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:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor growth is associated with neutrophilia, thrombocytosis, and extramedullar hematopoiesis. The mechanism(s) accounting for these phenomena is unclear, although granulocyte-macrophage colony-stimulating factor (GM-CSF) and/or granulocyte colony-stimulating factor (G-CSF) released by tumor cells have been involved. We studied whether CSF released by Ehrlich tumor (ET) may play a role. A comparative study was performed with two cell variants (ET and ET/0) growing in euthymic, nude, and SCID mice. Extramedullar hematopoiesis was assessed in the spleen by scoring organ enlargement, wheat germ agglutinin ve+ cells, and interleukin 3-dependent granulocyte-macrophage colony-forming unit (GM-CFU). Both cell lines showed the same cytokine profile by reverse transcriptase polymerase chain reaction, including GM-CSF, G-CSF, and macrophage colony-stimulating factor (M-CSF); yet, only ET cells produced detectable colony-stimulating activity in vitro, mainly due to GM-CSF. No differences in tumorigenicity were noted between ET and ET/0 cells inoculated to normal or immunodeficient mice. An increase in extramedullar hematopoiesis, accompanied by neutrophilia and thrombocytosis, was associated with tumor progression irrespective of the cell line. A strong correlation was obtained between the increase in splenic GM-CFU and tumor mass (r = 0.96, p < 0.0001) that was independent on the tumor cell line, strain of mice, or stage of tumor development. The results point against CSF released by tumor cells and/or reactive host T cells as the only factors involved in the extramedullar hematopoiesis in this tumor model. The remarkable correlation between splenic GM-CFU and the tumor mass still suggests that a factor(s) of tumor origin may play a critical role.
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PMID:Ehrlich tumor stimulates extramedullar hematopoiesis in mice without secreting identifiable colony-stimulating factors and without engagement of host T cells. 1064 93

Dendritic cells (DCs) are essential for the presentation of antigens in the primary immune response. To examine the generation of DCs from hemopoietic stem cells in the bone marrow (BM), lineage-negative (Lin-)/CD71- bone marrow cells (BMCs) from C57BL/6 mice were separated into major histocompatibility complex (MHC) class Ihigh/ c-kit(low) and MHC class Ihigh/c-kit(low)(phenotypically c-kit-negative, but c-kit message only detected by reverse transcriptase-polymerase chain reaction) populations. A large number of cells with the morphological, phenotypical, and functional characteristics of DCs was generated from both c-kit(low) and c-kit(low) populations when cultured with a combination of cytokines (GM-CSF, tumor necrosis factor-a [TNF-a], interleukin 7 [IL-7], IL-3, stem cell factor [SCF], and flt3 ligand); the cytokine combination studies revealed that SCF and IL-3 in addition to GM-CSF and TNF-a are essential for DCs to be generated from these primitive populations. To our surprise most (>80%) generated cells expressed high levels of DC surface markers such as DEC205 and MHC class II, and they were potent stimulators in the primary allogeneic T cell activation. The development of DCs from c-kit(<low) cells was slower than that from c-kit(low) cells. These results indicate that c-kit(<low) cells are more primitive than c-kit(low) cells, although both c-kit*(low) cells and c-kit(<low) cells can differentiate into DCs. It should be noted that the combination of these cytokines selectively induces DCs from both c-kit(<low) and c-kit(low) cells in vitro, suggesting that the ex vivo expansion of DCs using these primitive cells would be applicable to immunotherapy.
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PMID:Development of mouse dendritic cells from lineage-negative c-kit(low) pluripotent hemopoietic stem cells in vitro. 1066 72

