by the IMWG.Patients: We retrospectively reviewed 180 patients with MM admitted to the Department of Hematology/Oncology at Kameda Medical Center, Kamogawa, Japan, from January 2006 to May 2014.Seventeen patients were excluded from the analysis due to lack of appropriate follow-up data.Method: An OB was defined as the presence of a serum and/or urine IFE monoclonal spike that was different from the original myeloma protein in heavy and/or light chains, as well as a different IFE migration pattern. IFE was performed at least every three months after obtaining very good partial response (VGPR) and then until the disease progression or relapse was confirmed. Overall survival (OS) and progression free survival (PFS) were analyzed in 173 MM patients by the Kaplan–Meier method, and differences between the curves were calculated by two-sided log-rank test. Free light chain (FLC) and minimal residual disease measurement by multicolour flowcytometory (MFC) were performed to evaluate the response to treatment.Results: Myeloma response more than VGPR and CR were achieved in 87 (53.3%) and 54 (33.1%) patients, respectively. None of the patients with less than PR developed OB, and OB developed in 36.3% (12/33) and 51.9% (28/54) of the patients with VGPR and CR, respectively. Among the 30 patients who received SCT, 18 patients (60.0%) developed OB, whereas only 12 of 133 patients who did not receive SCT developed OB. The emergence of OB was significantly higher in patients receiving SCT (P < 0.001). The median PFS of the patients with and without OB were 79.4 months and 19.2 months (P = 0.028), respectively, and those of OS did not reached and 41.1 months (P < 0.001), respectively (Figure 1). However, if patient response was limited to CR, median PFS and OS of patients with and without OB were not significantly different between the two groups (79.4 months vs. 80.1months, respectively, P = 0.646; and not reached and not reached, respectively, P = 0.776; Figure 2). OB was observed in 60% of patients after SCT, and in 36.6% of patients more than VGPR without SCT (P<0.001). In the patients who received SCT, the presence of OB was not associated with either PFS or OS (20.0 months vs 44.7 months, P=0.543 and not reached vs not reached, P= 0.739, respectively; Figure3). We also analyzed the association between residual myeloma cells assessed by the MFC in the patients who achieved CR according to the development of OB. Although the patients with OB showed slightly lower levels of residual myeloma cells than those without OB (2.49 x10-4vs 4.15 x10-4), there was no significant difference between the two groups (P= 0.054). As the presence of OB may result in an abnormal serum FLC kappa/lambda ratio, we examined the association of FLC kappa/lambda ratio and development of OB in 28 patients who achieved CR. Abnormal FLC kappa/lambda ratio was observed in 10 (35.7%) and 4 (15.3%) patients with and without OB, respectively, among those with CR (P = 0.118). Conversely, OB was detected in 10 of the 14 patients with an abnormal FLC ratio (71.4%) versus 18 of 40 (45.0%) with a normal serum FLC ratio (P = 0.164) among those with CR.Conclusions: In conclusion, we showed that the emergence of OB occurred exclusively in patients with favourable myeloma responses (more than VGPR) and was associated with prolonged survival. Patients with OB appeared to have fewer residual myeloma cells compared to those without OB. However, its development did not confer an additional survival benefit among the patients who achieved CR. In addition, it is possible that the emergence of OB affects the sCR response criteria proposed by the IMWG. [Display omitted] [Display omitted] [Display omitted] DisclosuresNo relevant conflicts of interest to declare.

Chorzy na szpiczaka plazmocytowego leczeni w Klinice Neurochirurgii i Neurochirurgii Dziecięcej UM w Lublinie

Multiple myeloma is the neoplastic proliferation of plasma cells. There is a significant heterogeneity to the clinical presentation. Neurologic complications are quite common. The causes include metabolic derangements, vertebral compression fractures, base of skull and other bony involvement, but direct involvement of the central nervous system is rare. We describe the patients with multiple myeloma treated in Department of Neurosurgery, Medical University of Lublin.

