Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphology, immunologic and functional properties of peripheral blood and bone marrow cells or cultured cells from 2 patients with clinically aggressive non-T, non-B lymphoma/leukemia are described. The leukemic cells possessed medium to large granules in the cytoplasm, antigens against CD38, CD2, CD25, OKIa1, CD16, TA-1, CD9, CD24 and NKH-1 (N901) monoclonal antibodies on their cell surface, and also showed a high natural killer (NK) activity. Phenotypically, the cells in these disorders were quite different from T gamma leukemia cells bearing Fc receptor or the traditionally reported NK leukemia cells possessing HNK-1 (Leu 7) antigens on their surface. In addition, these leukemias/lymphomas belonged to neither T- nor B-cell lineage, proved by studying clonal gene rearrangement for the T beta and T gamma receptor, and immunoglobulin. Hence, a quite interesting and important point, as suggested by our data, is that all our cases expressed an antigen for NKH-1 (N901), which is detectable on all NK cell surfaces and they lacked the antigen for Leu 7 (HNK-1), which is usually detected on the surface of leukemic NK cells. These facts indicate that we are dealing with a leukemic NK cell subset which is quite different from cells of all other reported cases of NK cell leukemias. We therefore concluded that such disorders with an aggressive clinical nature and a poor prognosis as in our cases belong to a new clinical entity originating from a portion of the NK cell subset.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aggressive natural killer cell leukemia/lymphoma with N901-positive surface phenotype: evidence for the existence of a third lineage in lymphoid cells. 246 36

A case of chronic lymphocytic leukemia (CLL) treated with chlorambucil, followed by the development of an acute monoblastic leukemia, is described. Cytofluorometric quantitative immunophenotype was determined during the blastic phase. Whereas small lymphocytes displayed a CD19+; CD24+; CD37+; CD5+ phenotype, the blastic population exhibited, besides CD13, CD14 and CD15 positivity, which is usually noted in such a monoblastic leukemia, definite CD9, CD10, CD22, CD24, CD37, CD5 and CD4 staining. Such results argue against a complete independence between the two clones, although their similarity could not be demonstrated.
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PMID:Acute monocytic leukemia with B cell markers expression following B chronic lymphocytic leukemia. 258 3

Two children with acute lymphoblastic leukemia (ALL) received autologous bone marrow transplantation (BMT) using remission bone marrow treated in vitro with the monoclonal antibodies, CD24 (BA-1), CD9 (BA-2) and CD10 (BA-3), and with rabbit complement. In one child with second remission ALL, hematopoietic recovery after BMT was prompt but, 81 days after BMT, isolated central nervous system (CNS) relapse occurred. Bone marrow relapse developed three months later, and she died 11 months after BMT. In patients with CNS leukemia prior to BMT, as in the present case, more intensive pretransplant CNS treatment and/or a conditioning regimen may reduce the risk of relapse. In the other patient, with primary refractory ALL in first remission, marrow reconstitution was slower. The patient developed interstitial pneumonitis with pleural effusion, and died 54 days after BMT. No infectious causes could be detected by culture or from serological studies of the pleural effusion. The rationale for applying autologous BMT to children with second remission ALL and first remission refractory ALL is discussed.
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PMID:Autologous bone marrow transplantation in acute lymphoblastic leukemia following in vitro treatment with monoclonal antibodies and with complement: analyses for two cases of failure. 303 35

Fresh bone marrow from 43 cases of myeloma and three cases of plasma cell leukaemia has been phenotyped both by indirect immune-rosetting and, on fixed cytospin preparations, by indirect immunofluorescence. Both clustered and unclustered B cell associated antibodies from the IIIrd International Workshop on Human Leucocyte Differentiation Antigens were used. The results confirm the lack of many pan-B antigens on the surface of myeloma plasma cells, i.e. CD19-23, 37, 39, w40. Strong surface reactivity is seen with CD38 antibodies and with one CD24 antibody (HB8). Weak reactions are sometimes obtained with CD9, 10 and 45R. On cytospin preparations CD37, 39 and w40 are sometimes weakly positive, and anti-rough endoplasmic reticulum antibodies are always strongly positive. Specific and surface-reacting antiplasma cell antibodies are still lacking.
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PMID:An analysis of myeloma plasma cell phenotype using antibodies defined at the IIIrd International Workshop on Human Leucocyte Differentiation Antigens. 304 3

