Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dsi-1 is a region of chromosomal DNA that underwent proviral insertion in 3 of 24 Moloney murine leukemia virus-induced rat thymomas. In one of these tumors, a provirus is also integrated adjacent to the proto-oncogene c-myc. The proviruses in Dsi-1 have been characterized and appear to be complete. The proviruses were located within a 2-kilobase region that contained four prominent DNase I-hypersensitive sites. These hypersensitive sites were observed in Moloney murine leukemia virus-induced thymomas but not in NRK cells. The region of Dsi-1 immediately 3' to the insertions cross-hybridized with human and chicken DNA, indicating that it contains highly conserved sequences. No evidence could be found for the expression of this highly conserved region. Dsi-1 was mapped to mouse chromosome 4. This location demonstrates that Dsi-1 is different from 16 of the known proto-oncogenes (c-abl, c-erbA c-erbB, c-ets-1, c-ets-2, c-fes, c-fos, c-myb, c-myc, c-raf, A-raf, c-Ha-ras, c-Ki-ras, N-ras, c-sis, and c-src) and 12 cellular regions of tumor-associated integrations in retrovirus-induced tumors (c-erbB, Fis-1, int-1, int-2, Mis-1/pvt-1, Mlvi-1, Mlvi-2, c-mos, c-myb, c-myc, Pim-1, and c-Ha-ras). Hybridization experiments indicated that Dsi-1 is probably different from five additional proto-oncogenes (c-fgr, c-fms, c-mos, neu, and c-yes) and from two additional frequent integration regions (lck and Mlvi-3).
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PMID:Dsi-1, a region with frequent proviral insertions in Moloney murine leukemia virus-induced rat thymomas. 302 11

A rat type C virus spontaneously activated from the NRK (normal rat kidney) cell line was found to have two major size classes of viral RNA subunits sedimenting at 35 and 30 S. Virus-producing cells contained both RNA species, while normal "virus-free" rat cells contained primarily virus-specific 30S RNA species. A DNA transcript, specific for Kirsten sarcoma virus, prepared from virus activated in nonproducer BALB/c cells originally transformed by Kirsten sarcoma virus and rendered specific for the virus by absorption of sequences related to mouse helper virus hybridized only with the 30S RNA species of virus-producing rat cells and normal rat cells. These findings are consistent with the hypothesis that sarcoma-specific nucleic acid sequences in kirsten sarcoma virus emerged through a process that incorporated some portions of 30S RNA species from rat cells (either normal or virus-producing) into the Kirsten leukemia virus during passage in vivo of that virus. The virus designated M-MSV(RaLV), which originally derived from tumor induced by Moloney sarcoma virus (M-MSV) in rats, contained 35S RNA species of rat type C viruses and 30S RNA species specific for both rat and mouse viruses. It appears striking that for these two animal species, sarcoma-virus-specific information resides on a 30S subunit.
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PMID:Sarcoma-virus-related RNA sequences in normal rat cells. 414 May 5

