scholarly journals A window into immunoglobulin quantitation and plasma cell disease: antigen epitopes defined by the junction of immunoglobulin heavy and light chains

Leukemia ◽  
2013 ◽  
Vol 27 (1) ◽  
pp. 1-2 ◽  
Author(s):  
J A Katzmann ◽  
S V Rajkumar
Keyword(s):  
Plasma Cell ◽  
Light Chains ◽  
Cell Disease ◽  
Disease Antigen

scholarly journals Successful eradication of leptomeningeal plasma cell disease

2018 ◽  
Vol 2018 (7) ◽  
Author(s):  
Øyvind Bruserud ◽  
Bent-Are Hansen ◽  
Nils Vetti ◽  
Silje Johansen ◽  
Håkon Reikvam
Keyword(s):  
Plasma Cell ◽  
Cell Disease

scholarly journals Phenotypic analysis of human myeloma cell lines

Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 566-572
Author(s):  
C Duperray ◽  
B Klein ◽  
BG Durie ◽  
X Zhang ◽  
M Jourdan ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Lines ◽  
Plasma Cell ◽  
Plasma Cells ◽  
Myeloma Cell ◽  
Light Chains ◽  
Cell Phenotype ◽  
Phenotypic Analysis ◽  
Barr Virus ◽  
Human Myeloma Cell

Multiple myeloma (MM) is a B-cell malignancy characterized by the accumulation, primarily in bone marrow, of a clone of plasma cells. The nature of the stem cells feeding the tumoral compartment is still unknown. To investigate this special point, we have studied the phenotypes of nine well-known human myeloma cell lines (HMCLs) and compared them with those of normal lymphoblastoid cell lines (LCLs). Twenty-four clusters of differentiation involved in B lymphopoiesis were investigated using a panel of 65 monoclonal antibodies (MoAbs). For each cluster, the percentage of positive cells and the antigen density were determined, giving rise to a “quantitative phenotype”. We thus classified the HMCLs into two different groups: those with cytoplasmic mu chains (c mu+) and those without (c mu-). In the first (c mu+) group, comprising seven cell lines, the HMCLs had a phenotype of pre-B/B cells close to that of Burkitt's lymphoma cell lines. They expressed low densities of surface mu chains, without detectable cytoplasmic or surface light chains. Three of them were infected with the Epstein Barr virus (EBV). These c mu+ HMCLs bore most of the B-cell antigens except CD23. They expressed the CALLA antigen (CD10) and lacked the plasma-cell antigen PCA1. In contrast, LCLs expressed surface light chains, high densities of CD23, low densities of PCA1 antigen, and no CD10 antigen. The c mu- HMCLs had a plasma-cell phenotype, lacking most of the B-cell antigens and expressing high densities of PCA1 antigen.(ABSTRACT TRUNCATED AT 250 WORDS)

Sensitivity of whole-body CT and MRI versus projection radiography in the detection of osteolyses in patients with monoclonal plasma cell disease

2014 ◽  
Vol 83 (7) ◽  
pp. 1222-1230 ◽  
Author(s):  
Maya B. Wolf ◽  
Fritz Murray ◽  
Kerstin Kilk ◽  
Jens Hillengass ◽  
Stefan Delorme ◽  
...  
Keyword(s):  
Plasma Cell ◽  
Whole Body ◽  
Cell Disease ◽  
Whole Body Ct ◽  
Projection Radiography ◽  
Ct And Mri ◽  
Body Ct

kappa/lambda index for confirming urinary free light chain in amyloidosis AL and other plasma cell dyscrasias

1991 ◽  
Vol 37 (6) ◽  
pp. 1122-1126 ◽  
Author(s):  
Stanley S Levinson
Keyword(s):  
Plasma Cell ◽  
Electrophoretic Pattern ◽  
Light Chains ◽  
Plasma Cell Dyscrasia ◽  
Serum Samples ◽  
Kappa Chain ◽  
Immunofixation Electrophoresis ◽  
Patient Groups ◽  
Bone Marrow Analysis ◽  
Serum And Urine

