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P Roy-Burman

Publications and source records attributed to P Roy-Burman.

At least 19 recordsLinked to original sources
PubMed1992

A revised estimate of twin concordance in systemic lupus erythematosus.

OBJECTIVE: Based on a small clinical series and previously published case reports, concordance for systemic lupus erythematosus (SLE) among monozygous (MZ) twins has been reported to be as high as 69%. Using a larger and less biased sample, we provide another estimate of this percentage. METHODS: We established a registry of twins with SLE, based upon self-reports and information provided by the patients' physicians. We used DNA fingerprinting to validate the reported zygosity in a sample of these twins. RESULTS: Of 107 twin pairs meeting the American College of Rheumatology 1982 revised criteria for the diagnosis of SLE, 24% of 45 MZ pairs and 2% of 62 dizygous (DZ) pairs were concordant. The frequency distributions of diagnostic criteria and disease symptoms in the SLE patients were similar to those in other published reports of SLE patients. Zygosity was confirmed by DNA fingerprinting in a subsample of 15 self-described MZ twins and 7 self-described DZ twins. All individuals had correctly predicted their zygosity. CONCLUSION: MZ concordance for SLE is similar to that for other autoimmune diseases and is much lower than previously believed.

Adolescent↗
PubMed1992

Biologically selected recombinants between feline leukemia virus (FeLV) subgroup A and an endogenous FeLV element.

In efforts to elucidate the proximal leukemogens that might be produced during a feline leukemia virus (FeLV) infection of cats, homologous recombinations between molecularly cloned exogenous and endogenous FeLV proviruses of known sequences were examined in cell cultures in vitro. A plasmid containing an infectious member of the most commonly occurring FeLV subgroup (FeLV subgroup A or FeLV-A) was coexpressed with noninfectious constructs containing the envelope (env) gene of an endogenously inherited FeLV-like feline genomic element in transfected feline fibroblasts. The viruses generated were selected for their ability to propagate in human cells which are resistant to infection by the parental ecotropic FeLV-A or the noninfectious endogenous constructs. An analysis of the recombinants thus derived identified a limited number of sites in the env gene which were preferentially utilized in the generation of recombinant FeLVs under the selection conditions used. These sites were clustered in the surface glycoprotein (SU) moiety of the env gene, and it appeared that most, but not all, of the SU gene product of FeLV-A, beginning from the N-terminus, can be replaced by sequences from an endogenous element, still allowing the virus to be biologically viable. In fact, these substitutions in the env gene expanded infectivity of the parental FeLV-A from ecotropic to polytropic cell tropism. Additionally, substitutions in the SU region yielded many recombinants in which a primary neutralizing pentapeptide epitope of FeLV-A was altered because of its variance in the endogenous element. In several of the recombinants, this sequence was also found to be frequently mutated. Consistent with the changes identified in this antibody-binding domain, the recombinant viruses were only weakly inhibited by a monoclonal antibody directed against this epitope, while FeLV-A was highly sensitive to neutralization.

Amino Acid Sequence↗
PubMed1991

Recombination between feline leukemia virus subgroup B or C and endogenous env elements alters the in vitro biological activities of the viruses.

An important question in feline leukemia virus (FeLV) pathogenesis is whether, as in murine leukemia virus infection, homologous recombination between the infecting FeLV and the noninfectious endogenous FeLV-like proviruses serves as a significant base for the generation of proximal pathogens. To begin an analysis of this issue, several recombinant FeLVs were produced by using two different approaches: (i) the regions of the viral envelope (env) gene of a cloned FeLV (subgroup B virus [FeLV-B], Gardner-Arnstein strain) and those of two different endogenous proviral loci were exchanged to create specific FeLV chimeras, and (ii) vectors containing endogenous env and molecularly cloned infectious FeLV-C (Sarma strain) DNA sequences were coexpressed by transfection in nonfeline cells to facilitate recombination. The results of these combined approaches showed that up to three-fourths of the envelope glycoprotein (gp70), beginning from the N-terminal end, could be replaced by endogenous FeLV sequences to produce biologically active chimeric FeLVs. The in vitro replication efficiency or cell tropism of the recombinants appeared to be influenced by the amount of gp70 sequences replaced by the endogenous partner as well as by the locus of origin of the endogenous sequences. Additionally, a characteristic biological effect, aggregation of feline T-lymphoma cells (3201B cell line), was found to be specifically induced by replicating FeLV-C or FeLV-C-based recombinants. Multiple crossover sites in the gp70 protein selected under the conditions used for coexpression were identified. The results of induced coexpression were also supported by rapid generation of FeLV recombinants when FeLV-C was used to infect the feline 3201B cell line that constitutively expresses high levels of endogenous FeLV-specific mRNAs. Furthermore, a large, highly conserved open reading frame in the pol gene of an endogenous FeLV provirus was identified. This observation, particularly in reference to our earlier finding of extensive mutations in the gag gene, reveals a target area for potentially productive homologous recombination upstream of the functional endogenous env gene.