Rare pancreas tumor mimicking adenocarcinoma: Extramedullary plasmacytoma

Neoplastic proliferation of plasma cells is called plasma cell dyscrasias, and these neoplasms can present as a solitary neoplasm or multiple myeloma. Extramedullary plasmacytoma, in particular pancreatic plasmacytoma, is a rare manifestation of multiple myeloma. Although computerized tomography is useful for the diagnosis of extramedullary plasmacytoma, there are no specific radiologic markers that distinguish it from adenocarcinoma. Histological confirmation by biopsy is necessary for accurate diagnosis and management of the tumor. Endosonography is the most sensitive method for the diagnosis of pancreatic tumors, and the use of fine needle aspiration by endosonography is associated with a lower risk for malignant seeding and complications. Here, we report a case of pancreatic plasmacytoma in newly identified multiple myeloma as diagnosed by endosonography. Endosonography is a reliable and rapid method for the diagnosis of extramedullary plasmacytoma. Therefore, endosonographic fine needle aspiration should be the first choice for histological evaluation when pancreatic plasmacytoma is suspected. Ideally, the pathology would be performed at the same site as endosonographic biopsy.

English

Plasmacytoma is a neoplastic proliferation of plasma cells that may manifest as multiple myeloma, primary amyloidosis, or monoclonal gammapathy of unknown significance. Plasmacytoma may be primary or secondary to disseminated multiple myeloma and may arise from osseous (medullary) or non-osseous (extramedullary) sites. Primary extramedullary plasmacytoma can be solitary or multiple1. The International Myeloma Working Group in 2003 recognized a separate classification of plasmacytomas that occur as multiple sites of disease in soft tissue, bone, or both soft tissue and bone as multiple solitary plasmacytoma. Primary extramedullary plasmacytoma is rare, accounting for only 4% of all plasma cell tumors. Here we report a rare case of extra medullary ethmoidal sinus plasmacytoma with intracranial extension with its clinical, radiological and histological features.

Multiple myeloma in a captive lion (&lt;i&gt;Panthera leo&lt;/i&gt;)

Multiple myeloma is a rare, systemic proliferation of neoplastic plasma cells. A case was reported in an 11-year-old male captive lion (Panthera leo) at the National Zoological Gardens of South Africa, Pretoria. The classic features of symptomatic multiple myeloma were all evident in this case; namely osteolytic lesions, monoclonal gammopathy in the serum with excretion of monoclonal proteins in the urine, neoplastic plasma cells in the bone marrow and associated renal failure and anaemia. In addition, similar to the common pattern of this disease in domestic felids, at least three extramedullary tumours were found and several organs were infiltrated by neoplastic plasma cells. The cytoplasm of approximately 50%of the neoplastic round cells, including a few giant myeloma cells, stained weakly to strongly using immunohistochemical stains for B-lymphocytes (CD79a). The normal haematological parameters and lack of any osteolytic lesions in the lion at the time of the first evaluation suggest that the primary neoplastic cells could have originated from one of the extramedullary tumour sites. Only two cases of multiple myeloma have previously been reported in captive wild felids. To the authors’ knowledge, there are no case reports of multiple myeloma in lions.

Why Proteasome Inhibitors Cannot ERADicate Multiple Myeloma

Proteasome inhibitors are key parts of our armamentarium against multiple myeloma, but the disease can become resistant through poorly defined mechanisms. In this issue of Cancer Cell, Leung-Hagesteijn and colleagues describe XBP1s(-) subpopulations of tumor cells that are resistant to bortezomib and may account for therapeutic failures in the clinic.

