Immunobeads Test (Antibody Coated Polyacrylamide Beads) in the Immunological Characterization of Lymphoproliferative Disorders

1987 ◽  
Vol 2 (3) ◽  
pp. 173-176
Author(s):  
Teodoro Chisesi ◽  
Michele Vespignani ◽  
Giovanni Capnist
Keyword(s):  
Multiple Myeloma ◽  
Chronic Lymphocytic Leukemia ◽  
Normal Subjects ◽  
Lymphoproliferative Disorders ◽  
Lymphocytic Leukemia ◽  
Immunological Characterization ◽  
Surface Immunoglobulin ◽  
Non Hodgkin Lymphoma ◽  
Patient Groups

Three groups of patients with immunoproliferative disorders (15 multiple myeloma, 11 non-Hodgkin's lymphoma, 21 chronic lymphocytic leukemia) were studied by immunological characterization and compared to a group of 20 normal subjects (controls) using anti-immunoglobulin coated polyacrylamide beads (T-B Quantigen test, QT), erythrocyte rosettes (ER), surface immunoglobulin (SIg), and monoclonal antibodies for T and B cells (OKT3; OKT11; OKT8; OKT4; IaDR); null cells (NC) and double marker (DM) cells were also considered. The values for normal subjects for T-B, NC and DM cells were comparable. Results for the patient groups strikingly differed. There were progressively larger differences between the T and B percentages obtained with different techniques. The largest differences were seen in patients with chronic lymphocytic leukemia and the smallest in multiple myeloma patients; values were intermediate in non-Hodgkin lymphoma. The different findings were related to the number of DM cells (ER +, SIg+ QT+) and the different tests used. The importance of these findings in the diagnostic appproach to lymphoproliferative disorders is discussed.

Tumor Marker CA 15-3 in Hematological Malignancies.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4329-4329
Author(s):  
Zoi Saouli ◽  
Athanasios Papadopoulos ◽  
Georgia Kaiafa ◽  
Fotios Girtovitis ◽  
Georg Charisopoulos ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Chronic Lymphocytic Leukemia ◽  
Acute Leukemia ◽  
Healthy Volunteers ◽  
Hodgkin Lymphoma ◽  
Hematological Malignancies ◽  
Myeloproliferative Disorders ◽  
Response To Therapy ◽  
Lymphocytic Leukemia ◽  
Non Hodgkin Lymphoma

Abstract Introduction: CA 15-3 is a glycoprotein expressed in several adenocarcinomas, especially of the breast. It is used to detect recurrent or metastatic disease. Elevated levels can also be found in adenocarcinomas of the ovary, lung, pancreas, and colon, and are also related to benign breast or ovarian disease, endometriosis, hepatitis, pregnancy and lactation. To our knowledge with the exception of multiple myeloma, there are no references for the significance of the CA 15-3 in hematological malignancies. Aim of our study was to evaluate the levels of CA 15-3 in patients with various hematological malignancies. Material and Methods: 84 patients with hematological malignancies were tested: MDS 27 pts, non Hodgkin lymphoma 12 pts, Hodgkin’s lymphoma 3 pts, chronic lymphocytic leukemia 13 pts, acute leukemia: 7 pts, multiple myeloma 8 pts, chronic myeloid leukemia 3 pts and other chronic myeloproliferative disorders 11 pts. 55% of the patients were men with average age of 55 (17–87) and 45% were women with average age of 52 (35–64). A group of 45 healthy volunteers’ blood donors was also tested. Immunoradiometric assay (IRMA) has been used to determine the circulating levels of the CA 15-3 marker. Results: None of the healthy volunteers had elevated Ca 15-3 levels. Among the 84 patients, 31 (36,9%) had elevated levels of CA 15-3. In MDS 10/27 pts, in Non Hodgkin Lymphoma 5/12 pts, in Hodgkin Lymphoma 1/3 pts, in Chronic Lymphocytic Leukemia 5/13 pts, in Multiple Myeloma 4/8 pts, in acute leukemia 1/7 pts and in other myeloproliferative disorders 4/11 pts. The CA 15-3 levels in hematological patients were higher than the ones in the healthy group. The difference was statistically significant (p <0.0001), (Table 1). 31 patients who where either untreated or had recurrent disease (subgroup a), had elevated CA 15-3 levels (36,8 ± 8,9 U/ml) while the rest 53 patients who were under therapy or were in remission (subgroup b) had normal levels (14,3 ± 5,2 U/ml). A statistically significant difference between the two subgroups was observed, (p <0.0001), (Table 2). The low risk MDS patients (RA, RARS) had normal level of CA 15-3, while the high risk MDS patients (RAEB, RAEB-t, CMML) had high levels of CA 15-3. Conclusions: CA 15-3 can be an indicative marker of the activity of a hematological malignancy. Also, it might be of value in monitoring hematological diseases and response to therapy. Table 1 Ca 15-3 (U/ml) Patients (total, n=84) 23 ± 12,3 Normal Subjects (n=45) 14,1 ± 4,6 p < 0.0001 Table 2 Ca 15-3 (U/ml) Subgroup a 36,8 ± 8,9 Subgroup b 14,3 ± 5,2 p < 0.0001

