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)

Cell cultures established from the spleen of a Macaca nemestrina with enzootic retroperitoneal fibromatosis (ERF) spontaneously released a unique retrovirus. Throughout 14 serial passages, the spleen cell cultures remained fibroblastic and no cytopathic effect was evident. The virus incorporates [3H]uridine, contains an RNA-dependent DNA polymerase (RDDP), has a buoyant density of 1.15 g/cm3 in sucrose, and was designated MNV-1. Virion-associated reverse transcriptase showed no preference for either Mg2+ or Mn2+ in standard RDDP assays. Complementary DNA (cDNA) transcribed from polyadenylated MNV-1 RNA hybridized to genomic DNA and RNA extracted from diseased tissues but not to nucleic acids from normal tissues of a healthy Macaca nemestrina or a Macaca mulatta. MNV-1 is therefore exogenous to these species. MNV-1 had no detectable homology to the endogenous macaque virus isolates MAC-1 and MMC-1. Liquid hybridization of MNV-1 cDNA to viral RNA derived from exogenous and endogenous subhuman primate retroviruses (SiSV(SSAV), GALV-SF, BaEV-M7, and BILN) did not reveal any significant sequence homologies. In addition, MNV-1 does not share homology with bovine leukemia virus or Mason-Pfizer monkey virus as determined by Southern blot hybridization. We conclude that MNV-1 is a unique retrovirus which has not previously been described. As the ultrastructure of virions in in vitro cell cultures, as well as disease involved tissue, show some particles with type C morphology and others with type D morphology, MNV-1 may be comprised of more than one component.
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PMID:Isolation of a unique retrovirus, MNV-1, from Macaca nemestrina. 686 69

A newborn baby boy was diagnosed with the mixed form of congenital mesoblastic nephroma (CMN) representing both classic and cellular histology features in the renal tumor. Additionally, the patient had skin and bone lesions consistent with multifocal involvement of a generalized infantile fibromatosis (IFS). Both skin and bone lesions were distinctly different from CMN and did not represent metastasis. The primary tumor cell line (MCH-MN-1), established from the resected right kidney tumor, had a diploid DNA content. Cytogenetic studies revealed deletion on the long arm of chromosome 3 (q21q24) and duplication on the short arm of chromosome 11 (p15). MCH-MN-1 cells expressed ETV6-NTRK3 gene fusion transcripts, characteristic of cellular and mixed forms of CMNs. The cells had high p21 and low Bax mRNA expression in the reverse transcriptase-polymerase chain reaction (RT-PCR) assay. The high level of proliferative marker (Ki67) mRNA expression correlated well with the pluripotent nature of MCH-MN-1 in tissue culture (cell doubling time = 12.4 h). Our results showed that MCH-MN-1 might be a good model cell line for investigations on mesoblastic nephroma.
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PMID:Cytogenetic and molecular characterization of a congenital mesoblastic nephroma. 1144 43

Infantile myofibromatosis (IM) is a distinctive mesenchymal disorder with different clinical forms, including solitary, multicentric, and generalized with visceral involvement. A wide morphologic spectrum is encountered, with the extremes resembling congenital infantile fibrosarcoma (CIFS) and infantile hemangiopericytoma. We report a series of lesions with mixed features of CIFS and IM and compare them in order to further define their clinicopathologic features and the significance of the so-called composite fibromatosis. Seven lesions with unusual overlapping morphologic "composite" features of both IM and CIFS were selected from a series of 106 myofibroblastic lesions. Three cases classified as composite infantile myofibromatoses (COIM) were highly cellular tumors with a diffuse growth of primitive mesenchymal cells and focal features of IM combined with areas resembling infantile fibrosarcoma (IF). Four cases were classified as IF. Three of these exhibited a biphasic pattern with foci resembling IM, including whorls of primitive and spindle cells and perivascular and intravascular projections of myofibroblastic nodules, and the 4th had a close histologic resemblance to a primitive, immature IM. With reverse transcriptase polymerase chain reaction, the ETV6-NTRK3 transcript was absent in 3 COIM and was detected in 3 CIFS; the other CIFS had typical cytogenetic aberrations. On the basis of currently available information, COIM represents a morphologic variant of IM that can mimic IF. Careful histologic evaluation to detect the typical features of IM is essential to avoid classification as IF. Molecular analysis for the ETV6-NTRK3 gene fusion is an important diagnostic tool in this group of lesions.
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PMID:Morphologic Overlap between Infantile Myofibromatosis and Infantile Fibrosarcoma: A Pitfall in Diagnosis. 1900 26