Profiling Bortezomib Resistance Identifies Secondary Therapies in a Mouse Myeloma Model

Multiple myeloma is a hematologic malignancy characterized by the proliferation of neoplastic plasma cells in the bone marrow. Although the first-to-market proteasome inhibitor bortezomib (Velcade) has been successfully used to treat patients with myeloma, drug resistance remains an emerging problem. In this study, we identify signatures of bortezomib sensitivity and resistance by gene expression profiling (GEP) using pairs of bortezomib-sensitive (BzS) and bortezomib-resistant (BzR) cell lines created from the Bcl-XL/Myc double-transgenic mouse model of multiple myeloma. Notably, these BzR cell lines show cross-resistance to the next-generation proteasome inhibitors, MLN2238 and carfilzomib (Kyprolis) but not to other antimyeloma drugs. We further characterized the response to bortezomib using the Connectivity Map database, revealing a differential response between these cell lines to histone deacetylase (HDAC) inhibitors. Furthermore, in vivo experiments using the HDAC inhibitor panobinostat confirmed that the predicted responder showed increased sensitivity to HDAC inhibitors in the BzR line. These findings show that GEP may be used to document bortezomib resistance in myeloma cells and predict individual sensitivity to other drug classes. Finally, these data reveal complex heterogeneity within multiple myeloma and suggest that resistance to one drug class reprograms resistant clones for increased sensitivity to a distinct class of drugs. This study represents an important next step in translating pharmacogenomic profiling and may be useful for understanding personalized pharmacotherapy for patients with multiple myeloma.

Solitary extramedullary plasmocytoma of the liver

Solitary extrameduallary plasmacytomas represent approximately 3% of all plasma cell neoplasms. Extramedullary plasmacytoma of the liver is a very rare tumor, although a few cases of extramedullary plasmacytoma of the liver have been reported. We report an unusual case of liver plasmacytoma without systemic disease, diagnosed by percutaneous needle biopsy of the hepatic lesion. The patient was a 67 year old female who exhibited a solitary liver mass on dynamic computed tomography (Panel A). We performed percutaneous needle biopsy of the hepatic lesion. Histologically, the tumor was composed of CD 138 positive plasma cells with mild atypia (Panel B: H&Ex40 black arrow), and 80% of them demonstrated Kappa light chain (Panel C: H&Ex40 red circle – white arrow). There was no evidence of a monoclonal protein in the serum and urine, lytic bone lesions, anemia, renal insufficiency, or hypercalcemia. The bone marrow examination revealed no abnormalities. The patient was treated with local radiation and is doing well without further evidence of disease after one year of follow-up. Primary extramedullary plasmacytoma (EMP) is defined as an extraosseous proliferation of neoplastic plasma cells, without evidence of bone or B

Anaplastic solitary plasmacytoma of mandible, masquerading as sarcoma

Plasma cell neoplasm is characterized by a monoclonal neoplastic proliferation of plasma cells and solitary plasmocytoma of bone (SPB) is a localized form. It usually occurs in vertebrae and secondarily in long bones. Its presence in mandible is extremely rare event. A 48-year-old man consulted to our clinic with a chief complaint of pain in his mandible. Radiography revealed a destructive lesion in body and ramus. The initial pathologic evaluation revealed a high grade pleomorphic neoplasm. The diagnosis was confirmed by immunohistochemical markers. Overall, plasmacytoma with anaplastic features can be confused with high grade sarcoma clinically and histologically.

Plasma Cell Myeloma Initially Presenting as Lung Cancer

Sun Young Cho, M.D., Jae-Heon Jeong, M.D., Woo-In Lee, M.D., Juhie Lee, M.D., Il Ki Hong, M.D., Jin-Tae Suh, M.D., Hee Joo Lee, M.D., Hwi-Joong Yoon, M.D., and Tae Sung Park, M.D.. Ann Lab Med 2013;33:225-8. https://doi.org/10.3343/alm.2013.33.3.225

Characterization and Prognostic Impact of Oligoclonal Humoral Response in Patients with Multiple Myeloma After Autologous Stem-Cell Transplantation: Long-Term Results From a Single Institution

