Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A series of 217 trephine bone marrow biopsies from adult patients and specimens from 16 fetuses and 5 infants were examined for the presence of stromal myoid cells (MCs) using a monoclonal antibody recognizing alpha-smooth muscle actin. In the normal adult bone marrow, stromal cells did not contain alpha-smooth muscle actin, whereas during fetal life, many alpha-smooth muscle actin-containing MCs were connected with vascular sinusoids in the primitive bone marrow. This cell type reappeared in various characteristic distribution patterns in adult bone marrow during different neoplastic and non-neoplastic conditions including metastatic carcinoma, Hodgkin's disease, multiple myeloma, hairy cell leukemia, acute myeloid leukemia (FAB M4, 5, 7) and chronic myelo-proliferative diseases. In general, the appearance of MCs was associated with a slight to pronounced increase in the deposition of reticulin and collagen fibers. We propose that bone marrow MCs represent a distinct subpopulation of fiber-associated or adventitial reticular cells undergoing cytoskeletal remodeling in response to various stimuli.
Virchows Arch B Cell Pathol Incl Mol Pathol 1989
PMID:Alpha-smooth muscle actin is expressed in a subset of bone marrow stromal cells in normal and pathological conditions. 257 Apr 90

The incidence of acute myeloid leukemia (AML) in CBA/H mice following exposure to single acute doses of ionizing radiation has previously been determined. A high proportion of these AMLs are characterized by rearrangement of murine chromosome 2 in the C2 and/or E5-F regions, and there is evidence that these events are a direct consequence of radiation damage to multipotential hemopoietic cells. Using a combination of in situ chromosome hybridization and mRNA analyses, we show that the cytokine gene interleukin-1 beta (IL-1 beta) is encoded in the chromosome 2 F region and is translocated in a chromosome 2---2 rearrangement in an x-ray-induced AML (N36). Also, IL-1 beta is specifically deregulated in N36 and in two other chromosome 2-rearranged AMLs but not in a fourth, which has two cytogenetically normal chromosome 2 copies. We suggest that radiation-induced specific chromosome 2 rearrangement associated with IL-1 beta deregulation may initiate murine leukemogenesis through the uncoupling of normal proliferative control mechanisms in multipotential hemopoietic cells.
Mol Carcinog 1989
PMID:Interleukin-1 beta gene deregulation associated with chromosomal rearrangement: a candidate initiating event for murine radiation-myeloid leukemogenesis? 257 38

The Philadelphia chromosome (t9:22;q34:q11) is found in more than 90% of patients with chronic myelogenous leukemia, in 10 to 20% of patients with acute lymphocytic leukemia, and in 1 to 2% of patients with acute myelogenous leukemia. Alternative chimeric oncogenes are formed by splicing different sets of BCR gene exons on chromosome 22 across the translocation breakpoint to a common set of ABL oncogene sequences on chromosome 9. This results in an 8.7-kilobase mRNA that encodes the P210 BCR-ABL gene product commonly found in patients with chronic myelogenous leukemia or a 7.0-kilobase mRNA that produces the P185 BCR-ABL gene product found in most Philadelphia chromosome-positive patients with acute lymphocytic leukemia. To compare the efficiency of growth stimulation by these two proteins, we derived cDNA clones for each with identical 5' and 3' untranslated regions and expressed them from retrovirus vectors. Matched stocks were compared for potency to transform immature B-lymphoid lineage precursors. The growth-stimulating effects of P185 for this cell type were found to be significantly greater than those of P210. Structural changes in BCR may regulate the effectiveness of the ABL tyrosine kinase function, as monitored by lymphocyte growth response. Changes in mitogenic potency may help to explain the more acute leukemic presentation usually associated with expression of the P185 BCR-ABL oncogene.
Mol Cell Biol 1989 May
PMID:Alternative forms of the BCR-ABL oncogene have quantitatively different potencies for stimulation of immature lymphoid cells. 274 38