Defective Kirsten murine sarcoma virus was present as leukemia virus pseudotype [Ki-MSV(MLV)] in a 10- to 100-fold excess over its helper, Kirsten murine leukemia virus (Ki-MLV), when the two viruses were propagated in an NRK rat cell line. The s(omega,20) of the fastsedimenting RNA complex of Ki-MLV and of Ki-MSV-(MLV) was 62 S and 55 S, respectively. Gel electrophoresis in buffered aqueous or formamide solution of the dissociated 62S RNA complex of Ki-MLV showed a single major peak of molecular weight about 2.5 x 10(6). Dissociated 55S RNA of Ki-MSV(MLV) was resolved into a major component with a higher electrophoretic mobility than that of Ki-MLV RNA and molecular weight about 2.3 x 10(6). Occasionally, a minor component with the same electrophoretic mobility as Ki-MLV RNA was observed in Ki-MSV(MLV) RNA; it is thought to be the RNA of Ki-MLV present as helper virus in our stocks of Ki-MSV(MLV). The RNA of an endogenous rat C-type RNA virus was electrophoretically different from both Ki-MLV RNA and Ki-MSV(MLV) RNAs. Oligonucleotide fingerprinting of the RNAs digested with RNase T1 indicated that the RNAs of Ki-MSV(MLV) and Ki-MLV are different. However, the extent of the difference between the two RNAs could not be estimated by this method. The heat-dissociated 50-70S RNAs of two other defective murine sarcoma-leukemia viruses; Harvey-MSV(MLV) and Moloney-MSV(MLV) and of defective spleen-focus-forming Friend virus were resolved electrophoretically into two components. The larger components had the same electrophoretic mobility as the RNA of Ki-MLV or Moloney MLV. The smaller were not present in leukemia virus. It is suggested that the small RNA components of the two murine viruses and of Friend virus represent specific genetic information of these replication-defective transforming viruses. Possible relationships between the RNAs of murine leukemia viruses and replication-defective murine sarcoma and Friend viruses are discussed.
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PMID:Ribonucleic acid components of murine sarcoma and leukemia viruses. 435 79

BALB/c mouse sarcoma virus (BALB-MSV) is a spontaneously occurring transforming retrovirus of mouse origin. The integrated form of the viral genome was cloned from the DNA of a BALB-MSV-transformed nonproducer NRK cell line in the Charon 9 strain of bacteriophage lambda. In transfection assays, the 19-kilobase-pair (kbp) recombinant DNA clone transformed NIH/3T3 mouse cells with an efficiency of 3 X 10(4) focus-forming units per pmol. Such transformants possessed typical BALB-MSV morphology and released BALB-MSV after helper virus superinfection. A 6.8-kbp DNA segment within the 19-kbp DNA possessed restriction enzyme sites identical to those of the linear BALB-MSV genome. Long terminal repeats of approximately 0.6 kbp were localized at either end of the viral genome by the presence of a repeated constellation of restriction sites and by hybridization of segments containing these sites with nick-translated Moloney murine leukemia virus long terminal repeat DNA. A continuous segment of at least 0.6 and no more than 0.9 kbp of helper virus-unrelated sequences was localized toward the 3' end of the viral genome in relation to viral RNA. A probe composed of these sequences detected six EcoRI-generated DNA bands in normal mouse cell DNA as well as a smaller number of bands in rat and human DNAs. These studies demonstrate that BALB-MSV, like previously characterized avian and mammalian transforming retroviruses, arose by recombination of a type C helper virus with a well-conserved cellular gene.
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PMID:Structural organization and biological activity of molecular clones of the integrated genome of a BALB/c mouse sarcoma virus. 627 97

The biological activity of a molecularly cloned DNA of a rat endogenous C-type leukaemia helper virus, RHHV, was assessed by intranuclear microinjection into normal rat kidney cells (NRK153). Release of rat C-type leukaemia helper viruses by the microinjected cells was examined by superinfection of Kirsten-transformed non-producer cells (K-NRK). Immediate release of helper leukaemia viruses at a very low level was observed only in the NRK153 m3 . 5/cir cells microinjected with the supercoiled form of RHHV DNA in toto, suggesting that the circular form of the virus DNA might have expedited the replication and expression of virus particles. Genome rescue experiments were also performed by co-cultivating the microinjected NRK153 m cells carrying various linear RHHV DNAs, in toto or of subgenomic sizes, with K-NRK cells. The results indicated that both the total and the 5.8 to 6.2 kb DNA fragment proximal to the 5' terminus of the cloned RHHV 8.8 kb DNA were able to rescue successfully a transforming replication-competent pseudotype virus. Subgenomic DNA fragments derived from the centre or the 3' end of the RHHV DNA were ineffective in the genome rescue experiments.
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PMID:Biological activity of cloned rat endogenous C-type virus DNA transferred by microinjection. 629 32

