Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression, tissue distribution, and preliminary characterization of a cell surface molecule, apparently a glycolipid, recognized by a monoclonal antibody, anti-PAA, were described. This antibody (anti-PAA) was produced by the fusion of myeloma cells NS-1 with spleen cells from a BALB/c mouse, which were sensitized with activated human T-cells generated by allogeneic stimulation in mixed-lymphocyte culture (MLC). Resting human peripheral blood T-cells, B-cells, and monocytes demonstrated weak anti-PAA binding. Binding of proliferating T-cells (phytohemagglutinin- and MLC-activated T-cells) and thymocytes to anti-PAA was two to six times greater than that of resting T-cells. A fifteenfold-increased binding was observed with acute lymphocytic leukemia T-cell lines. Epstein-Barr virus-transformed B-cell lines bound anti-PAA up to sixteenfold greater than resting B-cells. Tumor cell lines of various nonlymphoid origins demonstrated marked reactivity with this antibody. Both benign and malignant cells in hyperplastic tissues, of various origins, bound anti-PAA, whereas their normal, nonproliferating counterparts did not. Normal proliferating cells in these tissues, including cells of the placental chorionic villi and trophoblasts, also bound anti-PAA. Of all lymphoid and nonlymphoid cell lines examined, only chronic lymphocytic leukemia (CLL) cells and some cell lines derived from Burkitt's lymphoma showed weak or no binding. This antibody also failed to react with a variety of nonprimate cell lines. Anti-PAA antibody did not immunoprecipitate any protein from lymphoid tumor cell lines to which it demonstrated a quantitatively high degree of binding, nor did protease treatment of these lines decrease antibody binding. Anti-PAA did, however, bind to glycolipids extracted from these cell lines. Binding of this monoclonal antibody to a minor neutral glycolipid, isolated from the erythroleukemia cell line K562, was about sixfold greater than that of any other K562 neutral glycolipid or ganglioside. Anti-PAA demonstrated weak or undetectable binding to purified, predominant, lymphoid cell membrane's neutral glycolipids and gangliosides. The monoclonal antibody anti-PAA appeared, therefore, to recognize a unique, proliferation-associated, neutral glycolipid present on normal as well as on benign and malignant proliferating cells. The antigen appeared to be universally expressed on proliferating cells from all human tissues with the exception of some Burkitt's cell lines and CLL cells. Nonhuman cell lines, except those for closely related primates, did not express PAA.
 ...
PMID:Unique proliferation-associated marker expressed on activated and transformed human cells defined by monoclonal antibody. 354 53

A new enzymoimmunoassay, specific for the measurement of placental ferritin (PLF) isotype, has been described. Two monoclonal antibodies (McAbs) with different binding specificities to placental ferritin have been used in this assay. One antibody (CM-G-8) binds to all ferritins, whereas the second (CM-H-9) binds to placental ferritin only. In addition, a second enzymoassay was developed for the measurement of total common serum ferritin using CM-G-8 McAb. Serum levels of total ferritin and PLF were measured in healthy individuals and in patients with lymphoproliferative diseases and multiple myeloma. The majority of normal subjects were deficient in PLF in the serum. Increased serum levels of PLF were observed in patients with Hodgkin's lymphoma and non-Hodgkin's lymphoma of low and intermediate grades, as well as in patients with acute lymphocytic leukemia (ALL). Total ferritin was also elevated in these patients. Chronic lymphocytic leukemia (CLL) and multiple myeloma patients exhibited normal levels of common serum ferritin, whereas PLF in the serum was lacking.
 ...
PMID:New monoclonal antibody enzymoassay for the specific measurement of placental ferritin isotype in hematologic malignancies. 381 52

