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

A leukaemic phase is uncommon in large cell lymphoma, particularly at presentation of the disease, and very few cases have been reported since immunological markers became available. We have studied 24 cases presenting over a period of 15 years. 16 were B-lineage and eight T-lineage. In five patients the large cell lymphoma represented a transformation of a preceding low grade, small cell lymphoproliferative disease. Three other patients with T-lineage large cell lymphoma presented with skin infiltration (two cases) or lymphoma-associated nephrotic syndrome (one case) 3-9 months before leukaemia occurred. The other 16 patients (12 B-lineage and four T-lineage) presented with de novo large cell leukaemia/lymphoma. With the exception of skin infiltration, clinical features did not differ between T and B-lineage cases. Prognosis was generally poor although a minority of patients lived 1-2 years. Median survival was 7 months. In the B-cell lymphomas immunological markers were those expected but among the T-cell cases there were many unusual immunophenotypes with frequent failure to express markers which are usually positive in peripheral T cells. Without the availability of immunological markers diagnosis would have been difficult, with acute myeloid leukaemia being the most important differential diagnosis. T-lineage and B-lineage cases could not be distinguished on cytological features. In the majority of cases the cells were very pleomorphic with nuclear lobulation, prominent nucleoli and marked cytoplasmic basophilia being commonly observed. Marked nuclear lobulation was not confined to T-lineage cases but was seen also in seven of 12 cases of de novo B-lineage leukaemia/lymphoma; it was readily apparent in histological sections and on ultrastructural examination.
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PMID:Leukaemia as a manifestation of large cell lymphoma. 201 54

Southern blot analysis was employed to analyze the structural alterations of the c-myc oncogene in genomic DNA derived from tumor specimens of 35 adults with pathologically classified and immunophenotyped non-AIDS-related, non-Hodgkin's lymphoma in Japan. In this study, seven cases (20%), including one peripheral T-cell lymphoma and six B-cell lymphomas of various histological types, were demonstrated to have additional c-myc fragments. An interesting feature is that c-myc rearrangements were found in three out of eight primary gastrointestinal lymphomas. Analyses with several restriction enzymes revealed that the breakpoints in these cases were clustered in a region spanning the first exon, first intron and nearby 5'-flanking sequences of the c-myc gene, suggesting that the alteration of this region may represent an important molecular event in activating the oncogenic potential of the c-myc gene.
Leukemia 1991 Jun
PMID:Genomic rearrangement of the c-myc proto-oncogene in non-AIDS-related lymphoma in Japan. 205 71

Split-dose X-irradiation efficiently induced Thy-1-positive thymic lymphomas (80%) in intact NFS mice within 12 months after irradiation. A high incidence (67%) of nonthymic lymphomas and leukemias was observed in the thymectomized NFS mice. Development of nonthymic lymphomas and leukemias in these mice started about 2 months later than that of thymic lymphomas and increased significantly 10 months onward after the last irradiation, when the development of thymic lymphomas in intact mice had already come to an end. These nonthymic lymphomas and leukemias involved predominantly the spleen and the mesenteric lymph nodes. Twelve out of 18 lymphomas and leukemias were examined immunocytologically. All of these tumors except one were diagnosed as lymphomas including one plasmacytoma. One case was diagnosed as myelomonocytic leukemia because the leukemic cells were highly positive for nonspecific esterase and negative for chrolacetate esterase. All lymphomas tested were negative for thy-1.2, and five of them expressed surface immunoglobulins. From these results, nonthymic lymphomas developed in thymectomized and X-irradiated NFS mice were classified as B-cell lymphomas probably including non-T/non-B cell lymphomas. Present findings demonstrated that a low incidence of nonthymic lymphomas in intact NFS mice exposed to split-dose X-irradiation should be ascribed to a longer latency since most of the mice died of thymic lymphomas prior to the development of overt nonthymic lymphomas.
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PMID:Development of nonthymic lymphomas in thymectomized NFS mice exposed to split-dose X-irradiation. 209 58

DBA/2 mice carry a single endogenous ecotropic murine leukemia provirus, Emv-3, that is replication defective because of a single nucleotide substitution in codon 3 of p15gag. However, when weanling DBA/2 mice are treated percutaneously with 7,12-dimethylbenz(a)anthracene (DMBA), ecotropic virus replication is induced in almost all of the treated mice. Previous studies have shown that this induction results from DMBA-induced reverse mutations in codon 3 that allow efficient virus replication. In addition to ecotropic virus replication, DMBA also induces lymphomas in 100% of the treated mice. These results have raised the possibility that ecotropic virus replication is causally associated with the development of lymphomas in DBA/2 mice, perhaps via the insertional activation or mutation of cellular proto-oncogenes. To test this possibility, we compared lymphoma incidence after percutaneous DMBA treatment in DBA/2J-dv/dv mice, which carry two copies of Emv-3, with lymphoma incidence in DBA/2J-d+18J/d+18J mice, which lost both copies of Emv-3 by homologous recombination involving the long terminal repeat sequences. The results of this study conclusively demonstrated that Emv-3 is not causally associated with the development of DMBA-induced lymphomas in DBA/2J mice. Interestingly, histopathological and molecular analyses of the lymphomas indicated that the majority of the lymphomas in both strains of mice were of the B-cell lineage. This was unanticipated, since the majority of chemically induced lymphomas in other inbred strains are thymic lymphomas, presumably of the T-cell lineage. Thus, DBA/2 mice appear to present a unique model system for the investigation of chemically induced B-cell lymphomas in mice.
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PMID:Lack of ecotropic virus involvement in induction of lymphomas in DBA/2J mice by 7,12-dimethylbenz(a)anthracene. 216 96