Human osteoblasts were derived in culture from explants of bone from patients who had recently suffered osteoporotic fractures and from patients with no evidence of osteoporosis. The expression of cytokine mRNA in these osteoblasts was subsequently determined by reverse transcriptase-linked polymerase chain reaction (RT-PCR). We have detected mRNA for IL-1beta, IL-3, IL-6, IL-8, TNF-alpha and -beta, and the three TGF-beta isoforms in the cells. The profile of cytokines expressed by osteoblasts derived from patients with osteoporotic fractures was consistent with profiles observed in osteoblasts derived from patients with no evidence of reduced bone mass--the latter included children undergoing corrective surgery and adult subjects ranging from 31 to 80 years undergoing elective surgery for osteoarthritis and other bone pathologies.
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PMID:Cytokine expression by cultured osteoblasts from patients with osteoporotic fractures. 1076 43

Interleukin-9 (IL-9) has been implicated in the pathogenesis of allergic disorders. To examine the interaction between IL-9 and eosinophils, we evaluated mature peripheral blood eosinophils for their expression of the specific alpha-subunit of the IL-9 receptor (IL-9R-alpha). The expression of IL-9R-alpha by human eosinophils was detected at the messenger RNA (mRNA) and protein levels by reverse transcriptase-polymerase chain reaction (RT-PCR), flow cytometry, and immunocytochemical analysis, respectively. Functional analyses demonstrated that recombinant human (rh)IL-9 inhibited in vitro peripheral blood human eosinophil apoptosis in a concentration-dependent manner. We then examined the role of IL-9 in eosinophil differentiation using the human cord blood CD34(+) cells and human promyelocytic leukemia cells (HL-60). The addition of IL-9 to CD34(+) cells cultured in IL-3 and IL-5 enhanced eosinophil development, and IL-9 alone induced the expression of IL-5R-alpha. IL-9 also up-regulated the IL-5R-alpha chain cell surface expression during terminal eosinophil differentiation of the HL-60 cell line. Our findings suggest that IL-9 may potentiate in vivo eosinophil function by increasing their survival and IL-5-mediated differentiation and maturation. Taken together, these results suggest a mechanism by which IL-9 potentiates airway and tissue eosinophilia.
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PMID:Interleukin-9 enhances interleukin-5 receptor expression, differentiation, and survival of human eosinophils. 1097 62

CD34(+) cells and megakaryocyte progenitors were lower in marrow from patients after hematological recovery from the first cycle of 5-fluorouracil, leucovorin, adriamycin, cyclophosphamide (FLAC) chemotherapy plus PIXY321 (GM-CSF/interleukin 3; IL-3 hybrid) than in FLAC + GM-CSF or pre-FLAC marrows. Marrow stromal layers, an in vitro model of the marrow microenvironment, express a combination of stimulatory and inhibitory factors that modulate hematopoietic progenitor cell proliferation and differentiation. The TaqMan assay and quantitative reverse transcriptase-polymerase chain reaction were used to measure monocyte chemoattractant protein-1 (MCP-1), melanoma stimulatory growth activity, and monokine inducible by interferon-gamma (Mig) (inhibitory chemokines for primitive or megakaryocyte progenitors) mRNA levels in in vitro PIXY and GM-CSF-treated and patient post-FLAC marrow stromal layers. Chemokine mRNA was increased after in vitro GM-CSF and to a lesser extent after PIXY treatment. MCP-1 mRNA levels were fivefold higher in FLAC + PIXY than in FLAC + GM-CSF layers, and Mig mRNA was elevated in FLAC + GM-CSF layers. Thrombopoietin (TPO), insulin-like growth factor I (IGF-I), and IGF-II (stimulatory factors for primitive and megakaryocyte progenitors) mRNA were also measured. TPO mRNA levels were 30% lower in GM-CSF and PIXY-pretreated than in control layers with no decrease in IGF mRNA. TPO mRNA in stromal layers of patients who developed grade 3 thrombocytopenia (platelets < 20 x 10(9)/l) during the third cycle of FLAC was only 24% of levels in stromal layers of marrow from other post-FLAC patients. Results demonstrate that patient and in vitro treatment had modulatory effects on TPO and chemokine mRNA expression in marrow stromal layers.
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PMID:Thrombopoietin and chemokine mRNA expression in patient post-chemotherapy and in vitro cytokine-treated marrow stromal cell layers. 1100 17

