Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598766 (leukemogenesis)
 4,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with antibodies to human T-cell leukemia virus type I and the presence of integrated sequences of this virus in T-lymphocytes was investigated. In contrast to previous reports, the T-cell lymphocytosis was found to be polyclonal by analysis of human T-cell leukemia virus type I integration sites and T-cell antigen receptor rearrangements. Polyclonal T-cell infection by human T-cell leukemia virus type I may represent an infrequently observed stage of leukemogenesis.
Cancer Res 1988 May 01
PMID:Polyclonal lymphocytosis of T-cells associated with human T-cell leukemia virus I. 289 81

Three mouse genomic domains, Fim1, Fim2, and Fim3, were previously described as proviral integration regions frequently involved in the early stages of myeloblastic leukemogenesis induced in vivo or in vitro by the Friend murine leukemia virus. Fim2 was identified as the 5' end of the c-Fms protooncogene, which encodes the receptor of the macrophage colony stimulating factor (Csflr). The functions of Fim1 and Fim3 are not yet known, but these regions are highly conserved among different species. To examine whether these regions could correspond to known human loci involved in genetic alterations specific to some human leukemias, we undertook their chromosomal mapping. The localization of FIM2/c-FMS on 5q33 was confirmed. FIM1 and FIM3 were localized on human chromosomes 6p22.3-p23 and 3q27 respectively. Interestingly, translocations involving these two regions have been described in various hematopoietic malignancies: the t(6;9)(p23;q34) in acute nonlymphocytic leukemias and the 3q26-q28 translocations in a large variety of leukemias.
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PMID:The human homologues of Fim1, Fim2/c-Fms, and Fim3, three retroviral integration regions involved in mouse myeloblastic leukemias, are respectively located on chromosomes 6p23, 5q33, and 3q27. 292 Oct 36

Remarkable progress has been achieved in our understanding of the biology of acute lymphoblastic leukemias (ALL) occurring in childhood. Morphologic, immunologic, and cytogenetic studies of ALL have resulted in more accurate classification and risk assessment, permitting tailoring of therapy in this heterogeneous group of diseases. Studies of tumor cell biology have begun to pinpoint genes whose altered functions may be etiologically linked to cancer, and have provided insights into the biochemical processes involved in leukemogenesis.
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PMID:Acute lymphocytic leukemia in childhood: immunologic marker, cytogenetic, and molecular studies. 295 21

The association of Down's syndrome and leukemia has been documented for over 50 years. Multiple studies have established the incidence of leukemia in Down's syndrome patients to be 10- to 20-fold higher than that in the general population. The age of onset for leukemia in these children is bimodal, peaking first in the newborn period and again at 3-6 years. This increased risk extends into adulthood. All cytogenetic types of Down's syndrome apparently predispose to leukemia. The proportion of acute lymphoblastic leukemia and acute nonlymphoblastic leukemia in patients with Down's syndrome is similar to non-Down's syndrome leukemia patients matched for age. There are case reports in which leukemia, Down's syndrome, and other chromosomal aberrations cluster within a family. In these kindreds, there may be a familial tendency toward nondisjunction. Congenital leukemia also occurs with increased frequency in Down's syndrome patients, and is characterized by a preponderance of acute nonlymphoblastic leukemia (similar to non-Down's syndrome patients). Transient leukemoid reactions have been observed in Down's syndrome patients, as well as in phenotypically normal children with constitutional trisomy 21 mosaicism. The transient leukemoid reactions are characterized by a high spontaneous remission rate. However, in some Downs syndrome patients with apparent transient leukemoid reaction, leukemia relapse following periods of spontaneous remission have been reported. Cytogenetic studies of leukemic cells in Down's syndrome patients show a tendency toward hyperdiploidy. Besides trisomy 21, there is no other specific cytogenetic abnormality that is characteristic of the leukemia cells in Down's syndrome patients. The possible mechanisms for leukemogenesis in Down's syndrome patients may involve factors at the levels of the organism, the organ/system, the cell, the chromosomes or the DNA.
Cancer Genet Cytogenet 1987 Sep
PMID:Down's syndrome and leukemia: epidemiology, genetics, cytogenetics and mechanisms of leukemogenesis. 295 86

