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

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

The pattern of 115 cases of malignant lymphomas diagnosed in the years 1979-1987 is presented using the updated Kiel's classification for non Hodgkin's lymphomas and after application of monoclonal antibodies L 26 and UCHL1 for the identification of B and T lymphocytes. Ninety-six cases (83.5%) were non Hodgkin's lymphomas and 19 cases (16.5%) Hodgkin's disease. Among non Hodgkin's lymphomas, B-cell lymphomas were predominant with a total number of 91 cases (94.8%). An analysis of B-cell lymphomas showed the following relevant features: a high frequency of lymphoplasmacytic/oid immunocytoma, a low frequency of Burkitt's lymphoma with a predominance of abdominal localisations, a high frequency of extranodal lymphomas (47.3%) and high grade lymphomas (48.4%); a 65% increase in high grade and extranodal lymphomas and a 76% increase in Burkitt's lymphomas and immunoblastic lymphomas in the period 1984-87 compared to the period 1979-83. For T-cell lymphomas, relevant features were the presence of one case of pleomorphic T-large cell lymphoma or adult T-cell leukemia-lymphoma and the fact that four out of five cases were large cell (high grade) lymphomas. More than 50% (57.9%) of Hodgkin's disease were of mixed cellularity type, only 15.8% being of nodular sclerosing type. The disease seemed to affect adolescents and young adults, more than 80% (83.3%) being aged 15-40 years. These features are compared to those observed by other authors and possible pathogenetic mechanisms are discussed.
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PMID:Pattern of malignant lymphomas in Rwanda. 130 35

Lymphocytes leave the blood via post-capillary venules by binding initially to their specialized endothelium. CD44 is a 80-90 kDa hyaluronate-binding glycoprotein involved in binding to endothelium of high endothelial venules (HEV). LECAM-1 is a 75-85 kDa glycoprotein with lectin activity interacting with human peripheral lymph node vascular addressin (PNAd) on HEV. This immunohistochemical study shows that CD44 and LECAM-1 are essentially coordinately expressed on B-lymphocytes. The mode and level of CD44/LECAM-1 expression dissect the peripheral B-cell development into stages that are closely linked to morphologically defined B-cell compartments. Although statistically correlated in B-cell leukaemias (p < 0.0009) and extranodal B-cell lymphomas (p < 0.003), expression of both molecules was less stringently coordinated in 127 B-cell neoplasms examined. B-cell chronic lymphocytic leukaemia, hairy cell leukaemia and mantle zone lymphoma were CD44/LECAM-1 positive, thus corresponding to their reactive counterparts. Correspondingly, follicular centre cell-derived lymphomas were devoid of both markers. Conversely, CD44 and LEC-AM-1 were infrequently detectable in extranodal malignant B-cell neoplasms, irrespective of their maturational state. Presence versus absence of CD44 and LECAM-1, alone or together, determined neither the leukaemic versus aleukaemic state nor the nodal versus extranodal tumour-forming phenotype of a B-cell tumour.
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PMID:Venular endothelium binding molecules CD44 and LECAM-1 in normal and malignant B-cell populations. A comparative study. 138 25

ABL-MYC, a murine retrovirus that encodes the v-abl and c-myc oncogenes, was constructed from Abelson murine leukemia virus (A-MuLV) in order to assess the biological consequences of co-expression of these genes in lymphoid cells. When inoculated into mice this retrovirus induced plasmacytomas in up to 100% of infected mice and less frequently induced pre-B lymphomas. Both tumor types contained genome-length proviruses in one or a few chromosomal locations, were mono- or oligoclonal as judged by immunoglobulin gene rearrangement and had unrearranged endogenous c-myc loci. The type of tumor induced depended upon the age and strain of mouse, and whether helper virus was present in the inoculated virus pool. ABL-MYC induced plasmacytomas with or without helper virus, with or without pretreatment of the mice with pristane, and in strains of mice resistant to pristane-induced plasmacytomas. Pristane treatment prior to ABL-MYC infection shortened the latent period of plasmacytomagenesis and produced mostly IgM-secreting tumors rather than IgA-secreting tumors, which predominantly arose in the absence of pristane. Control viruses for ABL-MYC with either a deletion in v-abl or a frameshift mutation in c-myc caused predominantly monocyte/macrophage tumors and pre-B-cell lymphomas respectively. Histopathological analysis of ABL-MYC-infected mice showed foci of transformed plasma cells as early as 14 days after infection. These results indicate that v-abl and c-myc act synergistically to transform mature B cells with high efficiency.
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PMID:A retrovirus that expresses v-abl and c-myc oncogenes rapidly induces plasmacytomas. 156 79