Abstract Primary systemic amyloidosis (AL), a disease involving the deposition of immunoglobulin light chains in tissue, is caused by a plasma cell dyscrasia. In the case of amyloidosis reported here, no monoclonal component was seen upon routine protein electrophoresis of serum or urine nor was a bone marrow analysis positive for AL. Immunofixation electrophoresis did not show a typical paraprotein band but did show, in the gamma region, two large diffuse bands and a lower concentration of oligoclonal-type bands, all of which stained for free lambda but not for free kappa chain. The ratio of kappa to lambda chains in urine was 0.178, much less than the ratio in serum (1.3). Six other urine samples from a group of patients with documented Bence Jones proteinuria also exhibited kappa/lambda ratios that differed manyfold from the ratios in their corresponding serum samples. On the other hand, the kappa/lambda ratios from seven controls (seven patients with generalized proteinuria unrelated to plasma cell dyscrasia) were similar in serum and urine. This difference between the kappa/lambda ratios from serum and urine can be expressed as a kappa/lambda index. The index was significantly different (P less than 0.01) between the two patient groups compared here, and was useful in confirming the presence of Bence Jones protein in this case with a difficult-to-interpret electrophoretic pattern. Although the kappa/lambda ratio has been widely used for confirmation and identification of monoclonal components in serum, its use in clinical laboratories has not been widely extended to urine. Comparison of serum and urine kappa/lambda ratios as a kappa/lambda index may help reduce the need for more complex immunoelectrophoresis techniques in identifying free light chains in urine.

Quantification by Ultrafiltration and Immunofixation Electrophoresis Testing for Monoclonal Serum Free Light Chains

2020 ◽  
Vol 51 (6) ◽  
pp. 592-600 ◽  
Author(s):  
Gurmukh Singh ◽  
Roni Bollag
Keyword(s):  
Plasma Cell ◽  
Light Chain ◽  
Limit Of Detection ◽  
Light Chains ◽  
Total Serum ◽  
Reliable Estimate ◽  
Free Light Chains ◽  
Serum Free ◽  
Immunofixation Electrophoresis ◽  
Serum Free Light Chains

Abstract Objective Measurement of monoclonal immunoglobulins is a reliable estimate of the plasma cell tumor mass. About 15% of plasma cell myelomas secrete light chains only. The concentration of serum free light chains is insufficient evidence of the monoclonal light chain burden. A sensitive quantitative estimate of serum free monoclonal light chains could be useful for monitoring patients with light chain myeloma. We describe such an assay that does not require mass-spectrometry equipment or expertise. Methods Serum specimens from patients with known light chain myelomas and controls were subjected to ultrafiltration through a membrane with pore size of 50 kDa. The filtrate was concentrated and tested by immunofixation electrophoresis. The relative area under the monoclonal peak, compared to that of the total involved light chain composition, was estimated by densitometric scanning of immunofixation gels. The proportion of the area occupied by the monoclonal peak in representative densitometric scans was used to arrive at the total serum concentration of the monoclonal serum free light chains. Results Using an ultracentrifugation and concentration process, monoclonal serum free light chains were detectable, along with polyclonal light chains, in all 10 patients with active light chain myelomas. Monoclonal light chains were identified in serum specimens that did not reveal monoclonal light chains by conventional immunofixation electrophoresis. The limit of detection by this method was 1.0 mg/L of monoclonal serum free light chains. Conclusion The method described here is simple enough to be implemented in academic medical center clinical laboratories and does not require special reagents, equipment, or expertise. Even though urine examination is the preferred method for the diagnosis of light chain plasma cell myelomas, measurement of the concentration of serum free light chains provides a convenient, albeit inadequate, way to monitor the course of disease. The method described here allows effective electrophoretic differentiation of monoclonal serum free light chain from polyclonal serum free light chains and provides a quantitation of the monoclonal serum free light chains in monitoring light chain monoclonal gammopathies.

A Diffuse Plasma-Cell Disease in a Golden Hamster (Cricitus auratus)

1970 ◽  
Vol 7 (2) ◽  
pp. 135-138 ◽  
Author(s):  
Leonard V. Crowley
Keyword(s):  
Plasma Cell ◽  
Golden Hamster ◽  
Prominent Feature ◽  
Cell Disease ◽  
Male Hamster ◽  
Secondary Degeneration ◽  
Plasma Cell Neoplasm ◽  
Cell Neoplasm ◽  
Reactive Plasmacytosis ◽  
The Brain

A 3 1/2 year-old male hamster with neurologic disturbances hud a systemic plasms-cell disease. The most prominent feature was widespread plasmacytic infiltration of the meninges with secondary degeneration of the brain. It is uncertain whether the disease should He considered a plasma-cell neoplasm or a florid reactive plasmacytosis.

scholarly journals Free Kappa and Lambda Light Chains in Plasma Cell Dyscrasias

2011 ◽  
Vol 20 (1) ◽  
pp. 64-66
Author(s):  
Clementine YF Yap ◽  
Pey Wah Wong ◽  
Tar Choon Aw
Keyword(s):  
Plasma Cell ◽  
Light Chains ◽  
Plasma Cell Dyscrasias

Heavy/Light Chain Quantification Identifies Clonal Plasma Cell Disease in Patients with AL Amyloidosis and Normal Serum Free Light Chain Ratio

