A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.
Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) isolated from spontaneous leukemia in AKR strain mice.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) producing leukemia of the reticulum-cell type with massive infiltration of liver, spleen, and bone marrow. It infects DBA/2 and Swiss mice.
A replication-defective murine sarcoma virus (SARCOMA VIRUSES, MURINE) isolated from a rhabdomyosarcoma by Moloney in 1966.
An enzyme that synthesizes DNA on an RNA template. It is encoded by the pol gene of retroviruses and by certain retrovirus-like elements. EC 2.7.7.49.
Virus diseases caused by the RETROVIRIDAE.
A replication-defective strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) capable of transforming lymphoid cells and producing a rapidly progressing lymphoid leukemia after superinfection with FRIEND MURINE LEUKEMIA VIRUS; MOLONEY MURINE LEUKEMIA VIRUS; or RAUSCHER VIRUS.
Deoxyribonucleic acid that makes up the genetic material of viruses.
Family of RNA viruses that infects birds and mammals and encodes the enzyme reverse transcriptase. The family contains seven genera: DELTARETROVIRUS; LENTIVIRUS; RETROVIRUSES TYPE B, MAMMALIAN; ALPHARETROVIRUS; GAMMARETROVIRUS; RETROVIRUSES TYPE D; and SPUMAVIRUS. A key feature of retrovirus biology is the synthesis of a DNA copy of the genome which is integrated into cellular DNA. After integration it is sometimes not expressed but maintained in a latent state (PROVIRUSES).
A group of replication-defective viruses, in the genus GAMMARETROVIRUS, which are capable of transforming cells, but which replicate and produce tumors only in the presence of Murine leukemia viruses (LEUKEMIA VIRUS, MURINE).
Conditions in which the abnormalities in the peripheral blood or bone marrow represent the early manifestations of acute leukemia, but in which the changes are not of sufficient magnitude or specificity to permit a diagnosis of acute leukemia by the usual clinical criteria.
Proteins coded by the retroviral gag gene. The products are usually synthesized as protein precursors or POLYPROTEINS, which are then cleaved by viral proteases to yield the final products. Many of the final products are associated with the nucleoprotein core of the virion. gag is short for group-specific antigen.
A species of GAMMARETROVIRUS causing leukemia, lymphosarcoma, immune deficiency, or other degenerative diseases in cats. Several cellular oncogenes confer on FeLV the ability to induce sarcomas (see also SARCOMA VIRUSES, FELINE).
The functional hereditary units of VIRUSES.
Established cell cultures that have the potential to propagate indefinitely.
Duplex DNA sequences in eukaryotic chromosomes, corresponding to the genome of a virus, that are transmitted from one cell generation to the next without causing lysis of the host. Proviruses are often associated with neoplastic cell transformation and are key features of retrovirus biology.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.
Strains of MURINE LEUKEMIA VIRUS discovered in 1976 by Hartley, Wolford, Old, and Rowe and so named because the viruses originally isolated had the capacity to transform cell foci in mink cell cultures. MCF viruses are generated by recombination with ecotropic murine leukemia viruses including AKR, Friend, Moloney, and Rauscher, causing ERYTHROLEUKEMIA and severe anemia in mice.
Insertion of viral DNA into host-cell DNA. This includes integration of phage DNA into bacterial DNA; (LYSOGENY); to form a PROPHAGE or integration of retroviral DNA into cellular DNA to form a PROVIRUS.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A strain of MURINE LEUKEMIA VIRUS associated with mouse tumors similar to those caused by the FRIEND MURINE LEUKEMIA VIRUS. It is a replication-competent murine leukemia virus. It can act as a helper virus when complexing with a defective transforming component, RAUSCHER SPLEEN FOCUS-FORMING VIRUS.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Ribonucleic acid that makes up the genetic material of viruses.