Immunoprecipitation of radioiodinated hairy cell leukaemia (HCL) cell lysates with monoclonal antibody (MoAb) HML-1, originally reported to recognize intraepithelial T cells, and with MoAb B-ly7, originally reported to react with HCL, led to identical biochemical characteristics. In SDS-PAGE under reducing conditions, a major band of 143 kDa, a broad band ranging from 112 to 122 kDa, and two additional faint bands of 175 and 100 kDa could be determined. Deglycosylation of N-linked sugar moieties by treatment of immunoprecipitates with endoglycosidases indicated that the two main protein cores of the antigen are predominantly if not exclusively glycosylated by complex and hybrid types of oligosaccharide chains. Competitive binding inhibition demonstrated that both MoAb are directed against different epitopes. Immunohistochemically, the staining patterns obtained with both MoAb in normal tissues, in T- and B-cell lymphomas, and in HCL were identical except for a single case of HCL which was HML-1-/B-ly-7+. We conclude that MoAb HML-1 and B-ly7 recognize the same antigen.
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PMID:Identity of HML-1 antigen on intestinal intraepithelial T cells and of B-ly7 antigen on hairy cell leukaemia. 169

The Cas-Br-E murine leukemia virus is a nondefective retrovirus that induces non-T-, non-B-cell lymphomas in susceptible NIH/Swiss mice. By using a DNA probe derived from Cas-Br-E provirus-flanking sequences, we identified a DNA region, originally called Sic-1, rearranged in 16 of 24 tumors analyzed (67%). All proviruses were integrated in a DNA segment smaller than 100 bp and were in the same 5'-to-3' orientation. Ecotropic as well as mink cell focus-forming virus types were found integrated in that specific DNA region. On the basis of Southern blot analysis of somatic cell hybrids and progeny of an interspecies backcross, the Sic-1 region was localized on mouse chromosome 9 near the previously described proto-oncogenes or common viral integration sites: Ets-1, Cbl-2, Tpl-1, and Fli-1. Restriction map analysis shows that this region is identical to the Fli-1 locus identified in Friend murine leukemia virus-induced erythroleukemia cell lines and thus may contain sequences also responsible for the development of mouse non-T-, non-B-cell lymphomas.
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PMID:Identification of a common viral integration region in Cas-Br-E murine leukemia virus-induced non-T-, non-B-cell lymphomas. 184 10

A study was conducted to evaluate the usefulness of paraffin-immunohistochemistry for histopathological classification of non-Hodgkin's malignant lymphomas (NHML). the phenotypes of lymphoma cells and other cells were examined using 11 monoclonal and 3 polyclonal antibodies by the ABC method on paraffin-embedded tissue sections of 226 cases of NHML, comprising 94 B-cell lymphomas (B-ML) and 132 T-cell lymphomas (T-ML). In 219 NHML cases (96.8%), lymphoma cells reacted with more than one of these antibodies. A set of MB-1, Mx-pan B, L26, LN-1, LN-2 and anti-immunoglobulin light chain antibodies characterized each subtype of B-MLs, categorized according to the Kiel classification. Mantle-zone lymphoma (MzML) was added as one subtype. L26 stained the largest number of B-MLs (82.8%). B-cell chronic lymphocytic leukemia (B-CLL) was labeled most frequently by MB-1. MzML was characterized by reactivity of lymphoma cells with LN-2 and by the appearance of monoclonal immunoglobulin light chain along the cell membrane. Follicle center cell lymphomas were stained by LN-1 and LN-2, although a small number of proliferating cells were labeled by LN-1 in B-CLL, MzML and the immunocytoma lymphoplasmacytic/cytoid variant. MT-1 and/or UCHL-1 showed various degrees of reactivity with the cell membranes of lymphoma cells in 94.8% of T-MLs. Among the T-cell pleomorphic lymphomas of Suchi and Lennert, the adult T-cell leukemia/lymphoma type, defined by stippled heterochromatin distribution and peculiar huge cells, reacted selectively (p less than 0.05) with anti-phosphokinase C antibody. Anaplastic large cell T-ML reacted with a set of Ber H2, LN-2 and Leu M1. In T-zone lymphomas without hyperplastic follicles, angioimmunoblastic lymphadenopathy with dysproteinemia-type T-ML, lymphoepithelioid cell lymphomas and some pleomorphic lymphomas comprising clear large lymphoma cells, there were many intermingling B cells, and their constitution varied. In some lymphoblastic lymphomas of both the T cell and B-cell type, phenotypes of T cells and B cells were expressed. Consequently, it was shown that paraffin immunohistochemistry was useful for the practical histopathological diagnosis of NHML even in the area where human T-cell leukemia virus type 1 is endemic.
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PMID:Paraffin-immunohistochemical analysis of 226 non-Hodgkin's malignant lymphomas in the endemic area of human T-cell leukemia virus type 1. 186 99