The current use of allogeneic bone marrow transplantation in various hematologic diseases is reviewed. Bone marrow transplantation (BMT) involves infusion of bone marrow from a suitable donor into a properly conditioned recipient. Most BMT is allogeneic, in which the donor is genetically dissimilar but shares some common tissue antigens with the recipient. Almost all patients undergoing allogeneic BMT must be "prepared" with high-dose cyclophosphamide to prevent graft rejection. Most patients with hematologic malignancy also receive total body irradiation to eradicate malignant cells located in areas inaccessible to the systemic circulation. Bone marrow transplantation is the treatment of choice for severe aplastic anemia. In acute myelogenous leukemia, the best results are observed in young patients undergoing BMT in first remission. In acute lymphoblastic leukemia, BMT is usually reserved for patients in second or subsequent remission. Early results are promising in patients with chronic myelogenous leukemia who receive BMT before the accelerated phase or blast crisis of this disease. Allogeneic BMT offers an opportunity for cure in some patients with relapses of Hodgkin's disease or those with certain subtypes of non-Hodgkin's lymphoma. Other diseases for which BMT has been used include severe combined immune deficiency disease, Fanconi's anemia, and multiple myeloma. Complications of BMT include graft failure or rejection, acute and chronic graft-versus-host disease, and infectious complications; late complications, such as restrictive and obstructive pulmonary disease, cataracts, sterility, and secondary malignancies, may also occur. Bone marrow transplantation has become an important treatment for many hematologic diseases, but it will probably remain a treatment reserved for only a few highly specialized centers. If morbidity and mortality caused by transplant-related complications can be reduced, BMT may be offered to older patients and those without HLA-identical sibling donors.
 ...
PMID:Allogeneic bone marrow transplantation in the treatment of hematologic diseases. 388 73

Malignant lymphomas and leukemias are related to maturation stages of distinct subpopulations of hematopoietic or lymphoid cells as defined by immunocytological methods. We first describe various monoclonal antibodies, and the methodology employed in our investigations and report on recent developments in the standardization of these reagents (part 1). The maturation sequence of normal lymphoid cells and their precursors in the bone marrow, thymus and the peripheral lymphoid organs are discussed in part 2. Typical immunomorphological findings in Non Hodgkin Lymphomas (NHL) are summarized in respect to lymphocytic NHL (CLL, lymphoplasmocytoid NHL, hairy cell and prolymphocytic leukemia, some lymphomas of peripheral T-lymphocytes), to NHL of follicular center cells (centroblastic-centrocytic, centrocytic NHL), to "large cell" NHL (centroblastic, immunoblastic NHL, large cell NHL derived from T-lymphocytes or "lymphomas" of macrophage origin) and to lymphoblastic NHL (derived from T-lymphocytes, pre-B lymphocytes and Burkitt-type). Findings in multiple myeloma are also summarized in part 3. Immunocytological features of the normal Myelo-, Mono-, Erythro- and Thrombopoieses are discussed in part 4. The reactivity of some monoclonal antibodies with precursor cells of these cells (CFU-GM, BFU-e and CFU-e, CFU-M) are also described. Finally we summarized the immune phenotype of acute leukemias (part 5) in respect to acute lymphoid leukemias (cALL, T-ALL, O-ALL, B-ALL), to acute non lymphoid leukemias (M1-M6 type according to the FAB-Classification) and to blastic stages of chronic leukemias.
 ...
PMID:[Immunocytologic diagnosis of leukemia and lymphoma: monoclonal antibodies in the differential diagnosis of hematologic neoplasms]. 391 83

Marrow transplantation is effective treatment for a number of hematological diseases in patients under the age of 50 who have an HLA-identical sibling donor. It is successful in the treatment of aplastic anemia with 70-85% long-term survival. It offers 10-30% apparent cures for patients with acute leukemia who have relapsed at least once, and for those with chronic myelocytic leukemia in blast crisis. Although still somewhat controversial, it appears to be the treatment of choice for patients with acute nonlymphoblastic leukemia in first chemotherapy induced remission, and for those with chronic myelogenous leukemia in the chronic phase since approximately 50-60% of these patients experience long-term, disease-free survival. Patients with acute lymphoblastic leukemia grafted in second or subsequent remission may expect a 30% "cure" of their disease. Marrow grafting is the only effective treatment for many patients with inherited immunologic deficiencies and certain genetic storage diseases. Cures of congenital Fanconi's anemia, Blackfan-Diamond anemia, osteopetrosis, paroxysmal nocturnal hemoglobinuria and thalassemia major have been achieved. Marrow transplantation is being explored for the therapy of patients with lymphoma, Hodgkin's disease, preleukemia, multiple myeloma, hairy cell leukemia, small cell lung cancer, testicular cancer, ovarian cancer and neuroblastoma. Marrow transplantation has been limited by the fact that many patients do not have HLA-identical siblings and very few have monozygotic twins. More recently, marrow transplants from HLA-nonidentical family members and even from unrelated donors have been successfully explored.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Marrow transplantation: the Seattle experience. 391 47