A case of plasma cell leukaemia of non-producer type is described. The patient presented with typical clinical features of plasma cell myeloma, including multiple osteolytic lesions, hypercalcaemia, renal failure and reduced polyclonal immunoglobulins, except that M-component was not detected in either the serum or urine. Morphological examinations showed a plasmacytoid appearance of the neoplastic cells, while immunological studies failed to detect cytoplasmic immunoglobulin or secretory capacity. The surface phenotype of CD38+, PCA-1+, DR-, CD20-, CD24-, CD9-, CD10- and surface immunoglobulin- was compatible with mature plasma cells. Chromosomal analysis showed the 14q+ marker due to translocation (6;14) and deletion of the short arm of chromosome 1. Analysis of immunoglobulin genes revealed the presence of heavy chain gene rearrangement, but the light chain genes, both kappa and lambda, remained in germline configuration. Such defective immunoglobulin gene rearrangement may be responsible for the failure of immunoglobulin biosynthesis and secretion by the neoplastic plasma cells. Furthermore, it is suggested that the morphological and phenotypic development of B cells may not necessarily depend on immunoglobulin light chain gene rearrangement, and that the oncogenic event in myeloma may occur at an earlier stage of B cell differentiation.
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PMID:Plasma cell leukaemia of non-producer type with missing light chain gene rearrangement. 313 42

A 66-year-old male patient was admitted with dyspnea; physical examination revealed petechiae and systemic lymphadenopathy. Laboratory findings showed leukemia. The blasts in the peripheral blood were negative for cytochemical myeloperoxidase, and had condensed nuclear chromatin with a nucleolus. The histological diagnosis of the biopsied neck lymph node was lymphoblastic lymphoma. The leukemia cells expressed CD2, CD6, CD7, CD13low, CD56, beta chain of IL-2 receptorlow (IL-2R beta), and HLA-DR antigens, but not other pan-T (CD5, CD3, CD4, and CD8); pan-B (CD10, CD19, CD20, and CD24); natural killer (NK) (CD16, CD57); or myeloid (CD33) antigens. Electronmicroscopy revealed convoluted nuclei with conspicuous nucleoli and peripherally condensed heterochromatin. Membrane-bound granules containing an electron dense matrix were observed in the cytoplasm, indicating the NK cell nature of the neoplastic cells. While terminal deoxynucleotidyl transferase (TdT) and cytoplasmic CD3 were not detected by immunofluorescence on fixed smears, Northern blot analysis revealed the gene expression of CD3 epsilon, CD3 zeta, and TdT. Gene rearrangement analysis revealed that the beta, gamma, and delta chains of T-cell receptor (TCR) and immunoglobulin heavy chain (IgH) were of germline genotype. While the overall interpretation of the phenotype and genotype was difficult, the derivation of an immature stage of NK lineage was strongly suggested, based predominantly on the electronmicroscopic features. Despite initially successful chemotherapy, the patient died 14 months after initial presentation.
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PMID:Novel leukemic lymphoma with probable derivation from immature stage of natural killer (NK) lineage in an aged patient. 753 82

Murine AIDS (MAIDS) is induced by infection with the replication-defective virus (BM5def) component in the LP-BM5 murine leukemia virus (MuLV) mixture. The disease is characterized by polyclonally activated CD4+ T cells and B cells. It is known that BM5def is expressed at highest levels in B lymphocytes and that B cells serve as viral antigen-presenting cells. Full and sustained activation of CD4+ T cells against a conventional Ag usually requires both TCR and costimulating signals. Among various molecules known to provide costimulatory function, the expression of CD54 (ICAM-1) and CD11a/CD18 (LFA-1) on MAIDS B cells was increased, whereas that of CD2, heat-stable Ag (CD24), CD80 (B7-1), and CD86 (B7-2) was unchanged from normal. C57BL/6 mice depleted of both CD54 and CD11a expression as a result of chronic administration of mAb had developed no MAIDS at 4 wk and 8 wk after LP-BM5 MuLV infection. In addition, the proliferative response of B cells to mitogen was well conserved, whereas MAIDS-associated increases in serum Ig levels were inhibited. Replication of BM5def was suppressed markedly in infected mice treated with the CD54 and CD11a mAbs. These results suggest that the CD54/CD11a signal transduction pathway is a critical determinant of MAIDS development, and the lack of an immune response against viral Ag is enough to suppress BM5def replication and to prevent MAIDS.
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PMID:Rapid development of murine AIDS is dependent of signals provided by CD54 and CD11a. 760 73