Antibody to a synthetic peptide (anti-C3 serum) with the predicted sequence of the C terminus of the Moloney murine sarcoma virus (strain 124) v-mos gene was used in immunoprecipitation experiments with cytoplasmic extracts of a clone of NRK cells infected with ts110 Moloney murine sarcoma virus, termed 6m2 cells. ts110 Moloney murine sarcoma virus codes for two viral proteins of 85,000 and 58,000 M(r), termed P85 and P58, respectively, in nonproducer 6m2 cells maintained at 33 degrees C. Anti-C3 serum specifically recognized [(3)H]leucine-labeled P85, but not P58, from infected cells maintained at 33 degrees C, whereas antiserum prepared against murine leukemia virus p12 recognized both proteins. Normal serum and anti-C3 serum pretreated with excess C3 peptide did not precipitate P85. Immunoprecipitation experiments after metabolic labeling of 6m2 cells with (32)P(i) showed that P85 is phosphorylated. Both anti-C3 and anti-p12 sera specifically detected (32)P-labeled P85. Cell-free translation of ts110 murine sarcoma virus/murine lukemia virus RNA produces P85, P58, and helper virus protein Pr63(gag). Anti-C3 serum specifically precipitated P85 but neither P58 nor Pr63(gag). We conclude from these studies that P85 is a product of both the gag and mos genes of ts110 murine sarcoma virus, and, therefore, it is referred to as P85(gag-mos). We have not detected any other v-mos gene product in ts110-infected cells.
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PMID:P85: a gag-mos polyprotein encoded by ts110 Moloney murine sarcoma virus. 630 Apr 56

The myeloproliferative sarcoma virus (MPSV) induces extensive hematopoietic changes, including spleen foci in adult mice, and transforms fibroblasts in vitro. NRK nonproducer cell lines of MPSV and ts temperature-sensitive mutants were analyzed by restriction enzyme digestion and Southern blotting. EcoRI fragments containing the proviral DNAs of MPSV and two temperature-sensitive mutants and rat cellular sequences homologous to c-mos were molecularly cloned. By comparing restriction enzyme cleavage sites, it was shown that the MPSV genome consists only of sequences related either to Moloney murine leukemia virus or to the c-mos mouse oncogenic sequences. Two regions of fragment heterogeneity were observed: (i) in the defective pol gene, where MPSV and the two cloned temperature-sensitive mutants were different from Moloney murine sarcoma virus and from each other, although MPSV wild-type retained more of the pol gene than any of the Moloney murine sarcoma virus isolates; (ii) in the area 3' to the mos gene, which was identical in MPSV and its temperature-sensitive mutants but different from other Moloney murine sarcoma virus variants. Transfection of cloned MPSV DNA in RAT4 cells and virus rescue on infection with Friend murine leukemia virus yielded MPSV which transformed fibroblasts in vitro and also induced spleen foci in adult mice, thus proving that both properties are coded by the same viral genome.
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PMID:Molecular cloning and characterization of a leukemia-inducing myeloproliferative sarcoma virus and two of its temperature-sensitive mutants. 632 1