A ribonuclease that specifically cleaves the RNA moiety of RNA:DNA hybrids. It has been isolated from a wide variety of prokaryotic and eukaryotic organisms as well as RETROVIRUSES.
Sequences of DNA or RNA that occur in multiple copies. There are several types: INTERSPERSED REPETITIVE SEQUENCES are copies of transposable elements (DNA TRANSPOSABLE ELEMENTS or RETROELEMENTS) dispersed throughout the genome. TERMINAL REPEAT SEQUENCES flank both ends of another sequence, for example, the long terminal repeats (LTRs) on RETROVIRUSES. Variations may be direct repeats, those occurring in the same direction, or inverted repeats, those opposite to each other in direction. TANDEM REPEAT SEQUENCES are copies which lie adjacent to each other, direct or inverted (INVERTED REPEAT SEQUENCES).
DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.
The type species of DELTARETROVIRUS that causes a form of bovine lymphosarcoma (ENZOOTIC BOVINE LEUKOSIS) or persistent lymphocytosis.
A genus of RETROVIRIDAE comprising endogenous sequences in mammals, related RETICULOENDOTHELIOSIS VIRUSES, AVIAN, and a reptilian virus. Many species contain oncogenes and cause leukemias and sarcomas.
Infections produced by oncogenic viruses. The infections caused by DNA viruses are less numerous but more diverse than those caused by the RNA oncogenic viruses.
DNA sequences that form the coding region for proteins associated with the viral core in retroviruses. gag is short for group-specific antigen.
The infective system of a virus, composed of the viral genome, a protein core, and a protein coat called a capsid, which may be naked or enclosed in a lipoprotein envelope called the peplos.
Specific molecular components of the cell capable of recognizing and interacting with a virus, and which, after binding it, are capable of generating some signal that initiates the chain of events leading to the biological response.
Retroviral proteins, often glycosylated, coded by the envelope (env) gene. They are usually synthesized as protein precursors (POLYPROTEINS) and later cleaved into the final viral envelope glycoproteins by a viral protease.
Layers of protein which surround the capsid in animal viruses with tubular nucleocapsids. The envelope consists of an inner layer of lipids and virus specified proteins also called membrane or matrix proteins. The outer layer consists of one or more types of morphological subunits called peplomers which project from the viral envelope; this layer always consists of glycoproteins.
Retroviral proteins that have the ability to transform cells. They can induce sarcomas, leukemias, lymphomas, and mammary carcinomas. Not all retroviral proteins are oncogenic.
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
Proteins found in any species of virus.
Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. Some are host-dependent defectives, meaning they can replicate only in cell systems which provide the particular genetic function which they lack. Others, called SATELLITE VIRUSES, are able to replicate only when their genetic defect is complemented by a helper virus.
Recombinases that insert exogenous DNA into the host genome. Examples include proteins encoded by the POL GENE of RETROVIRIDAE and also by temperate BACTERIOPHAGES, the best known being BACTERIOPHAGE LAMBDA.
An inheritable change in cells manifested by changes in cell division and growth and alterations in cell surface properties. It is induced by infection with a transforming virus.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
Proteins from the family Retroviridae. The most frequently encountered member of this family is the Rous sarcoma virus protein.
DNA sequences that form the coding region for retroviral enzymes including reverse transcriptase, protease, and endonuclease/integrase. "pol" is short for polymerase, the enzyme class of reverse transcriptase.
Viruses which enable defective viruses to replicate or to form a protein coat by complementing the missing gene function of the defective (satellite) virus. Helper and satellite may be of the same or different genus.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
DNA sequences that form the coding region for the viral envelope (env) proteins in retroviruses. The env genes contain a cis-acting RNA target sequence for the rev protein (= GENE PRODUCTS, REV), termed the rev-responsive element (RRE).
Production of new arrangements of DNA by various mechanisms such as assortment and segregation, CROSSING OVER; GENE CONVERSION; GENETIC TRANSFORMATION; GENETIC CONJUGATION; GENETIC TRANSDUCTION; or mixed infection of viruses.