A murine monoclonal antibody (anti-BL7) was raised by immunization of BALB/c mice with a precursor B-cell line (Josh-7) which detects a heat-stable, nonimmunoprecipitable antigen. The expression of BL7 was investigated in peripheral blood and/or bone marrow leukemic cell suspensions stained by indirect immunofluorescence and analyzed by flow cytometry. Lymphoblasts from 43 of 43 cases of "null" acute lymphoblastic leukemia were BL7-. Five cases of T-acute lymphoblastic leukemia and 5 cases of terminal deoxynucleotidyl transferase-positive blastic chronic myelogenous leukemia were also BL7-. All 63 cases of B-cell chronic lymphocytic leukemia were BL7+. Neoplastic cells in 22 of 28 cases of B-cell non-Hodgkin's lymphomas in leukemic phase were also BL7+. Expression of BL7 showed some correlation with Rappaport's histological classification. Four cases of multiple myeloma and plasma cell leukemia were BL7-. Twenty-three cases of acute nonlymphocytic leukemias were also analyzed. Of these, only the acute promyelocytic (M3,4 cases) and acute myelomonocytic (M4, one case) varieties expressed BL7 on a small proportion (approximately 15%) of the leukemic cells. All other subgroups were BL7-. The reactivity of anti-BL7 was compared to other B-cell antibodies on selected samples and was shown to be different from B1, B2, and the BA antibodies. Anti-BL7 is a unique monoclonal antibody useful in the study of B-cell cancers.
 ...
PMID:Distribution of a new B-cell-associated surface antigen (BL7) detected by a monoclonal antibody in human leukemic disorders. 392 96

A clone of murine monoclonal antibody HH 10 (IgM) was raised by fusing NS-1 myeloma cells and spleen cells of a mouse hyperimmunized with acute promyelocytic leukemia cells. Serological analysis by means of immune adherence assays showed that HH 10 reacts with immature hematopoietic cells including thymocytes and myeloid precursor cells (defined as colony-forming units in culture assays). The antibodies were not reactive to either peripheral blood cells or bone marrow cells obtained from normal individuals. Lymphoid blasts induced with phytohemagglutinin, pokeweed mitogen, or concanavalin A were also non-reactive, and all non-hematopoietic cultured cells examined were also negative. The antibodies were, however, reactive to leukemia cells in 67 cases out of 91 cases (74%) of acute leukemia. In patients with acute lymphoblastic leukemia, 43 out of 52 cases (83%) were positive and, in particular, all of 12 T-cell-type acute leukemias were reactive to HH 10. Comparison of percent HH 10 positive cells in the bone marrow of patients with acute leukemia with the results of cytological studies showed a good correlation. Analysis of sequentially collected bone marrow cells of acute leukemia patients using HH 10 revealed its usefulness for monitoring leukemia cells.
 ...
PMID:Production and analysis of HH 10 monoclonal antibodies reactive to immature hematopoietic cells and their use for monitoring acute leukemia cells. 392 83