Antiidiotype (Id) antibodies identify unique determinants within the surface immunoglobulin (Ig) that are present on B-cell tumors. Anti-Ids have been used for diagnosis and therapy of B-cell lymphoma and leukemia. A panel of 29 anti-Id monoclonal antibodies (MoAbs) that recognize shared idiotypes (SIds) on B-cell lymphomas was tested for reactivity with both B-cell leukemias and lymphomas. Ten of 40 (25%) cases of chronic lymphocytic leukemia (CLL) reacted with at least one of the 29 anti-SId MoAbs. Three cases reacted with more than one anti-SId MoAb, but there was no repetitive pattern of a single anti-SId MoAb reacting with a large proportion of CLL cases. In contrast, for B-cell lymphoma, in which 11 of 31 (36%) cases reacted, one anti-SId (B4-1) reacted with five of the positive cases; all were diffuse histology. Restricted anti-SId reactivity may lead to important insights into the etiology of certain B-cell lymphomas. In addition, these anti-SIds may obviate the need to develop "tailor-made" antibodies for individual patients.
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PMID:Shared idiotype expression by chronic lymphocytic leukemia and B-cell lymphoma. 222 30

Immunophenotypic analysis on 34 cases of T-cell malignancies using monoclonal antibodies against T-cell receptors (TCR) revealed 25 cases of alpha beta-type and two of gamma delta-type. The two patients with gamma delta-type showed cutaneous involvement of tumor cells. Immunoblastic lymphadenopathy (IBL)-like T-cell lymphoma is divided into three histologic categories; inconspicuous type, patchy type and diffuse type. DNA hybridization analysis revealed that 11 of 16 cases showed clonal rearrangement of TCR beta-chain gene without rearrangement of immunoglobulin heavy chain gene, providing strong evidence for clonal proliferation of T-cells. Among 185 patients with adult T-cell leukemia (ATL), 18 cases (9.7%) were found not to be associated with human T-cell leukemia virus type I (HTLV-I). They consisted of 10 of acute type, five of chronic type, two of lymphoma type and one of smoldering type, indicating a diversity in clinical features. Two Japanese patients with ATL developed secondary monoclonal B-cell lymphomas of diffuse, large cell, non-Burkitt type. They were seropositive for HTLV-I but negative for human immunodeficiency virus (HIV). They also suffered from pulmonary tuberculosis, and one from adenovirus type 11-induced hemorrhagic cystitis, indicating an immunodeficient state. Epstein-Barr virus genome was found in lymphoma cells from one patient. It is suggested that opportunistic B-cell lymphomas may occur in the immunodeficient stage of ATL.
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PMID:[Recent advances in clinical research on T-cell lymphoma]. 239 7

Several monoclonal antibodies (MAbs) directed to blood group P1 (Gal alpha 1-4Gal beta 1-4GlcNAc beta-O) and Pk (Gal alpha 1-4Gal beta 1-4Glc beta-O) determinants were produced with high efficiency by using synthetic neoglycoproteins as immunogens. The specificity of IgM and IgG1 MAbs was characterized by binding to defined oligosaccharides and glycoconjugates. Antibodies that bound equally well to P1 and Pk determinants and to Gal alpha 1-4Gal beta 1-O-derivatives were obtained, together with others that showed selective recognition of the entire trisaccharide chain. Selected antibodies were shown to be useful as reagents for detection of the blood group P antigens in glycolipid extracts of erythrocytes and on the surface of erythrocytes of different P phenotypes, demonstrated both by radioimmune assays and hemagglutination. Six IgM MAbs directed to the Pk determinant bound selectively to Burkitt lymphoma cells and 2 of these antibodies (424/3D9 and 424/6A2) could be used as auxiliary reagents in immunofluorescence for diagnosis and classification of B-cell lymphomas and leukemias using flow cytometric analysis. Eight normal individuals and 37 patients with lymphoma or leukemia were studied. Tumor cells of 2/2 patients with "Burkitt-like" lymphoma, 1 patient with centroblastic lymphoma and 2 patients with acute leukemia were strongly stained for the Pk antigen. The staining patterns for differentiation markers classified the tumor cells to a developmental stage closely related to the Burkitt cell type.
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PMID:Monoclonal antibodies produced by immunization with neoglycoproteins containing Gal alpha 1-4Gal beta 1-4Glc beta-O and Gal alpha 1-4Gal beta 1-4GlcNAc beta-O residues: useful immunochemical and cytochemical reagents for blood group P antigens and a differentiation marker in Burkitt lymphoma and other B-cell malignancies. 245 94