Previously, it has been shown that E mu-pim-1 transgenic mice are predisposed to T-cell lymphomas, whereas E mu-myc transgenic mice are predisposed to pre-B-cell lymphomas. Here we show that double-transgenic E mu-myc E mu-pim-1 mice exhibit pre-B-cell leukemia in utero. Upon transplantation into recipient mice, embryo-derived double-transgenic leukemic cells frequently progressed to highly malignant monoclonal tumors, indicating that additional (epi)genetic events had occurred during the progression of the disease.
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PMID:Mice bearing the E mu-myc and E mu-pim-1 transgenes develop pre-B-cell leukemia prenatally. 199 Feb 73

The absence of wild type retinoblastoma (Rb) gene expression in a wide variety of human solid tumors suggests an etiologic role for this tumor suppressor gene in human cancer. We have evaluated the involvement of Rb gene inactivation in the pathogenesis and progression of human lymphoma and leukemia. We examined the genomic configuration and transcription of the Rb gene in cultured cell lines and primary cases of T- and B-cell lymphomas and leukemias. By Southern analysis, abnormalities of the Rb locus were identified in 1 of 5 T-cell acute lymphoblastic lymphoma (T-ALL) cell lines, 1 of 26 primary cases of T-ALL, 1 of 40 primary cases of chronic lymphocytic lymphoma/well-differentiated lymphoma (CLL/WDL), and 1 of 15 primary cases of intermediately differentiated lymphoma (IDL). By Northern analysis, markedly reduced or abnormal expression of the Rb gene was identified in 2 of 5 T-ALL cell lines, 1 of 7 primary cases of T-ALL, 1 of 5 primary cases of CLL/WDL, and 1 of 6 primary cases of IDL. These findings show that Rb gene inactivation can be associated with a broad range of lymphoid neoplasms and that loss of the tumor suppressor function of Rb may influence the pathogenesis and progression of lymphoma/leukemia.
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PMID:Inactivation of the retinoblastoma gene in human lymphoid neoplasms. 199 22

A series of T-cell proliferations in peripheral blood, bone marrow, or tissue samples were analyzed for clonality. The technique used employs the polymerase chain reaction to amplify portions of the rearranged T-cell receptor beta chain genes, using primers recognizing conserved sequences of the variable, diversity, and joining region segments. We examined 17 cases of T-cell lymphoma or leukemia; a clone was identified in 13 cases (76%) overall and in 7 of 8 cases (87.5%) in which both beta-chain alleles were known to be rearranged, as shown by restriction enzyme analysis. No clonal rearrangements were detected in samples from 13 non-T-cell disorders, including B-cell lymphomas, reactive lymphoid proliferations, and nonlymphoid tumors. This method is useful for detecting clones in thymic and post-thymic T-cell malignancies and has the advantages of being extremely rapid (a result is obtained within hours of the biopsy procedure), requiring no radiolabeling, using only a small amount of tissue, and being applicable to formalin-fixed, paraffin-embedded tissue.
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PMID:The rapid detection of clonal T-cell proliferations in patients with lymphoid disorders. 201 72


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