The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.
Widely used technique which exploits the ability of complementary sequences in single-stranded DNAs or RNAs to pair with each other to form a double helix. Hybridization can take place between two complimentary DNA sequences, between a single-stranded DNA and a complementary RNA, or between two RNA sequences. The technique is used to detect and isolate specific sequences, measure homology, or define other characteristics of one or both strands. (Kendrew, Encyclopedia of Molecular Biology, 1994, p503)
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
Tumors or cancer of the THYMUS GLAND.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Biologically active DNA which has been formed by the in vitro joining of segments of DNA from different sources. It includes the recombination joint or edge of a heteroduplex region where two recombining DNA molecules are connected.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Nucleotide sequences repeated on both the 5' and 3' ends of a sequence under consideration. For example, the hallmarks of a transposon are that it is flanked by inverted repeats on each end and the inverted repeats are flanked by direct repeats. The Delta element of Ty retrotransposons and LTRs (long terminal repeats) are examples of this concept.
A general term for various neoplastic diseases of the lymphoid tissue.
Cis-acting DNA sequences which can increase transcription of genes. Enhancers can usually function in either orientation and at various distances from a promoter.
The transfer of bacterial DNA by phages from an infected bacterium to another bacterium. This also refers to the transfer of genes into eukaryotic cells by viruses. This naturally occurring process is routinely employed as a GENE TRANSFER TECHNIQUE.
A genus of the family HYLOBATIDAE consisting of six species. The members of this genus inhabit rain forests in southeast Asia. They are arboreal and differ from other anthropoids in the great length of their arms and very slender bodies and limbs. Their major means of locomotion is by swinging from branch to branch by their arms. Hylobates means dweller in the trees. Some authors refer to Symphalangus and Nomascus as Hylobates. The six genera include: H. concolor (crested or black gibbon), H. hoolock (Hoolock gibbon), H. klossii (Kloss's gibbon; dwarf siamang), H. lar (common gibbon), H. pileatus (pileated gibbon), and H. syndactylus (siamang). H. lar is also known as H. agilis (lar gibbon), H. moloch (agile gibbon), and H. muelleri (silvery gibbon).
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)
Carnivores of genus Mustela of the family MUSTELIDAE. The European mink, which has white upper and lower lips, was widely trapped for commercial purposes and is classified as endangered. The American mink, lacking a white upper lip, is farmed commercially.
A neoplasm originating from thymic tissue, usually benign, and frequently encapsulated. Although it is occasionally invasive, metastases are extremely rare. It consists of any type of thymic epithelial cell as well as lymphocytes that are usually abundant. Malignant lymphomas that involve the thymus, e.g., lymphosarcoma, Hodgkin's disease (previously termed granulomatous thymoma), should not be regarded as thymoma. (From Stedman, 25th ed)
A transfer RNA which is specific for carrying proline to sites on the ribosomes in preparation for protein synthesis.
A species of GAMMARETROVIRUS causing leukemia in the gibbon ape. Natural transmission is by contact.
A species of ALPHARETROVIRUS causing anemia in fowl.
Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.
A group of heterogeneous lymphoid tumors representing malignant transformations of T-lymphocytes.
Enzymes that are part of the restriction-modification systems. They catalyze the endonucleolytic cleavage of DNA sequences which lack the species-specific methylation pattern in the host cell's DNA. Cleavage yields random or specific double-stranded fragments with terminal 5'-phosphates. The function of restriction enzymes is to destroy any foreign DNA that invades the host cell. Most have been studied in bacterial systems, but a few have been found in eukaryotic organisms. They are also used as tools for the systematic dissection and mapping of chromosomes, in the determination of base sequences of DNAs, and have made it possible to splice and recombine genes from one organism into the genome of another. EC 3.21.1.
Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.
