Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.6 (RNA polymerase)
34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient was a 62-year-old man. His hematological data in April 2000 had shown no abnormalities, but he was referred to our hospital because of a fever and leukocytosis in June 2000. The peripheral blood showed 29.8 x 10(9)/L white blood cells, with 68.0% blasts. A bone marrow aspirate showed hypercellularity with a proliferation of large leukemic blasts. The leukemic cells were positive for CD13 (91%), CD33 (54.8%), CD34 (94.5%), and HLA-DR (97.9%). Some leukemic cells (15.6%) also expressed CD14. Cytogenetic analysis revealed 92,XXYY,t(9;22)(q34;q11)x2 in all 20 metaphase cells. Reverse transcriptase polymerase chain reaction analysis detected the minor BCR/ABL messenger RNA (mRNA) but failed to detect the major BCR/ABL mRNA. The patient achieved complete remission after induction chemotherapy, with no evidence of Philadelphia chromosome (Ph) or minor BCR/ABL mRNA. Ph-positive acute myeloid leukemia (Ph-AML) has rarely been reported. Herein, we report a case of Ph-AML with tetraploidy and review the previously reported Ph-AML cases.
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PMID:Philadelphia chromosome-positive acute myeloid leukemia with tetraploidy. 1184 93

Angiogenesis is a critical step in tumor growth and metastatic invasion. We here report the study of the vascular status of 10 benign and 9 malignant pheochromocytomas. We examined the vascular architecture after immunostaining endothelial cells (CD34) and vascular smooth muscle cells (alpha-actin) and identified a vascular pattern characteristic of malignant lesions. To define a gene expression profile indicative of the invasive phenotype, we studied by in situ hybridization the expression of genes encoding several pro- and anti-angiogenic factors [hypoxia-inducible factor (HIF-1 alpha), EPAS1, vascular endothelial growth factor (VEGF), VEGF receptors, angiopoietins and their receptor Tie2, five genes of the endothelin system, and thrombospondin 1]. A semiquantitative evaluation of the labeling revealed an induction of genes encoding EPAS1, VEGF, VEGFR-1, VEGFR-2, endothelin receptor, type B (ETB) and endothelin receptor, type A (ETA) in malignant pheochromocytomas as compared to benign tumors. These differences were observed in tumor cells, in endothelial cells, or in both. Quantification by real-time reverse-transcriptase polymerase chain reaction showed an increase of EPAS1, VEGF, and ETB transcripts of 4.5-, 3.5-, and 10-fold, respectively, in malignant versus benign tumors. Furthermore, we observed a strong correlation between the expression of EPAS1 and VEGF in tumoral tissue and between EPAS1 and ETB in endothelial cells. Altogether, our observations show that analysis of angiogenesis provides promising new criteria for the diagnosis of malignant pheochromocytomas.
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PMID:Angiogenesis and vascular architecture in pheochromocytomas: distinctive traits in malignant tumors. 1236 97

The authors studied mineralocorticoid receptor (MCR)-mediated effects of steroids on CD34(+) progenitor cells. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed the presence of mRNA for both the MCR and the alpha subunit of the epithelial sodium channel, a member of the amiloride-sensitive sodium channel (ASSC) superfamily, in human CD41(+) megacaryoblastic cells derived from cultured bone marrow CD34(+) isolates, as well as in the human erythromegakaryoblastic leukemia (HEL) cell line. Immunofluorescence also revealed the presence of both the MCR and ASSC in circulating CD34(+) and medullar CD41(+) megacaryoblastic cells, the former as a nucleocytoplasmic protein and the latter as a membrane-bound protein, as expected from earlier studies using MCR-specific targets. In a selective medium, the formation of erythrocyte burst-forming units, and of the granulocyte-macrophage colony-forming units, by circulating CD34(+) cells was influenced by the agonists deoxycorticosterone and aldosterone, as well as by the antagonists RU 26752 and ZK 91587, targeted for the MCR. The multiplication of the leukemic HEL progeny, derived from CD41(+) cells, was similarly altered by these steroids targeted for the MCR. In contrast, in the optimal growth medium, the multiplication, and colony formation by bone marrow CD34(+) progenitor cells were not altered by either aldosterone or ZK 91587. These and other studies reveal that the receptor-mediated action of mineralocorticoids may influence the functional maturation of the hematopoietic progenitor lineage, contrary to the classical notion where the mineralotropic effect would be a unique feature of the epithelial cell.
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PMID:Mineralocorticoid hormones exert dramatic effects on pluripotent human stem cell progeny. 1293 24