Abstract 3948 Background:Multiple myeloma (MM) is characterized by the production of a monoclonal immunoglobulin of constant isotype and light chain restriction due to the clonal proliferation of neoplastic plasma cells. The optimal treatment in patients younger than 65 years includes induction therapy followed by high- dose therapy/autologous stem-cell transplantation (ASCT). On the other hand, the emergence of oligoclonal bands is a benign phenomenon frequently associated with complete remission (CR) after ASCT. The aim of the present study was to investigate the incidence, biological characteristics, duration and prognostic value of the oligoclonal bands in patients with MM who underwent ASCT at our institution in the last 18 years. Methods:Two-hundred and eleven patients underwent melphalan-based ASCT at our institution from March 31st, 1994, to December 27th, 2011. Of these, 199 patients (109M/90F; median age 55 years, range 25 to 70) who achieved at the least a partial response (PR) after ASCT are the basis of this study. Initial baseline demographics, clinical and laboratory data, and information concerning treatment and follow up were collected. No patient was lost to follow-up. The median follow-up for alive patients was 4.7 years (range 4 months to 18 years). A retrospective systematic review of all serum and urine immunofixation (IFE) studies was carried out. An oligoclonal humoral response was defined as the presence of a serum and/or urine IFE monoclonal spike different from the original myeloma protein either in heavy and/or light chains, as well as at IFE migration pattern. Response, relapse, and progression were defined according to European Blood and Marrow Transplantation (EBMT) criteria. Results:Median PFS was 87 out of the 199 patients (43.7%) achieved CR. The median progression-free survival (PFS) and overall survival (OS) after ASCT were 3.2 and 6.6 years, respectively. Oligoclonal bands were observed in 34% of the patients, but with different prevalence according to the use of novel agents vs. conventional chemotherapy (63% vs. 22%; p=0.0001) in induction. This phenomena was almost exclusive of patients in CR compared to other degrees of response (92% vs. 8%; p=0.0001). Five patients with IgA and five with Bence Jones MM were the only ones being in PR and having a very transient coexistence of the original M-protein with IgG oligoclonal bands in serum. The median number of different isotypes accounting for oligoclonal humoral response was 2 (range 1 to 6) and this phenomena lasted for a median of 1.35 years. Serum bands were more frequent (75.4%) than those in urine and the main involved serum heavy-chain was IgG (73%), with almost the same distribution kappa/lambda. Kappa light-chain was the predominant isotype in urine (60%).In the overall series, all the oligoclonal bands disappeared before serological and clinical progression, except in two settings. First, patients (n=6) who progressed with extramedullary disease with soft-tissue plasmacytomas without significant bone marrow or serological involvement, had persistent oligoclonal bands for several months. Second, patients with Bence Jones MM (n=6), showing urine M-protein progression at the time of relapse had also a transient persistence of serum oligoclonal bands.The presence of oligoclonal bands after ASCT resulted in a significantly longer PFS (p=0.004). This translated in a significantly longer OS in patients with this humoral oligoclonal response (median OS not reached vs. 5.58 years; p=0.003) (Figure 1). An oligoclonal humoral response stable more than one year after ASCT was associated with a significantly longer clinical PFS and OS than those with shorter duration (p=0.008 and p=0.0001, respectively). Of note, the estimated survival of patients with oligoclonal bands lasting for more than one year at 10 years is 70% (Figure 2). In contrast, the PFS ad OS of patients with oligoclonal bands lasting for less than one year were similar to those who never developed this phenomena. Conclusions:The emergence of oligoclonal bands after ASCT is a prognostic factor and it is usually observed in patients in CR. They reflect a robust humoral immune response and consequently an immune system reconstitution. Duration of this humoral response is also associated with a significant survival prolongation. [Display omitted] [Display omitted] Disclosures:No relevant conflicts of interest to declare.

Initial Finding of Mandible Mass in Multiple Myeloma

Multiple myeloma is characterized by a monoclonal neoplastic proliferation of plasma cells. Systematically, multiple myeloma would bring on hypercalcemia, anemia, renal failure, and bone lesions. The vertebrae, ribs, pelvic bone, and skull are usually involved in bone lesions. We report a 46-year-old man whose initial finding of multiple myeloma was a mandible mass. Mandible mass is not rare in multiple myeloma, but it is not that frequently seen as an initial finding.