3T3 Cells↗
PubMed1987

Enhanced expression and state of the c-myc oncogene in chemically and X-ray-transformed C3H/10T1/2 Cl 8 mouse embryo fibroblasts.

We examined expression of the c-myc oncogene in nontransformed, in three chemically transformed, and in two X-ray-transformed C3H/10T1/2 Cl 8 cell lines. In nontransformed C3H/10T1/2 cells, c-myc was expressed when cells were logarithmically growing, and expression decreased as cells reached confluence. In a methylcholanthrene-transformed cell line, MCA Si 24, c-myc expression was similar to that observed in nontransformed cells, while in two chemically transformed cell lines, Bleo Cl 2 and DMBA Cl 2, and in two radiation-transformed cell lines, F17 and F29, steady-state levels of the c-myc transcript were 5-7-fold greater than observed in nontransformed C3H/10T1/2 cells. All cell lines, both transformed and nontransformed, produced a 2.3-kilobase c-myc transcript. There was no detectable amplification or rearrangement of c-myc DNA sequences in any of the cell lines examined as determined by DNA dot blot and restriction endonuclease-Southern blotting analyses. In addition, the c-myc gene in nontransformed and transformed cell lines showed similar methylation patterns as determined by HpaII/MpsI digestion analysis, except that F19 and F29 cells lost a 0.95-kilobase HpaII band, suggesting extra region-specific methylation in these two cell lines compared to C3H/10T1/2 cells. Therefore, increased c-myc expression in the four transformed lines did not generally correlate with changes in DNA methylation in the vicinity of the c-myc gene. Our results suggest that expression of the c-myc gene is growth related and that elevated steady-state levels of c-myc RNA in certain chemically and X-ray transformed C3H/10T1/2 cell lines, such as Bleo Cl 2, DMBA Cl 2, F17, and F29, are correlated with and may participate in conversion to or maintenance of cells in the transformed state.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

Molecular analysis of several classes of endogenous feline leukemia virus elements.

Five recombinant DNA clones of endogenous feline leukemia virus-related DNA sequences were isolated by screening a lambda phage genomic library of cat placental DNA with a probe specific to the gag-pol region of infectious feline leukemia virus. The clones containing retroviral long terminal repeat-like sequences demonstrated the existence of different size classes of endogenous elements in the cat genome, including those of nearly full length in which the gag region is heterogeneous but all of pol and most of env are highly conserved. Other size classes included elements with major deletions in gag or pol. A genomic DNA analysis suggested that the majority of endogenous elements were close to full length in size and that the highly truncated sequences which we described previously (Soe et al., J. Virol. 46:829-840, 1983) represented only a subset of the elements present. A restriction analysis of genomic DNA suggested a high degree of conservation in pol and the 5' portion of env among the various endogenous sequences present in the cat genome. We also found by using DNA transfection that while all of the endogenous clones were noninfectious, there was differential expression of the elements which we examined. These findings correlate with the subgenomic expression of endogenous feline leukemia virus sequences in cat placental tissue.

Animals↗
PubMed1979

Reversion of Kirsten sarcoma virus transformed human cells: elimination of the sarcoma virus nucleotide sequences.

The virus-specific nucleotide sequences in the RNA and DNA of a Kirsten mouse sarcoma virus (Ki-MSV)-transformed non-producer human osteosarcoma cell clone and two subclones of these cells that reverted to a normal phenotype have been analysed by hybridization of sarcoma virus-specific complementary DNA (cDNA) to cellular RNA or DNA. Whereas the transformed clone had acquired de novo Ki-MSV sequences in the RNA and DNA of the cells, both the revertant cell lines seemed to have lost most or all of this information from the cellular nucleic acids. The DNA from the revertant cells lacked the sequences represented either in the Ki-MSV-specific cDNA or in the total cDNA of the leukaemia-sarcoma virus complex. Thus, the reversion of the virus-transformed human cells to normal morphology is associated with the loss of most or all of the proviral sequences from the cellular DNA.

