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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical, pathologic, immunologic and electron microscopic findings in three cases of young men who had T cell leukemia and lymphoma are presented. The disease in this older age group appears to have the same characteristics as that seen in children. It is an aggressive, rapidly fatal disease with a poor response to the usual chemotherapeutic regimens for acute leukemia or poorly differentiated lymphocytic lymphoma, with which this T cell disorder is frequently grouped. An example of Burkitt's lymphoma in another young man is presented briefly to illustrate the clinical, morphologic and immunologic similarities to and differences from an aggressive B cell lymphoma.
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PMID:T cell leukemia--lymphoma in young adults. 14 86

Human B cell lymphoma and murine T cell leukemia can be initiated by several agents. The present paper formulates some thoughts on the role of cytogenetic changes in the subsequent neoplastic process. Initiation creates long-lived preneoplastic cells. In some respects, they are comparable to in vitro-transformed ("immortalized") cell lines that maintain a diploid karyotype and are not tumorigenic in vivo. The development of a tumorigenic ("autonomous") clone is dependent on additional changes at the genetic level. In human B and murine T cell lymphoma, there are characteristic nonrandom chromosomal changes. The 14q+ marker appears to play a key role in human B cell lymphomas. The reciprocal 8;14 translocation in Burkitt lymphoma is a specialized subclass within this category. In murine T cell leukemia, trisomy 15 is the predominant change. The clustering of these nonrandom changes to tumors derived from a certain cell type rather than to tumors induced by a given etiological agent has important implications for the understanding of the genetic control of cellular responsiveness to growth-regulating forces in vivo.
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PMID:Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution. 22 25

To determine if cell membrane phenotypes change under the selective pressures of therapy we have conducted a prospective study of 54 children with lymphoid malignancies of T-like, B-like, common, and null cell types. Membrane phenotypes were determined at diagnosis in all patients and again 1-24 mo later in 18 children who either failed induction therapy or had one or more relapses. In 7 patients the cells tested were from relapse sites different than those of the original diagnoses. The data indicate that at relapse most children with lymphoid neoplasias had the same cell membrane phenotype as established at diagnosis, and suggest that the site of relapse did not affect the expression of cell surface markers. However, there were three exceptions: (1) a child initially diagnosed as having null cell acute lymphocytic leukemia had 90% T-antigen-positive blasts in her second-relapse bone marrow; (2) only membrane IgM was present on relapse blasts from a B-cell lymphoma that had both membrane IgM and IgD before initiation of treatment; (3) at diagnosis, bone marrow blasts from a child with T-like leukemia expressed both T antigen and E receptors, but at relapse, bone marrow and pleural fluid cells expressed only T antigens. We postulate that these phenotype shifts may be due to selective effects of therapy on cells at different stages of differentiattion.
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PMID:Shifts in expression of cell membrane phenotypes in childhood lymphoid malignancies at relapse. 28 8

Prolymphocytic leukaemia occurred in two women aged 75 and 57 years, respectively. In both instances the lymphatic cells fulfilled the morphological criteria of the disease picture. In one patient the disease was characterised by immunological and physical methods as being a B-cell lymphoma, in the other a T-cell lymphoma. Acid phosphatase was of special significance among cytochemical studies. While the patient with the T-cell lymphoma died after three months, the one with B-cell lymphoma is still alive 16 months later. Splenectomy resulted in marked improvement in the latter patient's condition and may turn out to be the treatment of choice in prolymphocytic leukaemia.
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PMID:[Prolymphocytic leukaemia (author's transl)]. 31 Mar 85

318 cases of 682 malignant B-cell lymphomas reacted positive for cIg. 66 of them showed Dutcher bodies (DB). DB were found in about 22% of plasmacytomas, 17% of immunocytomas, and in 7.5% of follicular lymphomas and polymorphic centroblastomas, respectively. Regarding only the cIg-positive cases, DB occurred in about 27% of immunocytomas, 20% of follicular lymphomas and 18% of polymorphic centroblastomas. A single case of prolymphocytic leukaemia, centrocytoma, monomorphic centroblastoma, and immunoblastoma each showed also DB. Usually, DB-positive plasmacytomas showed kappa, alpha, and J-chains. The remaining lymphomas mostly expressed kappa, my, and J-chains. In conclusion Dutcher bodies can occur with any cIg-producing B-cell lymphoma. They are not limited to immunocytomas.
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PMID:[Morphological and immunohistochemical findings on the frequency of intranuclear immunoglobulin inclusions (Dutcher bodies) in malignant B-cell lymphomas]. 128 64

Human Immunodeficiency Virus type 1 (HIV-1) infects CD4+ T lymphocytes and various other cell types, including B cells. Since HIV-1 seropositive individuals have high numbers of B cells carrying Epstein-Barr Virus (EBV), and are at high risk for development of EBV-associated lymphoproliferative diseases, we studied the mode of HIV-1 infection in four EBV-positive lymphoblastoid B-cell lines (LCLs) as well as some molecular and biological features of the B cells infected by both viruses. We found that LCL cells were successfully infected in vitro by HIV-1, despite the lack of CD4 antigen expression on the cell membrane. LCL cells displayed a persistent, productive, and non-cytopathic infection. Moreover, HIV-1 infection induced reactivation of EBV latent genomes in one cell line. Following HIV-1 infection, LCL cells showed a decrease in B-cell activation markers CD23 and CD39, and an increase in CD10 immature B-cell antigen. Not all cells in each LCL expressed HIV-1 antigens, but all CD10+ cells also co-expressed the HIV-1 envelope protein gp 120. Furthermore, HIV-1 infected LCL cells grew as disperse suspensions, and formed more agar colonies than control, non-HIV-1-infected LCLs. These findings raise the possibility that HIV-1 might play a role in EBV reactivation, and in B-cell lymphoma pathogenesis in AIDS patients.
Leukemia 1992
PMID:Morphological and phenotypical changes in EBV positive lymphoblastoid cells infected by HIV-1. 131 75