An amphotropic retroviral vector containing the bacterial neomycin phosphotransferase gene (neo) was used to infect blast cells from patients with acute myeloblastic leukemia. The infected cells acquired a G418-resistant phenotype that was stable as measured in a clonogenic assay and in long-term suspension culture. Thus, gene transfer into stem cells was accomplished by this procedure. This approach for manipulating gene expression in blast stem cells provides a means to assess the roles of a variety of genes in self-renewal, differentiation, and leukemogenesis.
Mol Cell Biol 1988 Feb
PMID:Introduction of new genetic material into human myeloid leukemic blast stem cells by retroviral infection. 283 45

Mitochondria from 25 patients with acute lymphoblastic leukemia (ALL) and 25 patients with acute myelogenous leukemia (AML) were compared in terms of their number, area, and shape index using a computer-controlled image analyzer. The number of mitochondria was greater in the AML than in the ALL patients. However, their size, as measured in electron micrographic profiles was similar in the two groups, in disagreement with conventional reports that mitochondria are small in granulocytes but large in lymphocytes. Two ALL patients had giant mitochondria. The mitochondria of the ALL cells were more irregular than those of the AML cells, and furthermore, within the ALL group, the degree of the irregularity was greater in those with a poor prognosis than in those in longstanding remission. The number of mitochondria was significantly greater in B-cell ALL than in null cell and T-cell ALL.
Virchows Arch B Cell Pathol Incl Mol Pathol 1986
PMID:Quantitative evaluation of leukemic mitochondria with a computer-controlled image analyzer. 287 44

Quantitative estimations of the mean areas of cell, nucleus and cytoplasm in polymorphonuclear leucocytes (PMN) were performed by automated image analysis of blood smears from six patients with acute myeloid leukaemia. The PMN were qualitatively separated by a cytochemical staining method into two well-defined subpopulations i.e. myeloperoxidase (MPO)-normal and MPO-deficient PMN. MPO-deficient PMN were characterized by a decreased size of the total cell (P less than 0.01), an increased size of the nucleus (P less than 0.01) and a decreased size of the cytoplasm (P less than 0.01). The resulting highly increased nucleus-to-cytoplasm ratio in this specific PMN subpopulation bears a striking resemblance to cells in malignant tumours. The planimetric results in this study further support the concept that MPO-deficient PMN may be the progeny of leukaemic precursors.
Virchows Arch B Cell Pathol Incl Mol Pathol 1986
PMID:Myeloperoxidase deficient polymorphonuclear leucocytes: computerized planimetric estimations of cellular and nuclear size. 288 56

Leukemic cells from 39 patients with acute leukemia (20 lymphocytic and 19 myelogenous) were examined by transmission electron microscopy and the nucleus and cytoplasm were measured on the micrographs with a computer-controlled image analyzer. The ratios between the areas of the nucleus and whole cell profile (nucleus/cell ratio), heterochromatin and euchromatin, the nucleolus and nucleus, and the degree of irregularity of the nucleus were compared between the two major types of leukemia studied. Acute lymphocytic leukemia (ALL) cells had a relatively larger nucleus and relatively less cytoplasm than acute myelogenous leukemia (AML) cells, and a greater proportion of the area of the nucleus was occupied by heterochromatin in ALL cells than in AML cells. According to the FAB classification, L1 cells are characterized by narrow, and L2 cells by wide cytoplasm based on light microscopic observation of smeared cells, and we confirmed these features by morphometry of May-Giemsa-stained blood smears. However, by electron microscopy there was no difference in the nucleus/cell ratio between L1 and L2 cells, this constituting a discrepancy between the results obtained by electron and light microscopic morphometry. In addition there was no difference in the degree of nuclear irregularity between L1 and L2 cells. Among AML subtypes, significant differences were observed only in the nucleus/cell ratio between M3 and M1, M2 or M4 cells, and in the heterochromatin/euchromatin ratio between M5 and M1, M2 or M3 cells. In conclusion, electron microscopic morphometry revealed marked differences between ALL and AML, but the differences among their subtypes defined by the FAB classification based on nonmorphometric light microscopy were less evident by electron microscopic morphometry.
Virchows Arch B Cell Pathol Incl Mol Pathol 1987
PMID:Morphometrical evaluation of acute leukemic cells by electron microscopy. Discrepancy between morphological characteristics in FAB classification and electron microscopic morphometry. 288 63