We are interested in the regulation of the tissue specificity of the megakaryocyte-specific platelet glycoprotein IIb gene. The murine embryonic stem (ES) cells are able to differentiate into erythroid, mast and granulomonocytic cells in appropriate culture conditions. Our goal is to optimize the production of myeloid cells including megakaryocytes (MKs) by ES cells. We have found that coculture with MS-5 stromal cells and the presence of a cocktail of hematopoietic growth factors (HGFs) [stem cell factor, interleukin 3 (IL-3), IL-6, IL-11, G-CSF and erythropoietin] had a high synergistic activity on differentiation of ES cells into pure and MK-containing myeloid colonies from day 12 embryoid bodies. Thrombopoietin increased the number of MKs only when added to the HGF cocktail in the presence of MS-5 cells. Interestingly, many MKs exhibited a "hairy" appearance evocative of pseudopodial proplatelet formation. Expression of genes specific for the megakaryocytic lineage, GPIIb, PF4, mpl and GPIIIa, was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) during differentiation of ES cells, and their relative time course was evaluated. This demonstrates that optimized culture conditions for the differentiation of ES cells into the MK lineage provide a useful tool for the study of the regulation of expression of genes during megakaryocytopoiesis.
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PMID:Hematopoietic differentiation of embryonic stem cells: an in vitro model to study gene regulation during megakaryocytopoiesis. 1101 21

We report a rare case of chronic eosinophilic leukemia (CEL) with a chromosomal abnormality of t(6;11)(q27;q23). The patient was diagnosed as having thyroid cancer with metastases to the lung and cervical lymph nodes in 1993. Percutaneous ethanol injection therapy (PEIT), total thyroidectomy, and radiotherapy were performed. The patient was also diagnosed as having prostatic cancer with bone metastasis in July 1999, and hormonal therapy was performed. At the time of the diagnosis of prostatic cancer, leukocytosis with eosinophilia was also revealed. Thereafter, cytogenetical analysis and reverse transcriptase polymerase chain reaction (RT-PCR) analysis of bone marrow showed t(6;11)(q27;q23) translocation and MLL/AF6 fusion products, respectively. No transcripts of the BCR/ABL chimeric gene were found by RT-PCR in bone marrow. Analysis of serum cytokines revealed a slight elevation of GM-CSF but no elevation of IL-3 or IL-5. Tissue damage due to infiltration of eosinophils was not observed throughout the clinical course. On the basis of the cytogenetic and molecular abnormality, the patient was diagnosed as having CEL, rather than reactive eosinophilia due to thyroid or prostatic cancer or other reactive inflammation. This is the first case report of CEL with t(6;11)(q27;q23) translocation.
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PMID:Chronic eosinophilic leukemia with t(6;11)(q27;q23) translocation. 1166 8

It was shown using complement-dependent cytolysis and monoclonal antibodies against CD4, CD8, and NK1.1 antigens that the cortisone-resistant CD3+4-8-NK1.1(-)-thymocytes spontaneously secreted a chemotactic transmitter inducing the release and directed migration of bone marrow cells. When estimating the general profile of the cytokines of these thymocytes by PCR with revertase, it was demonstrated the cells in question did not express cytokines with colony stimulating activities (SCF, IL-3, or GM-CSF) or cytokines affecting the migration of bone marrow stem elements (IL-2, 4, or 7). In addition, an active expression of gene bcl-2 was detected. Thus, the chemotactic cytokine inducing the release of bone marrow stem elements is a product of the cortisone-resistant long-living CD3+4-8-NK1.1(-)-T-cells of the thymus.
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PMID:[Characteristics of the cells producing thymic chemotactic factor for bone marrow stem cells]. 1196 78