A monoclonal antibody (SA-1) has been characterized. The antibody was derived from the fusion of the X-63 myeloma cell-line with splenocytes from a mouse immunized with human acute megakaryoblastic leukaemia cells. The antibody reacted with blast cells from 65% of patients with AML without correlation to morphologic classification. The antibody further reacted with a subset of myeloid cells from normal bone marrow, and with peripheral neutrophil granulocytes. In lymph nodes the antibody showed reactivity with subsets of dendritic reticulum cells. In skin biopsies the antibody reacted with subsets of Langerhans cells, subsets of indeterminate cells and activated T-lymphocytes. The antigen was not expressed on non-activated T-lymphocytes. Neither was it expressed on B-lymphocytes, erythrocytes, platelets nor blast cells from patients with ALL. The antigenic target for the antibody SA-1 was a surface exposed polypeptide (mol. wt. 15 000 D).
 ...
PMID:Expression of an antigen defined by a monoclonal antibody (SA-1) on normal and malignant cells. 408 40

The risk of developing a second primary cancer was evaluated in approximately 19,000 persons with initial cancers of the lymphatic and hematopoietic system in Connecticut between 1935 and 1982. Significant excesses for all second cancers were observed among patients with leukemia (34%), Hodgkin's disease (70%), non-Hodgkin's lymphoma (25%), and multiple myeloma (24%). In general, the risk of second cancers was greater in males than in females, even for cohorts not showing an excess of surveillance-related prostate cancer. Among patients with leukemia, significant excesses of cancers of the lung, kidney/ureter, and prostate were noted; cutaneous melanoma was elevated only in males. These excesses did not persist in the small number of long-term survivors. Possible etiologic factors included tobacco smoking for lung and kidney cancers, medical surveillance artifact for prostate cancer, and immunosuppression for malignant melanoma and lung cancer. The large number and good prognoses of patients with chronic lymphocytic leukemia strongly influenced the pattern of second cancers when all leukemias were analyzed together; no evidence was found for an increased risk of second cancer in patients with acute lymphocytic leukemia. A disproportionate number of subsequent cancers, particularly those of the kidney and ureter, were diagnosed incidentally at autopsy. Patients with Hodgkin's disease displayed significant excesses of cancers of the buccal cavity and pharynx, lung, female breast, and thyroid. The latter 3 sites remained significantly elevated in long-term survivors (10 yr or more postdiagnosis), so that radiation therapy may have contributed to their development. Among persons with non-Hodgkin's lymphoma, cancers of the stomach, lung, brain, and connective tissue occurred excessively. The first 3 sites, plus cancers of the urinary bladder, remained elevated among long-term survivors. The brain cancer excess, not previously reported, may represent misclassification of central nervous system lymphoma. The risk of gastric cancer is reminiscent of similar findings in patients with both acquired and genetically determined immunodeficiency disorders. The alkylating agent, cyclophosphamide, used extensively in the treatment of non-Hodgkin's lymphoma, is known to cause bladder cancer in man.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Second cancer following lymphatic and hematopoietic cancers in Connecticut, 1935-82. 408 98

A brilliant, coarsely granular nuclear antigen was detected by anti-complement immunofluorescence in the nuclei of acute myeloid leukemia myeloblasts. Designated as LANA (leukemia-associated nuclear antigen), the reactivity differs from that of the Epstein-Barr-virus-determined nuclear antigen (EBNA) in immunological specificity and morphological appearance, although it is visualized by the same method. Serum from acute myeloid leukemia patients gave positive reactions in 73% of the cases. In acute lymphatic leukemia, chronic myeloid leukemia, chronic lymphatic leukemia, and Burkitt's lymphoma the sera were positive in 35, 14, 19, and 24%, respectively. Two of five polycythemia and two of eleven myeloma sera were also positive. Among 61 healthy controls, 58 were negative, whereas three showed a diffuse nuclear staining with a different pattern. Among 24 carcinoma patients, 18 were negative, whereas six gave a nuclear staining with a different, diffuse pattern. Sera from 20 patients who had recovered from infectious mononucleosis were all negative. In addition to the blasts of acute myeloid leukemia, a similar reactivity was seen with two Epstein-Barr virus DNA and EBNA-negative African lymphoma biopsies and in a short-lived tissue culture line derived from one of them. LANA could be a fetal or tissue-specific antigen, a virally determined antigen, or a specific form of anti-nuclear reactivity.
 ...
PMID:Human leukemia-associated anti-nuclear reactivity. 459 70


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>