CD9, a member of the transmembrane 4 superfamily, is involved in cell adhesion, migration, and tumor metastasis. Little is known about its vascular expression pattern. In this study, we investigated CD9 expression on endothelial cells in the mucosa of the head and neck and compared it with vascular tumors. Using immunohistochemistry, expression of CD9 was studied in 17 samples of head and neck mucosa and skin (laryngeal mucosa: n = 2, oral: n = 6, and epidermis: n = 9) and a variety of vascular tumors (lymphangiomas: n = 9, juvenile nasopharyngeal angiofibromas: n = 4, hemangiomas: n = 7, angiosarcomas: n = 5, and Kaposi's sarcomas: n = 7) and compared with the expression of CD34 and PAL-E (blood vessel markers) and the lymphatic marker podoplanin. Regular lymphatic endothelium and lymphangiomas were strongly positive for CD9 and podoplanin but were mostly negative for PAL-E and CD34. By contrast, blood vessel endothelium and hemangiomas were strongly positive for PAL-E and CD34 but were mostly negative for CD9 and podoplanin. Weak to moderate CD9 reactivity was also observed on EC of juvenile nasopharyngeal angiofibromas, angiosarcomas, and Kaposi's sarcomas. Expression of CD9 by lymphatic EC was confirmed by reverse-transcriptase PCR and Western blot analyses. CD9 may be useful as a marker for lymphatic EC. It could promote the adherence of inflammatory and tumor cells to lymphatic EC and participate in the growth and maintenance of the lymphatic capillary net.
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PMID:CD9 expression on lymphatic vessels in head and neck mucosa. 1455 86

Recently, overlapping molecular phenotypes of hematopoietic and neuropoietic cells were described in mice. Here, we examined primary human CD34(+) hematopoietic stem and progenitor cells applying specialized cDNA arrays, real-time reverse-transcriptase-polymerase chain reaction (RT-PCR), and fluorescent-activated cell sorter (FACS) analysis focusing on genes involved in neurobiologic functions. We found expression of vesicle fusion and motility genes, ligand- and voltage-gated ion channels, receptor kinases and phosphatases, and, most interestingly, mRNA as well as protein expression of G protein-coupled receptors of neuromediators (corticotropin-releasing hormone 1 [CRH 1] and CRH 2 receptors, orexin/hypocretin 1 and 2 receptors, GABAB receptor, adenosine A(2)B receptor, opioid kappa 1 and mu 1 receptors, and 5-HT 1F receptor). As shown by 2-color immunofluorescence, the protein expression of these receptors was higher in the more immature CD38(dim) than in the CD38(bright) subset within the CD34(+) population, and completely absent in fully differentiated blood cells, suggesting that those receptors play a role in developmentally early CD34(+) stem and progenitor cells. The intracellular concentration of cyclic adenosine monophosphate (cAMP) in CD34(+) cells was diminished significantly upon stimulation of either CRH or orexin receptors, indicating that those are functionally active and coupled to inhibitory G proteins in human hematopoietic cells. In conclusion, these findings suggest a molecular interrelation of neuronal and hematopoietic signaling mechanisms in humans.
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PMID:Primary human CD34+ hematopoietic stem and progenitor cells express functionally active receptors of neuromediators. 1501 51

We have developed an in vitro reconstructed vaginal mucosa integrating Langerhans cells (LCs), obtained by differentiation of umbilical cord blood CD34(+) hematopoietic progenitor cells, and, in this model, we have investigated the infection of LCs by human immunodeficiency virus type 1 (HIV-1). Proviral DNA of X4 (LAI and NL4-3) and R5 (Ba-L) HIV-1 strains were detected in LCs integrated in the reconstituted mucosa. Infection of LCs could be specifically inhibited by the chemokines stromal cell-derived factor 1 (SDF-1) and RANTES (regulated on activation, normally T cell-expressed and -secreted), confirming the presence of functional coreceptors on LCs generated in vitro. A complete inhibition of LCs, by use of azidothymidine, a reverse-transcriptase inhibitor, was also observed. Moreover, HIV-1-infected LCs of the reconstructed mucosa were able to transmit R5 or X4 HIV-1 strains to activated peripheral blood mononuclear cells. Such a model could be a useful tool to study the mechanisms involved in transmission of HIV in the female genital tract.
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PMID:HIV-1 infection of Langerhans cells in a reconstructed vaginal mucosa. 1521 55