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2956-2956
Author(s):  
Tatiana Prokaeva ◽  
Brian Spencer ◽  
Fangui Sun ◽  
Nathaniel McConnell ◽  
Richard M O'hara ◽  
...  
Keyword(s):  
Overall Survival ◽  
Binding Site ◽  
Plasma Cell ◽  
Light Chain ◽  
Free Light Chain ◽  
Al Amyloidosis ◽  
Cell Disease ◽  
Serum Free ◽  
Serum Free Light Chain ◽  
Combined Use

Abstract Background: Serum and urine immunofixation electrophoreses (SIFE/UIFE) are routinely used for detection of clonal immunoglobulins (Ig) in AL amyloidosis. Serum free light chain (FLC) assays (Freelite®, The Binding Site Ltd., Birmingham, UK) have significantly improved the management of patients with AL amyloidosis by providing quantitative measure for the detection and monitoring of clonal plasma cell disease. However, up to 20% of patients with AL amyloidosis may have uninformative serum free light chain values. Objective: To assess the quantitative potential of serum Heavy/Light Chain (HLC) pairs (Hevylite®, The Binding Site Ltd., Birmingham, UK) assay in identification of clonal plasma cell disease in AL amyloidosis. Methods: One hundred and ninety-nine untreated patients with AL amyloidosis were included in this study. Patients with multiple myeloma or B cell lymphoproliferative diseases associated AL amyloidosis were excluded. Serum sampleswere obtained at initial evaluation and stored at -20°C. SIFE/UIFE were performed at the time of sample collection. HLC pairs were assessed by the Hevylite® assay. HLC κ/λ normal ratios (HLCR) were: 1.12-3.21 for IgG κ/λ; 0.78-1.94 for IgA κ/λ; and 1.18-2.74 for IgM κ/λ. FLCs were assessed by the Freelite® assay; FLC κ/λ normal ratio (FLCR) was 0.26-1.65. In 103 cases, FLC testing was performed at the time of sample collection; 96 cases were tested at The Binding Site. Vital status of patients was obtained from either medical records or Social Security Death Index. Follow-up ended in June 2014. Results: An abnormal HLCR was found in 74 (37.2%), an abnormal FLCR in 163 (81.9%), and SIFE/UIFE positivity in 187 (94%) of 199 patients with AL amyloidosis. Of 36 patients with a normal FLCR, 23 (63.9%) were noted with an abnormal HLCR compared to 51 (31.3%) patients in an abnormal FLCR group (P = 0.001). In total 186/199 (93.5%) patients with AL amyloidosis had abnormalities in either HLCR or FLCR, compared to 187/199 (94%) of patients who were SIFE/UIFE+ (Table 1). The combined use of both FLCR and HLCR yielded quantifiable information in 93.5% of cases; the use of both tests in combination with SIFE/UIFE identified plasma cell clonality in 100% of patients. Seventy-two cases presented with an abnormal HLCR for a single isotype and 2 in multiple Ig isotypes. In all cases, involved LC type of abnormal HLCR matched LC type identified by SIFE/UIFE. None of 12 cases that were negative on the SIFE/UIFE presented with an abnormal HLCR, however, all showed abnormalities in FLCR. Table 1. Comparative efficiency of FLCR, HLCR and Serum/Urine Immunofixation in AL Amyloidosis patients. SIFE/UIFE+ (n=187) SIFE/UIFE- (n=12) HLCR+/FLCR+ 51 (27.2%) - HLCR+/FLCR- 23 (12.3%) - HLCR-/FLCR+ 100 (53.5%) 12 (100%) HLCR-/FLCR- 13 (7%) - Overall survival was similar in patients with and without abnormal HLCR (Log rank p=0.092; Figure 1), whereas patients with an abnormal FLCR had a significantly inferior overall survival compared to those with a normal FLCR (Log rank p=0.027; Figure 2). Combined use of both HLCR and FLCR demonstrated a trend toward superior overall survival in a group of patients with an abnormal HLCR / normal FLCR (Wilcoxon p=0.037; Log rank p=0.107; Figure 3). Conclusions: The Hevylite® assay provided information in addition to other laboratory tests for clonal plasma cell disease in AL amyloidosis. The combined use of the HLCR and FLCR provided quantifiable information in 93.5% of patients. The use of both assays in combination with SIFE/UIFE detected clonal disease in all patients. HLCR has potential to quantify clonal disease in patients with uninformative FLCR results. An abnormal HLCR was not predictive of overall survival, while an abnormal FLCR was, in this series of patients. Combined use of HLCR and FLCR could be beneficial in prognostication of outcome in AL amyloidosis. Disclosures McConnell: The Binding SIte: Employment. O'hara:The Binding Site: Employment.

Sign in / Sign up

Export Citation Format

Share Document