scholarly journals Lymphocyte surface immunoglobulin density and immunoglobulin secretion in vitro in chronic lymphocytic leukemia (CLL)

Blood ◽  
1978 ◽  
Vol 52 (3) ◽  
pp. 601-608 ◽  
Author(s):  
YH Chen ◽  
P Heller
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Secretory Activity ◽  
Normal Subjects ◽  
Suppressive Effect ◽  
Lymphocytic Leukemia ◽  
Immunofluorescent Staining ◽  
Pokeweed Mitogen ◽  
Lymphocyte Surface ◽  
Surface Immunoglobulin

Lymphocyte surface immunoglobulin (SIg) and immunoglobulin (Ig) secretion were studied in 14 patients with chronic lymphocytic leukemia (CLL) and 12 healthy subjects. The determination of SIgM-bearing (SIgM+) cells by immunofluorescent staining and the quantification of SIgM by radioimmunoassay (RIA) permitted the calculation of the SIgM density. In 12 normal subjects the percentage of SIgM+ cells averaged 8% (range 4%-12%) and the SIgM density 10.2 ng antigenic equivalent/10(6) SIgM+ cells (SD 4.3). In 12 patients with CLL the respective figures were 68% (range 35%-90%) and 0.68 ng (SD 0.57). Ig secretion from pokeweed mitogen-stimulated CLL cells was markedly diminished as compared with normal lymphocytes. In coculture experiments CLL cells had no suppressive effect on Ig secretion of normal lymphocytes and normal lymphocytes did not enhance Ig secretion leukemic lymphocytes. These results indicate that the impaired secretory activity of CLL cells results from an intrinsic anomaly of these cells.

Evaluation and identification of protocols for safe and efficacious institutional administration of intravenous immune globulin in hypogammaglobulinemia associated with chronic lymphocytic leukemia, non-Hodgkin lymphoma, and multiple myeloma.

2018 ◽  
Vol 36 (30_suppl) ◽  
pp. 250-250
Author(s):  
Doron Feinsilber ◽  
Cole McCoy ◽  
Parameswaran Hari ◽  
Patrick C. Foy ◽  
Ravi Narra ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Chronic Lymphocytic Leukemia ◽  
Hematologic Malignancies ◽  
Iga Deficiency ◽  
Lymphocytic Leukemia ◽  
Data Capture ◽  
Cell Mediated Immunity ◽  
Nccn Guidelines ◽  
Quality Reporting ◽  
Non Hodgkin Lymphoma

250 Background: Hematologic malignancies effect both humoral and cell-mediated immunity. We hypothesize that for patients with Chronic Lymphocytic Leukemia (CLL), Non-Hodgkins Lymphoma (NHL), and Multiple Myeloma (MM) outcomes improve with adherence to National Comprehensive Cancer Network (NCCN) guidelines for intravenous immunoglobulin (IVIG).Our objective is to understand resource allocation and implementation of IVIG in outpatient and inpatient settings. We identified a cohort of patients with hypogammaglobulinemia for assessing incidence of sepsis, outcomes, and resource use. We initiated this project by undertaking a large descriptive study of current IVIG use. Methods: A retrospective Institutional Review Board (IRB) approved data capture was conducted covering 2016-2018. Inclusion criteria involved those on an active chemotherapy plan, age > 18 years and diagnosis of CLL, NHL, or MM. IgA deficiency, anaphylaxis to IVIG, planned chemotherapy, inherited immunodeficiency, and thymic deficiency were excluded. We considered patients to be suitable for IVIG if IgG was < 500 mg/dL for CLL and MM and < 400 mg/dL in NHL. Outcomes, number of admissions, sepsis, ICU care, infectious etiology, and monthly IgG levels were examined. Results: A preliminary i2b2 data capture identified a cohort of 563 patients that yielded 12% with bacteremia, 21% with sepsis, and 23% with pneumonia of which 87% were admitted. 28% received IVIG during the 2-year period. Of the 563, 77% were hospitalized and 21% required ICU care. 54% of ICU patients received inpatient IVIG. All influenza and parainfluenza cases were inpatient. Final data analysis will yield greater detail in comparing inpatient to outpatient IVIG use. Conclusions: Large academic institutions appear to have significant variability in use of IVIG in patients with lymphopenia and hematologic malignancies. With this data, we plan to assess for patient-level outcomes based on adherence to NCCN guidelines as a way to enhance Physician Quality Reporting System (PQRS) standards by prioritizing outpatient use of IVIG.