Base Sequence↗
PubMed1979

Heteroduplex analysis of the sequence relationships between the genomes of Kirsten and Harvey sarcoma viruses, their respective parental murine leukemia viruses, and the rat endogenous 30S RNA.

The sequence relations between Kirsten murine sarcoma virus (Ki-SV), Harvey murine sarcoma virus (Ha-SV), and a rat endogenous 30S RNA were studied by electron microscope heteroduplex analysis. The sequence relationships between the sarcoma viruses and their respective parental murine leukemia viruses (Kirsten and Moloney murine leukemia viruses), as well as between the two murine leukemia viruses, were also studied. The only observed nonhomology feature of the Kirsten murine leukemia virus/Moloney murine leukemia virus heteroduplexes was a substitution loop with two arms of equal length extending from 1.80 +/- 0.18 kilobases (kb) to 2.65 +/- 0.27 kb from the 3' end of the RNA. It is believed that this feature lies in the env gene region of the viral genomes. The Ha-SV and Moloney murine leukemia virus genomes (respective lengths, 6.0 and 9.0 kb) were homologous in a 1.0 +/- 0.05-kb region at the 3' end and possibly over a 200-nucleotide region at the 5' ends; otherwise, they were nonhomologous. Ha-SV and Ki-SV (length, 7.5 kb) were homologous in the first 4.36 +/- 0.37-kb region from the 3' end and in a 0.70 +/- 0.15-kb region at the 5' end. In between, there was a nonhomology region, possibly containing a short (0.23-kb) region of partial or total homology. The heteroduplex analysis between rat endogenous 30S RNA and Ki-SV shows that there are mixed regions of sequence homology and nonhomology at both the 5' and 3' ends. However, there is a large (4-kb) region of homology between Ki-SV and the rat 30S RNA in the center of the genomes, with only a small nonhomology hairpin feature. These studies help to define the regions of homology between the Ha-SV and Ki-SV genomes with each other and with the rat endogenous 30S RNA. These regions may be related to the sarcoma genicity of the viruses. In particular, the 0.7-kb region of homology of Ha-SV with Ki-SV at the 5' ends may be related to the formation of a 21,000-dalton phosphoprotein in cells transformed by either virus.

Animals↗
PubMed1978

RNA tumor virus phosphoproteins: primary structural analysis and identification of phosphopeptides.

Two-dimensional tryptic peptide mapping was used to compare the peptide sequences of the phosphoprotein (pp12) of cloned ecotropic and amphotropic wild mouse leukemia viruses, strains 1504 and 292. The maps of two ecotropic isolates were very similar to one another, as were the maps of two amphotropic isolates. There was also extensive similarity between the maps of this protein from ecotropic and amphotropic viruses, although characteristic peptide differences were readily recognized. These differences were consistent with the general type specificity of oncovirus phosphoproteins. The pp12 of the field isoalte of 292 virus contained five phosphopeptides, and the non-phosphorylated and variously phosphorylated species of this pp12 showed identical peptide maps, indicating differential phosphorylation of a single polypeptide.

Base Sequence↗
PubMed1977

Endogenous RD-114 virus genome expression in malignant tissues of domestic cats.

Endogenous xenotropic cat type C virus (RD-114)- and infectious feline leukemia virus (FeLV)-specific gene expressions were measured in spontaneous sarcomas carcinomas, and nonmalignant cat tissues by molecular hybridization for virus-specific RNA and competition radio-immunoassays for the major internal protein (p30) of these two viruses. The results indicate that RD-114 gene expression in sarcomas and carcinomas at both RNA and p30 levels is significantly higher than histologically normal tissues from cats free of cancer. In contrast, the levels of FeLV viral RNA and p30 are fount to be low or undetectable in the majority of these tumored and normal tissues examined. Whereas variability in the amounts of RD-114 OR FeLV RNA and p30 expressed is found in tissues from different cats, their expression is fairly uniform in multiple malignant tissues of the same cat. The finding of widespread occurrence of elevated RD-114 gene expression in sarcomas and carcinomas is consistent with our similar observation with natural lymphomas of domestic cats and suggests that expression of certain functions of this endogenous virus may be etiologically involved in the development of many different spontaneous neoplasms of cats.

Animals↗