Important insights into leukocyte differentiation and the cellular origin of leukemias have been achieved by the use of monoclonal antibodies for the detection of cellular antigens with impact on the diagnosis and classification of hematological malignancies. A successful rapid immunoenzymatic technique using application of microwave irradiation (MIWI) on bone marrow cells of various children with ALL is described. The MIWI-stimulated immunotyping of acute leukemia cells with a panel of monoclonal antibodies against differentiation antigens (i.e. CD2, CD7, CD10, CD19, CD20, CD24, HLA-DR and TdT) has been compared with the conventional APAAP procedure developed by Mason et al 1983. The commercial microwave oven we used operates at 2.45 GHz. Fifteen sec irradiation at 350 W during all incubation steps produced excellent color reactions with Fast Red TR and Fast Blue BB similar to the conventional immunoenzymatic method. The results so far have demonstrated that the application of the MIWI-technique eliminates the need for long incubation periods without loss of sensitivity. With this technique an immunological diagnosis of childhood leukemia cells is possible using air dried smears in an microwave oven within 30 minutes.
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PMID:Rapid immunodiagnosis of childhood leukemia using microwave-stimulated APAAP-complex system. 765 5

A correlation between CD24 expression and higher intrinsic radiation sensitivity has been described in B-lineage acute lymphoblastic leukaemia (B-ALL). We recently identified the SCLC surface antigen Cluster-4 (CL-4) to be identical to the B cell differentiation marker CD24, except for one amino acid residue. The CD24/CL-4 antigen is highly expressed on SCLC, but rarely on NSCLC cells. In order to investigate the influence of the expression of CD24/CL-4 on the radiation sensitivity in a non-leukaemic cell system, sublines of the human SCLC H249 cell line transfected with mutated ras oncogene, and differing in their CD24/CL-4 expression, were studied. In addition, we stably transfected the NSCLC A125 cell line and the mouse fibroblast NIH3T3 cell line with the CL-4 cDNA. The differential expression of CD24/CL-4 on the cells had no influence on morphology, proliferation and cloning efficiency. Radiation studies were done with cells in exponential growth phase. In the highly resistant NSCLC A125 cells no difference in radioresponsiveness was observed between CD24/CL-4 expressing and non-expressing cells. In the rather radiosensitive cells, similar responses to radiation were observed between CD24/CL-4 expressing and non-expressing SCLC H249-ras cells, whereas the CL-4 transfected NIH3T3 mouse fibroblasts showed a substantially higher radioresistance than the CD24/CL-4 non-expressing control cells. In conclusion, the correlation between CD24/CL-4 expression and radiation sensitivity is controversial and depends on the cell type.
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PMID:Radiation studies on B cell differentiation marker CD24/SCLC Cluster-4 antigen expressing and non-expressing lung cancer cell lines and mouse fibroblasts. 765 46

In order to define better the cytological and clinical features of atypical B-cell chronic lymphocytic leukaemia (B-CLL) with t(11:14)(q13;q32), sequential morphologic immunological and cytogenetic studies were performed in seven patients belonging to a series of 72 consecutive cases presenting with a diagnosis of CLL or atypical CLL according to the FAB criteria. Cytologic diagnosis in these seven patients with t(11;14) was typical CLL in two cases presenting with < 10% large lymphocytes (LL) and prolymphocytes (PL) and atypical CLL in five cases in which LL and PL comprised between 10% and 55%. The diagnosis was supported by histologic findings on bone marrow biopsy (five cases) or splenectomy specimens (two cases). A progressive increase of peripheral LL and PL was observed, resulting in a switch of FAB diagnosis over a 6-60-month period from typical CLL into atypical CLL in two cases and from atypical CLL into prolymphocytic leukaemia in five cases. Immunophenotyping showed a mature B-cell phenotype with CD19, CD22, CD24 positivity and CD10 negativity in all patients. A bright-staining pattern for surface immunoglobulins (SIg) was detected in 6/7 cases, CD5 positivity in 6/7 cases, and CD23 positivity in 1/7 cases. The FMC-7 monoclonal antibody was positive in > 40% cells in 5/6 cases. Chromosome changes in addition to t(11;14) were seen in five cases; in two cases unbalanced translocations involving the 3q21 chromosome region, resulting in partial trisomy for the long arm of chromosome 3, were detected early in the course of the disease. Karyotype evolution that was associated with disease progression occurred in 3/6 assessable patients. Comparison of these findings with similar data from 65 B-CLL patients without t(11:14) showed that atypical morphology, switch of FAB diagnosis during the course of the disease, and karyotype evolution were more frequently seen in cases with t(11;14) (5/7 v 15/65 cases, P = 0.015, 7/7 v 7/65 cases, P < 0.0001, and 3/6 v 5/45 assessable cases, P = 0.04, respectively). The frequency of positivity for CD23 and bright SIg staining differed significantly in the two groups. It is concluded that t(11;14) identifies a cytologically atypical subset of B-CLL, characterized by frequent cytologic and cytogenetic evolution and by a distinct immunological profile, sharing some biological features with mantle cell lymphoma.
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PMID:Atypical chronic lymphocytic leukaemia with t(11;14)(q13;q32): karyotype evolution and prolymphocytic transformation. 779 64


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