scholarly journals Histopathology of Canine Bone Marrow in Malignant Lymphoproliferative Disorders

1988 ◽  
Vol 25 (1) ◽  
pp. 83-88 ◽  
Author(s):  
R. E. Raskin ◽  
J. D. Krehbiel
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Acute Lymphoblastic Leukemia ◽  
Chronic Lymphocytic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Lymphoproliferative Disorders ◽  
Lymphocytic Leukemia ◽  
Metastatic Lesions ◽  
Multicentric Lymphoma

Bone marrow core biopsies from 63 dogs with malignant lymphoproliferative disorders and leukemic involvement were evaluated. Multicentric lymphoma (44), multiple myeloma (8), chronic lymphocytic leukemia (9), and acute lymphoblastic leukemia (2) were found. Four distinct bone marrow histologic patterns were identified: focal (6), mixed (20), interstitial (28), and packed (9). Of those with focal or mixed patterns, 77% (20/26) had paratrabecular distribution. Stromal changes were infrequent, with 6% (4/63) having necrosis, 3% (2/63) fibrosis, and 6% (4/63) osteolysis. For each condition, the interstitial and mixed patterns were the most common presentations, while focal and packed patterns occurred less frequently. Morphologically, cells of metastatic lesions of lymphoma resembled those of primary sites. Colonization of bone marrow by various cytologic types of lymphoma was independent of the histologic patterns.

scholarly journals Lymphocyte surface immunoglobulin density and immunoglobulin secretion in vitro in chronic lymphocytic leukemia (CLL)

Blood ◽  
1978 ◽  
Vol 52 (3) ◽  
pp. 601-608 ◽  
Author(s):  
YH Chen ◽  
P Heller
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Secretory Activity ◽  
Normal Subjects ◽  
Suppressive Effect ◽  
Lymphocytic Leukemia ◽  
Immunofluorescent Staining ◽  
Pokeweed Mitogen ◽  
Lymphocyte Surface ◽  
Surface Immunoglobulin

Abstract Lymphocyte surface immunoglobulin (SIg) and immunoglobulin (Ig) secretion were studied in 14 patients with chronic lymphocytic leukemia (CLL) and 12 healthy subjects. The determination of SIgM-bearing (SIgM+) cells by immunofluorescent staining and the quantification of SIgM by radioimmunoassay (RIA) permitted the calculation of the SIgM density. In 12 normal subjects the percentage of SIgM+ cells averaged 8% (range 4%-12%) and the SIgM density 10.2 ng antigenic equivalent/10(6) SIgM+ cells (SD 4.3). In 12 patients with CLL the respective figures were 68% (range 35%-90%) and 0.68 ng (SD 0.57). Ig secretion from pokeweed mitogen-stimulated CLL cells was markedly diminished as compared with normal lymphocytes. In coculture experiments CLL cells had no suppressive effect on Ig secretion of normal lymphocytes and normal lymphocytes did not enhance Ig secretion leukemic lymphocytes. These results indicate that the impaired secretory activity of CLL cells results from an intrinsic anomaly of these cells.