Mast cells are immunoregulatory effector cells capable of releasing different mediators and cytokines implicated in inflammatory tissue processes. Previous studies suggested that IL-3 regulates growth and function of murine mast cells and human mast cell precursors, but does not affect mature human mast cells. In the present study, we found expression of IL-3 receptors (IL-3R) in freshly isolated human intestinal mast cells by reverse transcriptase (RT)-PCR and in mast cells cultured with stem cell factor (SCF) using RT-PCR and flow cytometry. IL-3R expression was enhanced when the culture medium was supplemented with IL-4 in addition to SCF. In the presence of SCF, IL-3 significantly enhanced mast cell growth in a dose-dependent fashion (179+/-51% of control, p</=0.004, n=9, ED(50) approximately 15 ng/ml) by decreasing mast cell apoptosis rather than inducing proliferation. Furthermore, IL-3 selectively enhanced histamine (from 39.6+/-12.4 to 51.2+/-15.7% specific release, p<0.02, n=8) and leukotriene C(4) (LTC(4), 5.1+/-3.4 to 10.8+/-5.5 ng/10(6) mast cells, p<0.03, n=6) release triggered by IgE receptor cross-linking without affecting prostaglandin D(2) production. In conclusion, our data show that human intestinal mast cells express functional IL-3R, indicating that IL-3 not only regulates growth and function of immature, but also that of mature human mast cells.
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PMID:Cultured human intestinal mast cells express functional IL-3 receptors and respond to IL-3 by enhancing growth and IgE receptor-dependent mediator release. 1220 44

We have investigated constitutive and phytohaemagglutinin (PHA) + phorbol 12-myristate 13-acetate (PMA)-induced gene expression of tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-2, IL-3, IL-4, IL-10, IL-12 and granulocyte macrophage colony-stimulating factor (GM-CSF) in peripheral blood mononuclear cells (PBMCs) of 10 patients with Takayasu's arteritis (TA) and 10 healthy controls by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR). The constitutive mRNA expression of TNF-alpha (69.0 +/- 4.0%versus 27.5 +/- 18.0%; P = 0.001) and IL-4 (60.0 +/- 10.0%versus 0%; P = 0.001) was significantly higher in patients than controls; that of IL-3 was comparable in both groups (38.0 +/- 6.0%versus 32.0 +/- 5.0%; P = 0.651) while no constitutive mRNA expression was observed for the other cytokines studied. The stimulated PBMCs of patients, as compared with the controls, had higher mRNA gene expression of TNF-alpha (127.0 +/- 16.0%versus 54.0 +/- 6.0%; P = 0.001), IFN-gamma (93.0 +/- 13.0%versus 57.0 +/- 5.0%; P = 0.032), IL-2 (109.0 +/- 13.0%versus 68.0 +/- 6.0%; P = 0.015), IL-3 (60.0 +/- 8.0%versus 21.2 +/- 3.0%; P = 0.045) and IL-4 (68.0 +/- 7.0%versus 27.0 +/- 7.2%; P = 0.01) The mRNA expression of IL-10 was lower in patients than controls (35.0 +/- 8.0%versus 75.0 +/- 12.0%; P = 0.022). The GM-CSF mRNA was similar (102.0 +/- 6.0%versus 89.0 +/- 5.0%; P = 0.475) in both groups. Stimulation of cells with PHA + PMA showed no IL-12 expression but stimulation with lipopolysaccharide induced higher IL-12 mRNA in patients than controls (83.0 +/- 14.0%versus 33.0 +/- 4.0%; P = 0.005). Our data suggest that an inflammatory cytokine signature exists in TA with a key role for TNF-alpha, IL-4, IL-10 and IL-12 in different pathological processes of the disease.
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PMID:Cytokine mRNA repertoire of peripheral blood mononuclear cells in Takayasu's arteritis. 1549 51


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