The human T-cell leukemia virus (HTLV) types I and II are associated with specific hematological cancers. These viruses rapidly transform normal T-lymphocytes in vitro. The mechanism of HTLV-induced leukemogenesis is unknown. Structural analysis of HTLV-I and HTLV-II has revealed sequences of unknown function, termed X, at the 3' end of the proviral genome. The distal two-thirds of the X sequences are highly conserved between HTLV-I and HTLV-II. We have shown that these conserved X sequences contain a gene, termed x, that is expressed in both HTLV-I and HTLV-II by identifying a subgenomic X RNA as well as the proteins encoded by these messages. The function of this unique x gene is unknown; however, its conservation and expression suggest that it may play a role in HTLV replication and in HTLV-induced leukemogenesis.
Cancer Res 1985 Sep
PMID:Human T-cell leukemia virus x gene. 299 Jun 85

Removal of T-lymphocytes from marrow inoculum with monoclonal antibody plus complement permitted establishment of long-lived allogeneic chimeras between C57BL/6 and AKR/J mice. Development of leukemia was prevented for 15 mo. Protection from leukemia occurred with both young (4 wk) and older (4 mo) recipients. AKR mice reconstituted with syngeneic marrow or control AKR mice all developed leukemia-lymphoma before 1 yr of age. During spontaneous lymphomagenesis in AKR mice, amplified expression of gag or env gene-coded virus antigens on the surface of thymocytes preceded leukemia development and evidence for amplification of other virus genes. These changes generally appeared before 6 mo. Similar viral gene expression and viral gene amplification occurred in the thymus and spleen cells of leukemia-resistant chimeric mice. Using monoclonal antibodies to Mr 70,000 glycoprotein epitopes characteristic of ecotropic, xenotropic, or dualtropic viruses, antigens marking each virus form were found on thymocytes of allogeneic 4-wk and 4-mo chimeras as well as on the cells of AKR mice and of AKR mice reconstituted with syngeneic marrow. Flow cytometric analysis showed amplification of the virus genes in mice protected from leukemia-lymphoma by allogeneic bone marrow transplantation from leukemia-resistant mice. Allogeneic chimeras and syngeneically transplanted mice both showed evidence of accelerated viremia and of recombinant virus formation. The findings suggest that an event essential to leukemogenesis which occurs within the AKR lymphoid cells or their environment is lacking in the allogeneic chimeras. The nature of this influence of a resistance gene or genes introduced into AKR mice by allogeneic bone marrow transplantation deserves further study.
Cancer Res 1985 Dec
PMID:Expression of antigens coded in murine leukemia viruses on thymocytes of allogeneic donor origin in AKR mice following syngeneic or allogeneic bone marrow transplantation. 299

The expression of endogenous retroviral env products on primary leukemia cells of mice was studied with the use of a panel of monoclonal antibodies that discriminate between the various classes of murine leukemia viruses [MuLVs; ecotropic, xenotropic, and mink cell focus-forming (MCF)], as well as between various subtypes within each class. Most spontaneous AKR or Friend MuLV (F-MuLV)- or Moloney MuLV (M-MuLV)-induced AKR or NFS mouse leukemia cells expressed no xenotropic viral envelope antigens but always expressed MCF proteins. Spontaneous C58 lymphomas, on the other hand, often expressed xenotropic proteins in addition to MCF proteins. The subtype of MCF envelope antigens present on leukemia cells, as well as on isolated MCF viruses, varied in a reproducible manner, depending on the mouse strain inoculated and the ecotropic virus used (F-MuLV or M-MuLV). Specifically, F-MuLV consistently induced certain type(s) of MCF envelope antigens on leukemia cells of NFS mice, whereas M-MuLV induced different ones. Similar antigenic patterns were found on the MCF viruses isolated from these mice. Furthermore, MCF envelope antigens (on viruses or leukemia cells) induced in NFS mice by M-MuLV differed from those induced in AKR mice. This finding demonstrated a mouse strain influence on the endogenous MCF env sequences expressed following infection by a given ecotropic virus. The endogenous MCF env sequences in mice thus appear to be a set of genes highly expressed during leukemogenesis, with particular ones specifically expressed in a given mouse strain infected with a given ecotropic virus.
J Natl Cancer Inst 1987 Jan
PMID:Endogenous retroviral env expression in primary murine leukemias: lack of xenotropic antigens but presence of distinct mink cell focus-forming env subtypes correlating with ecotropic virus inoculated and mouse strain. 302 2