Granulocyte/macrophage progenitor cells (CFU-GM) and erythroid progenitor cells (BFU-E) have been assayed in peripheral blood (PB) and/or bone marrow (BM) from 12 patients with acute lymphocytic leukemia (ALL), 16 patients with chronic lymphocytic leukemia (CLL) and 31 patients with various forms of non-Hodgkin lymphoma (NHL) without BM involvement. Progenitor cell growth in PB and BM from the NHL patients did not differ statistically from controls (p greater than 0.1). CFU-GM and BFU-E per ml PB were markedly increased in ALL and CLL patients (p less than 0.001) while CFU-GM and BFU-E per plated BM cells from these patients were severely depressed (p less than 0.001). Lymphoblasts from one ALL patient failed to inhibit CFU-GM and BFU-E-derived colony growth from control PB mononuclear cells. The high levels of circulating progenitor cells in ALL and CLL patients clearly distinguish them from other cytopenic hematological malignancies, in which decreased progenitor cell levels have been demonstrated previously (acute myeloid leukemia, hairy cell leukemia). The cause of this finding and its pathophysiological implication still remains to be established.
Virchows Arch B Cell Pathol Incl Mol Pathol 1987
PMID:In vitro culture studies of granulocyte/macrophage and erythroid progenitor cells in lymphoproliferative disorders. 288 76

Somatic rearrangements of immunoglobulin (Ig) and T-cell receptor (TCR) genes are the basis for the production of receptors for antigen in B-cells and T-cells, respectively. Here, we have studied the extent and pattern of rearrangements at Ig and TCR loci in 17 patients presenting with acute myeloid leukemia (AML). Our data demonstrate illegitimate clonal rearrangements at Ig heavy and/or TCR beta chain genes in 5 of 17 AML patients. In four of these five patients, rearrangements at the TCR beta chain gene locus were also observed. Seven patients displayed clonal TCR gamma chain gene rearrangements as the only abnormality. Rearrangements at Ig light chain and TCR alpha chain gene loci were not detected. Illegitimate TCR gamma chain gene rearrangements in AML involve recombinations of only a subset of V gamma genes, predominantly with the J gamma 1 region. Rearrangements at the TCR beta chain gene locus are characterized by both D-J and V-D-J recombinations, with predominant use of the J beta 1 region. The absence or presence of illegitimate antigen receptor gene rearrangements in AML may constitute a prognostic marker. In addition, these alterations can be used to establish clonality in AML with direct applications in the monitoring of disease. Finally, the present data relate to the problem of lineage assignment of acute leukemias based on Ig and TCR gene rearrangements and strongly suggest that the latter cannot be regarded as unequivocal evidence for the B-cell or T-cell lineage, respectively.
Mol Biol Med 1987 Feb
PMID:Immunoglobulin heavy chain and T-cell receptor gamma and beta chain gene rearrangements in acute myeloid leukemias. 311 10

The distribution of Alu-family DNA repeats (AFRs) in chromosomes of phytohaemagglutinin-stimulated peripheral blood lymphocytes of four normal donors and non-stimulated bone marrow cells of four patients with acute leukemia (ALL and ANLL) was studied by in situ hybridization using DNA of recombinant phage lambda containing multiple inserts of AFR as a probe. Over some chromosome bands (14cen, 16p13, 16cen) from normal donors and from leukemic patients clusters of silver grains were detected. Over other three bands (3q26, 8p11-p12 and 14q24) the clusters were found only in chromosomes from the four acute leukemia patients, and were absent from chromosomes of healthy donors. The results suggest non-random long-range distribution of AFRs in human chromosomes, and somatic variations in the distribution of the repeats.
Mol Biol Rep 1988
PMID:'Conservative' and 'variable' clusters of Alu-family DNA repeats in human chromosomes. 322 44


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>