In animals, the bone marrow (BM) is a source of liver-repopulating cells with therapeutic potential in case of tissue damage. However, the early response of human BM-derived stem cells (SC) to liver injury is still unknown. Here, we studied 24 patients undergoing orthotopic liver transplantation (OLT) for end-stage liver disease or hepatocellularcarcinoma, and 13 patients submitted to liver resection. The concentration of circulating BM-derived SC was determined by phenotypic analysis and clonogenic assays. Moreover, we assessed the serum level of inflammatory and tissue-specific cytokines. Reverse transcriptase-polymerase chain reaction and fluorescence-in situ hybridization were also used to characterize mobilized SC. At baseline, patients showed a significant lower concentration of circulating CD133(+), CD34(+) SC and clonogenic progenitors (colony-forming unit cells) than healthy controls. However, the time-course evaluation of peripheral blood cells after OLT demonstrated the significant early mobilization of multiple subsets of hematopoietic and endothelial stem/progenitor cells. Cytogenetic and molecular analyses of CD34(+) cells showed the host origin of mobilized SC and the expression of transcripts for GATA-4, cytokeratin 19, and alpha-fetoprotein hepatocyte markers. In contrast with OLT, only total circulating CD34(+) cells significantly increased after liver resection. Mobilization of BM cells after OLT or liver surgery was associated with increased serum levels of granulocyte-colony stimulating factor, interleukin-6, stem cell factor, hepatocyte growth factor, and vascular endothelial growth factor. In summary, we demonstrate that tissue damage after OLT and liver resection induces increased serum levels of multiple cytokines but only ischemia/reperfusion injury associated with OLT results in the remarkable mobilization of BM stem/progenitor cells.
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PMID:Mobilization of bone marrow-derived hematopoietic and endothelial stem cells after orthotopic liver transplantation and liver resection. 1693 69

Bone marrow stromal cells (BMSCs) or mesenchymal stem cells (MSCs) are a heterogeneous population of cells that are multipotent. When rat BMSCs were seeded onto a 3-dimensional (3-D) tubular scaffold engineered from aligned type I collagen strands and cultured in osteogenic medium, they simultaneously matured and differentiated into osteoblastic and vascular cell lineages. In addition, these osteoblasts produced mineralized matricellular deposits. BMSCs were seeded at a density of 2 x 10(6) cells/15 mm tube and cultured in basal or osteogenic medium for 3, 6, and 9 days. These cells were subsequently processed for real-time reverse-transcriptase polymerase chain reaction (RT-qPCR), immunohistochemical, cytochemical, and biochemical analyses. Immunolocalization of lineage-specific proteins was visualized using confocal microscopy. In the present study, the expression pattern of key osteogenic markers significantly differed in response to basal and osteogenic media. Alkaline phosphatase activity and calcium content increased significantly over the observed period of time in osteogenic medium. The observed up-regulation of transcripts coding for osteoblastic phenotypic markers is reminiscent of in vivo expression patterns. Abundant sheets of Pecam (CD31) -, Flk-1 (vascular endothelial growth factor receptor-2) -, CD34-, tomato lectin-, and alpha-smooth muscle actin-positive cells were observed in these tube cultures. Moreover, nascent capillary-like vessels were also seen amid the osteoblasts in osteogenic cultures. Our 3-D culture system augmented the maturation and differentiation of BMSCs into osteoblasts. Thus, our in vitro model provides an excellent opportunity to study the concurrent temporal and spatial regulation of osteogenesis and vasculogenesis during bone development.
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PMID:A three-dimensional tubular scaffold that modulates the osteogenic and vasculogenic differentiation of rat bone marrow stromal cells. 1835 28