X-irradiation of purified primary cultures of mouse bone marrow stroma or permanent cloned marrow stromal cell lines in plateau phase decreases production of macrophage progenitor cell-specific colony-stimulating factor to a plateau minimum of 40% of control levels after doses of 50 to 500 Gy delivered at 2 Gy/min. After 50 Gy there is increased bioavailability of another growth factor(s) that is distinct from macrophage progenitor cell-specific colony-stimulating factor, granulocyte-macrophage progenitor cell colony-stimulating factor, or colony-stimulating factor for multipotential hematopoietic stem cells (interleukin 3). Liquid-phase cocultivation of irradiated stromal cells with either nonadherent cells from continuous marrow cultures or cloned dual granulocyte-macrophage progenitor cell colony-stimulating factor/interleukin 3-dependent hematopoietic progenitor cell lines induces evolution over 5 weeks of factor-independent colony-forming cells. Subcultured factor-independent colonies generated clonal malignant cell lines with multiple distinct karyotypic alterations. Inoculation of 10(6) cells s.c. from factor-independent clones into syngeneic mice produces local granulocytic monomyeloid tumors with spread to spleen, lymph nodes, and bone marrow. These data provide the first demonstration in vitro of indirect X-irradiation leukemogenesis through cells of the marrow stroma.
Cancer Res 1986 Sep
PMID:Induction of malignant transformation of cocultivated hematopoietic stem cells by X-irradiation of murine bone marrow stromal cells in vitro. 308 94

We report a case of acute nonlymphoblastic leukemia (M5) with a rare cytogenetic abnormality involving chromosomes 8 and 16, t(8;16)(p11;p13). The leukemic blasts were determined to be monocytic by cytochemical and immunochemical studies. Morphological changes of the leukemic cells in response to phorbol myristate acetate further supported their identification as monocytic in nature. This chromosomal abnormality has apparently been reported only thrice in the literature. Translocation (8;16)(p11;p13), though rare, may be of primary importance in the process of leukemogenesis in some cases of histiocytic/monocytic malignancies.
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PMID:Acute monoblastic leukemia with a single chromosomal rearrangement involving breakpoints on chromosomes 8 and 16, 46, XX, t(8;16)(p11;p13). 311 1

Although the origin of acute leukemia with the 4;11 translocation has been shown to be an early myeloid progenitor cell or a stem cell with the potential for differentiation into both lymphoid and myeloid lineage, few precise studies on acute leukemia with the 11;19 translocation have thus far been reported. This study focused on the clinical, morphologic, ultrastructural, and immunologic characteristics as well as the DNA in three cases of acute leukemia with the 11;19 translocation. All three patients were infants and showed hyperleukocytosis. The morphologic feature was French-American-British (FAB)-L2 in two patients, in one of which a few monocytoid blasts were also seen by electron microscopy. Cells from the third patient underwent morphologic changes from FAB-L2 at the time of diagnosis to M5b at relapse. Immunologic marker studies revealed that the blast cells from all three patients expressed Ia and B4, but none expressed B1, CALLA(J5), T antigens, or SIg. Cells from one patient simultaneously expressed myeloid antigen (MCS-II) both at diagnosis and relapse. Cells from two patients expressed myeloid antigen after being cultured for a short time in vitro. An analysis of immunoglobulin genes and T-cell receptor genes revealed rearrangements of the heavy chain genes and germ line configurations of the kappa and lambda light chain genes, and of the T-cell receptor beta chain genes. These findings suggest that acute leukemia with the 11;19 translocation has mixed lineage characteristics as a result of leukemogenesis in a stem cell with the potential for both lymphoid and myeloid, especially monocytic, differentiation.
Cancer 1988 Feb 15
PMID:Immunoglobulin heavy chain gene rearrangements and mixed lineage characteristics in acute leukemias with the 11;19 translocation. 312 49


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