In a series of 139 spleens involved by non-Hodgkin's lymphoma, we found that each type of lymphoma (as classified according to the Kiel classification) has a specific pattern of infiltration in the red and white pulp. Tumor infiltration in preexistent follicles was not a feature of B-cell lymphomas, but tumor nodules were found in the red pulp nonfiltering areas in cases of immunocytoma (small lymphocytic plasmacytoid) and centroblastic-centrocytic lymphoma (follicle center-cell lymphoma). B-chronic lymphocytic leukemia and centrocytic-centroblastic lymphoma were located along central arteries of T-cell areas. T-cell areas were infiltrated by B-prolymphocytic leukemia, immunocytoma, centrocytic lymphoma (lymphocytic lymphoma of intermediate differentiation), and T-cell lymphoma/leukemia. The red pulp showed diffuse involvement in leukemic cases. Additionally, there was pericapillary growth in all cases of low-grade B-cell lymphoma. The findings, which are related to the physiological counterparts of the lymphoma cells, contribute to our knowledge of the routes of circulation as well as the homing areas of lymphocytes in the human spleen.
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PMID:The distribution of non-Hodgkin's lymphoma in the lymphoid compartments of the human spleen. 250 66

Abelson murine leukemia virus (A-MuLV) can induce pre-B- or T-cell lymphomas (thymomas) in mice depending on the route and time of injection. Previous studies have shown that the choice of the helper virus used to rescue A-MuLV greatly influences its ability to induce pre-B-cell lymphomas. In this study, we investigated the role of the helper virus in A-MuLV-induced thymomas. A-MuLV rescued with the helper Moloney MuLV, BALB/c endogenous N-tropic MuLV, and two chimeric MuLVs derived from these two parents were injected intrathymically in young adult NIH Swiss mice. All four A-MuLV pseudotypes were found to be equally efficient in the induction of thymomas, whereas drastic differences were observed in their pre-B-cell lymphomagenic potential. Thymoma induction by A-MuLV was independent of the replication potential of the helper virus in the thymus, and no helper proviral sequences could be detected in the majority of thymomas induced by A-MuLV rescued with parental BALB/c endogenous or chimeric MuLVs. In the thymomas in which helper proviruses were present, none of them were found integrated in the Ahi-1 region, a common proviral integration site found in A-MuLV-induced pre-B-cell lymphomas (Y. Poirer, C. Kozak, and P. Jolicoeur, J. Virol. 62:3985-3992, 1988). In addition, helper-free stocks of A-MuLV were found to be as lymphomagneic as other pseudotypes in inducing thymomas after intrathymic inoculation, in contrast to their inability to induce pre-B-cell lymphomas when injected intraperitoneally in newborn mice. Restriction enzyme analysis revealed one to three A-MuLV proviruses in each thymoma, indicating the oligoclonality of these tumors. Analysis of the immunoglobulin and T-cell receptor loci confirmed that the major population of cells of these primary thymomas belongs to the T-cell lineage. Together, these results indicate that the helper virus has no effect in the induction of A-MuLV-induced T-cell lymphomas, in contrast to its important role in the induction of A-MuLV-induced pre-B-cell lymphomas. Our data also revealed distinct biological requirements for transformation of these two target cells by v-abl.
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PMID:Distinct helper virus requirements for Abelson murine leukemia virus-induced pre-B- and T-cell lymphomas. 253 5

We performed a cytogenetic study on 16 murine mature B-cell lymphomas and 10 T-cell lymphomas, using G-banding techniques. All tumors, with the exception of 3 spontaneous B-cell tumors, were induced by various slowly transforming murine leukemia viruses (MuLV). Metaphases were obtained from primary (10 B-cell tumors) and first or second transplant generation lymphomas (6 B-cell and 10 T-cell tumors), all of which were well characterized with respect to phenotypic, histologic and genotypic features. In the T-cell tumors we found relatively simple karyotypic abnormalities, including various numerical aberrations, such as trisomy 15, in line with many earlier reports. However, the majority of B-cell tumors showed a great variety of both structural and numerical chromosomal anomalies. Three B-cell lymphomas had an apparently normal karyotype. No single cytogenetic abnormality occurred commonly in the B-cell lymphomas, but some structural abnormalities were found in more than one stemline, in particular, ins (II) (A1; A2) in 3 tumors, and deletions involving the D-region of chromosome 14 in 3 other lymphomas. These cytogenetic results clearly indicate that the pathogenic mechanisms involved in MuLV-induced (long latency) B-cell lymphomagenesis and (short latency) T-cell lymphomagenesis differ considerably.
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PMID:Distinct chromosomal abnormalities in murine leukemia virus-induced T- and B-cell lymphomas. 254 44


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