We recently began a cytogenetic and molecular study of nondisjunction in leukemic Down syndrome individuals to determine whether the mechanism by which the extra chromosome 21 originates predisposes the individual to leukemia. In the present report, we summarize our observations on 18 patients with trisomy 21 and acute or transient leukemia, including 11 patients with acute lymphocytic leukemia, three with acute myeloid leukemia, one with B-cell lymphoma, one with acute megakaryoblastic leukemia, and two with transient leukemia. Results of DNA marker studies of the parental origin of the extra chromosome 21 indicated that 16 of the 18 cases (89%) were maternally derived, a percentage similar to that seen among nonleukemic Down syndrome patients. We noted that most leukemic Down syndrome patients had one locus or more in which parental heterozygosity was maintained in the trisomic individual, indicating a meiotic rather than a mitotic origin for the trisomy.
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PMID:Characterization and molecular analysis of nondisjunction in 18 cases of trisomy 21 and leukemia. 138 63

The B-cell lymphoma/leukemia oncogene bcl-2 takes part in crucial regulatory events in B-cell maturation and differentiation. The reciprocal chromosomal translocation t(14;18), leading to overexpression of this oncogene, can be found in the majority of follicular lymphomas and much less frequently in B-cell leukemias and diffuse lymphomas. We have studied the expression of this protein in different subtypes of Hodgkin's disease using monoclonal antibodies directed against a formalin-resistant epitope of the bcl-2 protein and also have investigated these cases by polymerase chain reaction for evidence of the t(14;18) translocation. We were particularly interested to determine whether nodular paragranuloma (lymphocyte-predominant, nodular), which differs from other subtypes of Hodgkin's disease by virtue of the B-cell nature of its malignant cell population, is characterized by expression of the bcl-2 protein. Our data indicate that only a small number of nodular paragranulomas express the bcl-2 protein and that the expression is not specific for this type of Hodgkin's disease. In a smaller number of cases this expression of bcl-2 could be explained by the presence of the translocation t(14;18).
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PMID:Expression of the bcl-2 oncogene product and chromosomal translocation t(14;18) in Hodgkin's disease. 142 49

A strategy is described for production of monoclonal antibodies against recombinant proteins that are produced using the baculovirus expression system and that requires no prior purification of the protein of interest. Crude lysates prepared from cultured Sf9 insect cells infected with recombinant or control baculoviruses are absorbed to nitrocellulose filters and used in a dot-immunobinding assay for screening hybridomas. The monoclonal antibody-producing hybridomas are derived by immunization of mice with a synthetic peptide corresponding to a hydrophilic region in the recombinant protein of interest. By using the baculovirus-produced recombinant protein as the screening antigen and by comparing antibody binding to filters containing control Sf9 lysates, hybridomas are identified that produce monoclonal antibodies with specific reactivity for the recombinant protein of interest and that can then subsequently be used to assist in the large-scale purification of the recombinant protein from baculovirus-infected cells. We applied this method to recombinant 26-kDa human Bcl-2 (B-cell lymphoma/leukemia-2), an integral membrane oncoprotein that regulates programmed cell death ("apoptosis") in hematolymphoid cells through unknown mechanisms. Two mouse monoclonal antibodies were produced that specifically bound the recombinant Bcl-2 baculoprotein in both solution and solid-phase assays.
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PMID:A strategy for generating monoclonal antibodies against recombinant baculovirus-produced proteins: application to the Bcl-2 oncoprotein. 144 60

The abnormal organization of actin-containing microfilaments and vimentin-containing intermediate filaments in neoplastic lymphocytes of T and B cell origin has been described. We investigated microtubules of pathologic cells from 34 lymphoid malignancies, by immunofluorescence microscopy, using monoclonal tubulin antibody. In most cases, apart from two cases of lymphoma, one T cell lymphoma and one B cell lymphoma, interphase leukemia cells, lymphoma cells, and myeloma cells were shown to contain well-organized microtubules which were associated with a microtubule organization center at one end. In the cells of a patient with T cell lymphoma, although microtubules were not visible in the lymphoma cells from lymph nodes, they became visible after 72 hours in culture with concanavalin A (Con A) and interferon alpha. Cap formation was observed with antitubulin monoclonal antibody in the peripheral blood lymphocytes from a chronic lymphocytic leukemia patient, but well-developed microtubules were observed on other occasions in the same patient. There were no obvious structural differences between microtubules in T and B cell lymphoid malignancies, but leukemia cells and lymphoma cells with irregularly shaped nuclei, such as adult T cell leukemia cells and B cell lymphoma cells with cleaved nuclei, had complicated microtubules surrounding their irregular nuclei. In general, after blastogenic stimuli with phytohemagglutinin-P (PHA-P), Con A, and pokeweed mitogen (PWM), the development of the microtubules was proportional to the incorporation of 3H thymidine (3H-TDR). In most cases, after incubation with granulocyte colony-stimulating factor (G-CSF) and interferon alpha, the number of intact cells decreased and the number of degenerated cells increased, but the intact cells had intact microtubules.
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PMID:Microtubule organization in lymphoid malignancies. 145 Apr 24


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