By the use of recombinant DNA technology and microinjection in cultured cells, the molecular genetic elements involved in the evolution of a retrovirus with the multipotential to infect, transform and replicate in host cell, have been critically examined in this investigation. Recently we have identified and purified the integrated and proviral DNA sequences specific for two rat endogenous helper leukemia viruses, WR- RaLV , originated from a chemically induced wild rat fibrosarcoma, and RHHV , isolated from a chemically induced rat hepatoma, HTC-H1 (1). By using a multidisciplinary approach combining restriction endonuclease analysis, reverse phase V-column chromatography, agarose gel electrophoresis, Southern blot transfer and filter nucleic acid hybridization, we were able to demonstrate that the rat helper leukemia viral DNA sequence was approximately 8.4-8.8 kb. The 8.8 kb RHHV DNA was molecularly cloned via the EK-1 certified vector pBR 322 plasmid into E. coli RRI cells. A successful recombinant clone, 8/32, that carried one entire RHHV 8.8 kb DNA sequence was mapped by restriction endonuclease analyses. Restricted DNA fragments of various sizes throughout the complete RHHV genome were isolated and purified for intranuclear microinjection into normal rat kidney cells. Release of type C infectious helper virus in these microinjected cells was investigated by superinfection on K-NRK, Kirsten sarcoma transformed non-producer cells. Recombination of the helper viral DNA sequence, en toto or of subgenomic sizes, carried in microinjected cells, with the sarcomagenic DNA sequence, carried in K-NRK cells, was also studied by genome-rescue and cell-transformation experiments. Our observations led to the conclusion that all critical genetic elements including the 5' LTR helper DNA sequence, gag, pol, and env genes, encoded for the biological activity of the type C helper virus resided within the 6.0 kb proximal to the 5' terminus of the endogenous rat type C helper virus DNA. They proved vitally essential for the recombination with the Src sequence during the evolution of an infectious, transforming and replication-competent retrovirus.
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PMID:Cloning of the rat endogenous helper leukemia virus DNA sequence and expression of the helper activity encoded by the cloned DNA sequence in normal rat kidney cells by microinjection. 632 7

Five rat strains were studied for immune responsiveness to SFFV-NRK, a normal rat kidney cell line non-productively infected with spleen focus-forming virus (SFFV) of the Friend leukaemia virus (FLV) complex. Antisera from ACI, JAR, Fischer and SD strains precipitated SFFV-specific gene product, gp55, whereas those from LEW did not. In the cross of Fischer X LEW, immune responsiveness to gp55 was controlled by a single or a few dominant genes. The immune responsiveness was neither related to the susceptibility to FLV infection, nor to the amount of SFFV-related RNA in spleen cells. Unresponsiveness of LEW rats to gp55 was not absolute; when LEW rats were immunized with FLV preparations from infected mice or xenotropic virus-infected NRK cells, they produced antibody that could precipitate gp55.
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PMID:Strain difference in immune response of the rat to NRK cells infected with spleen focus-forming virus of the Friend leukaemia virus complex. 641 46

Although the exact mechanism for the progression of myelofibrosis in acute megakaryoblastic leukaemia is unclear, certain humoral factors released from the proliferating megakaryoblasts that are unable to store these factors in their defective alpha-granules, including platelet derived growth factor (PDGF), fibroblast growth factors (FGF), platelet factor-4 (PF-4), transforming growth factor-beta (TGF-beta) and beta-thromboglobulin, could result in increased collagen synthesis by bone marrow fibroblasts. Recently, the human megakaryoblastic leukaemia cell line MEG-01 has been shown to produce both TGF-beta and PF-4 which have enhanced the growth of bone marrow fibroblasts. Therefore, we have examined the presence of a fibroblast growth stimulating activity and the humoral factors that might be responsible for it in the supernatant of the human megakaryoblastic leukaemia cell line ELF-153 recently established in our laboratory from a patient with acute myelofibrosis. A new fibroblast growth stimulating activity has been identified in the supernatant of the ELF-153 human megakaryoblastic leukaemia cell line that is independent of the percentage of fetal calf serum in NRK-49F fibroblast agar clonogenic assays and is not due to any of the known fibroblast growth stimulating humoral factors including PDGF, epithelial growth factor, TGF-alpha or beta, tumour necrosis factor-alpha, interleukin-1, 2, 4 or 6, FGF, fibronectin, PF-4 and factor VIII AG. Also, in vivo, subcutaneous injection of ELF-153 megakaryoblastic leukaemia cells into nude mice formed, in three out of the five mice after 6 weeks, subcutaneous tumours with a very rigid texture whose histological examination revealed dense infiltration by blast cells and pronounced reticular fibrosis. Immunohistochemistry demonstrated exclusive deposition of collagen III in the extracellular matrix whereas laminin and collagen IV were absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A new fibroblast growth stimulating activity from the human megakaryoblastic leukaemia cell line ELF-153: in vitro and in vivo findings. 748 50


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