Plasmocitoma ósseo solitário de mandíbula com apresentação imaginológica incomum: relato de caso clínico

The solitary plasmacytoma is a monoclonal unifocal neoplastic proliferation of plasma cells with histopathologic characteristics similar to those of multiple myeloma. Its etiology is unknown, and rarely the jaws. VMS patient, 56 years old, female, melanoderma in treatment of breast cancer, referred to oncologist for the preparation of the oral cavity in order to start the radiotherapy treatment. On physical examination, presence was seen as a fluctuation in the region of mandible body, with granulation tissue and purulent drainage without dental involvement. In-radiographic examination showed the presence of intraosseous lesion long, radiopaque, surrounded by radiolucent halo. The chance of diagnosis was chronic osteomyelitis diffuse, cement-osseous dysplasia, complex odontoma, osteoma and ossifying fibroma. After biopsy, was found to be a plasmacytoma. The objective of this work is to present a clinical case report of solitary bone plasmacytoma with primary involvement of the oral cavity, emphasizing their clinical, radiographic and histological features.

IgG Myeloma Presenting as a Large Mediastinal Mass and Pleural Effusion

Plasmacytoma, a rare form of plasma cell dyscrasia, refers to a neoplastic proliferation of plasma cells. Although the upper aerodigestive tract is the most common site for extramedullary plasmacytoma, mediastinal and pleural involvement is extremely rare. We report the case of a patient who presented with a large mediastinal mass and pleural effusion. Diagnosis was challenging and subsequently made as mediastinal extramedullary plasmacytoma with simultaneous myelomatous pleural effusion. Further investigations revealed multiple myeloma.

Plasma cell proliferations

Plasma cells (PC) are the terminally differentiated effector cells of the B-cell lineage. The aim of this review is to integrate relevant data on the phenotype of plasma cells, including reactive and malignant PC. The current World Health Organization classification of lymphoid neoplasm is based on correlation of their morphologic, histologic, immunophenotypic, genetic and clinical features. The extensive application of imunohistochemistry is necessary in diagnosis of plasma cell neoplasm, but also in determining prognosis as well as in evaluating residual/relapsing disease. This review focuses on immunohistochemical analysis non-neoplastic and neoplastic plasma cell proliferation in facilitating the diagnosis and highlights the recent advances that have been made with regard to their stratifying.

Plasmacytoma masquerading as an abscess

Plasma cell neoplasia is a lymphoid neoplastic proliferation of B cells and has been classified as multiple myeloma, solitary plasmacytoma, and extramedullary plasmacytoma. Extramedullary plasmacytoma is defined as neoplastic proliferation of plasma cells in the soft tissue. Extramedullary plasmacytoma of the head and neck is very uncommon tumors, representing approximately 0.4% of all head and neck malignancies; amongst them, plasmacytoma of the maxilla is extremely rare. We present a case of a 70-year-old male with swelling on the right middle third of the face, mimicking an abscess, but proven to be extramedullary plasmacytoma. This report discusses the clinical, radiographic, histological, and immunohistochemical features of extramedullary plasmacytoma.

Multiple myeloma with primary manifestation in the mandible: a case report

Plasma cell neoplasms (multiple myeloma, solitary plasmocytoma of bone and extra medullar plasmocytoma) are characterized by a monoclonal neoplastic proliferation of plasma cells. Multiple myeloma is a monoclonal malignant proliferation of plasma cells that causes osteolytic lesions in the vertebrae, ribs, pelvic bone, skull and jaw. We report a case of a 69-year-old male patient who presented with a tumefaction in the body of mandible, which had evolved over the previous two months. In the radiographic examination, an extensive osteolytic lesion was observed in the body of mandible. An incisional biopsy was performed and histopathological study revealed a malignant hematopoietic neoplasm formed by plasmacytoid cells. Knowledge about the maxillofacial manifestations of multiple myeloma is important for the early diagnosis of the disease, since its primary form can manifest itself in the jaw.