An Fc-Engineered Humanized Anti-CD40 Monoclonal Antibody, XmAb5485, Exhibits Potent Activity in Vitro and in Vivo against Non-Hodgkin Lymphoma, Chronic Lymphocytic Leukemia and Multiple Myeloma

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 881-881 ◽  
Author(s):  
Eugene A. Zhukovsky ◽  
Holly Horton ◽  
Matthias Peipp ◽  
Erik Pong ◽  
Matthew Bernett ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Cell Line ◽  
Hodgkin Lymphoma ◽  
Cell Lines ◽  
Lymphocytic Leukemia ◽  
Non Hodgkin Lymphoma

Abstract CD40, a transmembrane glycoprotein belonging to the tumor necrosis factor receptor family, is an attractive target for cancers of lymphoid origin since it is expressed on most mature B-cell malignancies, some early B-cell acute lymphocytic leukemias, and multiple myeloma. Finding efficient therapies for multiple myeloma (MM), chronic lymphocytic leukemia (CLL) and rituximab-refractory Non-Hodgkin Lymphoma (NHL) represents an unmet need. Several anti-CD40 antibodies, both agonistic and antagonistic, have demonstrated objective responses in early clinical NHL trials and thus validated this antigen as a target for lymphoproliferative diseases. Here we present the characterization of a novel Fc-engineered and humanized anti-CD40 antibody, XmAb®5485, that was generated using our XmAb antibody engineering technology. This antibody is highly cytotoxic against lymphoma, leukemia and multiple myeloma cell lines as well as primary cancer cells. XmAb5485 is characterized by: i) increased affinity for Fc gamma receptors (FcgR), ii) improved effector function, and iii) significantly increased antitumor potency. We investigated several direct and indirect (Fc-mediated) mechanisms of antibody-mediated cytotoxicity in vitro. The potency (EC50) of XmAb5485 in antibody-dependent cell-mediated cytotoxicity (ADCC) increased up to 150-fold relative to the native non Fc-engineered version (anti-CD40 IgG1) of the antibody in a screen of Burkitt’s lymphoma [BL], CLL and MM-derived cell lines. In the same cell lines, ADCC potency and maximal efficacy (% lysis) of XmAb5485 were also superior to that of rituximab: 74- and 1.3-fold higher in CLL, 12.5- and 1.4-fold higher in BL, and 190- and 1.9-fold higher in MM. In a MM cell line with low density of CD40 expression (~3500 per cell) XmAb5485 facilitated efficient ADCC whereas anti-CD40 IgG1 was virtually ineffective. Furthermore, using a BL cell line (Ramos) XmAb5485 displayed antibody-dependent cellular phagocytosis (ADCP) with potency and efficacy increased relative to rituximab (15- and 1.6-fold) and anti-CD40 IgG1 (5- and 1.2-fold). XmAb5485 also exhibited anti-proliferative apoptotic activity that was similar to that of rituximab. Ex vivo, XmAb5485 mediated potent ADCC of multiple primary patient-derived CLL, MCL, and plasma cell leukemia (PCL, an aggressive form of MM) cells, with substantially increased potency and efficacy relative to rituximab; in contrast, anti-CD40 IgG1 displayed minimal or no activity in these primary tumor cells. In vivo, in an established large (210–350 mm3) sc Ramos tumor xenograft model, 6 mg/kg XmAb5485 cured 80% of mice of detectable tumors and displayed statistically significant superiority over anti-CD40 IgG1. In contrast, only 7% of animals in the rituximab cohort were cured. In summary, our data suggest that XmAb5485, an anti-CD40 Fc variant antibody engineered for increased effector function, is a promising next-generation immunotherapeutic for leukemias, lymphomas, and multiple myeloma.

scholarly journals Lenalidomide and Chronic Lymphocytic Leukemia

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Ana Pilar González-Rodríguez ◽  
Angel R. Payer ◽  
Andrea Acebes-Huerta ◽  
Leticia Huergo-Zapico ◽  
Monica Villa-Alvarez ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Mechanism Of Action ◽  
Tumor Lysis Syndrome ◽  
Hematologic Malignancies ◽  
Lymphoproliferative Disorders ◽  
Lymphocytic Leukemia ◽  
Potential Mechanism ◽  
Non Hodgkin Lymphoma ◽  
Flare Reaction ◽  
Immunomodulatory Drug

Lenalidomide is an oral immunomodulatory drug used in multiple myeloma and myelodysplastic syndrome and most recently it has shown to be effective in the treatment of various lymphoproliferative disorders such as chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma. The mechanism of action of lenalidomide varies depending on the pathology, and in the case of CLL, it appears to primarily act by restoring the damaged mechanisms of tumour immunosurveillance. This review discusses the potential mechanism of action and efficacy of lenalidomide, alone or in combination, in treatment of CLL and its toxic effects such as tumor lysis syndrome (TLS) and tumor flare reaction (TFR), that make its management different from other hematologic malignancies.

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