Incorporation of circulating hematopoietic progenitor cells (HPCs) into damaged skeletal muscle has been proposed as a novel mechanism of tissue repair complementary to satellite cell-dependent regeneration. We studied the occurrence and myoendothelial differentiation of HPCs in muscle of patients with inflammatory myopathies. Muscle biopsies from untreated patients with dermatomyositis, polymyositis, inclusion body myositis, and controls were investigated for the expression of endothelial (CD31, von Willebrand factor, vascular endothelial growth factor receptor 2), hematopoietic (CD34, CD133, CD45), and myogenic (Pax7, MyoD) markers by immunohistochemistry and reverse-transcriptase-polymerase chain reaction. Confocal laser scanning microscopy was used to visualize coexpression of CD34, CD133, von Willebrand factor, or Pax7 on individual cells. Morphometric analysis revealed significantly increased numbers of CD133 cells per square millimeter in polymyositis and inclusion body myositis compared with controls (p < 0.001); this correlated with the density of CD45 infiltrates (p < 0.001). By confocal laser scanning microscopy, we detected several mononuclear cells that coexpressed either CD34/von Willebrand factor or CD133/Pax7 with or without CD34 reactivity, indicating endothelial or myogenic commitment of some HPCs in skeletal muscle. Rarely, CD133/CD34/Pax7 cells seemed to occupy satellite cell niches or to incorporate into preexisting myofibers. Our findings suggest that circulating HPCs colonize skeletal muscle in inflammatory conditions and provide evidence for in situ myoendothelial differentiation of some of these cells.
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PMID:Endothelial and myogenic differentiation of hematopoietic progenitor cells in inflammatory myopathies. 1859 42

Spindle epithelial tumor with thymus-like differentiation (SETTLE) is an extremely rare tumor of the thyroid and neck, first described by Chan and Rosai. SETTLE is a low-grade malignancy, with potential for late lung, lymph node, and other visceral metastases. The clinicopathologic features of SETTLE overlap significantly with those of synovial sarcoma. Thirteen cases previously diagnosed as "SETTLE" (11 cases) or "malignant neoplasm-SETTLE versus synovial sarcoma" (2 cases), were retrieved. Immunohistochemistry for low-molecular-weight cytokeratins, high-molecular-weight cytokeratins, cytokeratin 7, cytokeratin 20, epithelial membrane antigen, bcl-2, CD34, CD99, CD117, INI-1, and TLE1 were performed. Reverse transcriptase polymerase chain reaction for the SS18/SSX1 and SS18/SSX2 fusion genes and fluorescent in-situ hybridization for SYT rearrangement was performed. The 11 cases diagnosed, as "SETTLE" were negative for synovial sarcoma-associated fusion genes, whereas the other 2 cases were positive. SETTLE occurred in 7 females and 4 males (7 to 50 y of age, median 13.5 y) and involved the thyroid gland in 10 cases. Clinical follow-up showed 3 patients to be disease-free 7, 10, and 15 years after surgery. One patient had a lymph node metastasis at diagnosis and lung metastases 14 months after diagnosis. SETTLE infiltrated the thyroid, and consisted of a vaguely nodular admixture of fascicular, reticular, hyalinized, and microcystic areas. Spindled zones blended imperceptibly into areas showing epithelial differentiation, in the form of glomeruloid glandular structures, sertoli-like tubules, and small glands, lined by cuboidal to columnar cells. Mitotic activity was very low, necrosis was absent, and pleomorphism was not present. By immunohistochemistry, SETTLE showed extensive expression of high-molecular-weight cytokeratins in 7 of 8 cases (88%). Expression of low-molecular-weight cytokeratins and epithelial membrane antigen was limited, confined to only scattered cells in 7 of 8 (88%), and 4 of 8 (50%) of cases, respectively. Cytokeratin 7 expression was more widespread (7 of 8 cases, 88%). Cytokeratin 20 was negative. Expression of CD99 and bcl-2 was seen in 6 of 8 (75%) and 7 of 8 (88%) cases, respectively. CD117, INI-1, and TLE1 expression was seen in 6 of 8 (75%), 8 of 8 (100%), and 1 of 5 (20%) of cases, respectively. We conclude that traditional morphologic study and a limited panel of ancillary immunostains are sufficient for the distinction of SETTLE from synovial sarcoma in almost all instances. Molecular genetic study may, however, be helpful in selected cases, particularly in limited biopsies.
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PMID:Spindle epithelial tumor with thymus-like differentiation: a morphologic, immunohistochemical, and molecular genetic study of 11 cases. 1941 83


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