Serine-threonine protein kinases that relay signals from CYTOKINE RECEPTORS and are involved in control of CELL GROWTH PROCESSES; CELL DIFFERENTIATION; and APOPTOSIS.
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
A method (first developed by E.M. Southern) for detection of DNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.
Genes whose gain-of-function alterations lead to NEOPLASTIC CELL TRANSFORMATION. They include, for example, genes for activators or stimulators of CELL PROLIFERATION such as growth factors, growth factor receptors, protein kinases, signal transducers, nuclear phosphoproteins, and transcription factors. A prefix of "v-" before oncogene symbols indicates oncogenes captured and transmitted by RETROVIRUSES; the prefix "c-" before the gene symbol of an oncogene indicates it is the cellular homolog (PROTO-ONCOGENES) of a v-oncogene.
A strain of PRIMATE T-LYMPHOTROPIC VIRUS 1 isolated from mature T4 cells in patients with T-lymphoproliferation malignancies. It causes adult T-cell leukemia (LEUKEMIA-LYMPHOMA, T-CELL, ACUTE, HTLV-I-ASSOCIATED), T-cell lymphoma (LYMPHOMA, T-CELL), and is involved in mycosis fungoides, SEZARY SYNDROME and tropical spastic paraparesis (PARAPARESIS, TROPICAL SPASTIC).
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
The outer protein protective shell of a virus, which protects the viral nucleic acid.
Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The complete genetic complement contained in a DNA or RNA molecule in a virus.
Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.
Polyprotein products of a fused portion of retroviral mRNA containing the gag and pol genes. The polyprotein is synthesized only five percent of the time since pol is out of frame with gag, and is generated by ribosomal frameshifting.
The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.
Enzymes that catalyze the incorporation of deoxyribonucleotides into a chain of DNA. EC 2.7.7.-.
A continuous cell line of high contact-inhibition established from NIH Swiss mouse embryo cultures. The cells are useful for DNA transfection and transformation studies. (From ATCC [Internet]. Virginia: American Type Culture Collection; c2002 [cited 2002 Sept 26]. Available from http://www.atcc.org/)
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
An individual that contains cell populations derived from different zygotes.
Process of growing viruses in live animals, plants, or cultured cells.
Normal cellular genes homologous to viral oncogenes. The products of proto-oncogenes are important regulators of biological processes and appear to be involved in the events that serve to maintain the ordered procession through the cell cycle. Proto-oncogenes have names of the form c-onc.
Substances elaborated by viruses that have antigenic activity.
A myeloproliferative disorder characterized by neoplastic proliferation of erythroblastic and myeloblastic elements with atypical erythroblasts and myeloblasts in the peripheral blood.
Method for measuring viral infectivity and multiplication in CULTURED CELLS. Clear lysed areas or plaques develop as the VIRAL PARTICLES are released from the infected cells during incubation. With some VIRUSES, the cells are killed by a cytopathic effect; with others, the infected cells are not killed but can be detected by their hemadsorptive ability. Sometimes the plaque cells contain VIRAL ANTIGENS which can be measured by IMMUNOFLUORESCENCE.
Macromolecular molds for the synthesis of complementary macromolecules, as in DNA REPLICATION; GENETIC TRANSCRIPTION of DNA to RNA, and GENETIC TRANSLATION of RNA into POLYPEPTIDES.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Viruses whose genetic material is RNA.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
The property of objects that determines the direction of heat flow when they are placed in direct thermal contact. The temperature is the energy of microscopic motions (vibrational and translational) of the particles of atoms.
The introduction of functional (usually cloned) GENES into cells. A variety of techniques and naturally occurring processes are used for the gene transfer such as cell hybridization, LIPOSOMES or microcell-mediated gene transfer, ELECTROPORATION, chromosome-mediated gene transfer, TRANSFECTION, and GENETIC TRANSDUCTION. Gene transfer may result in genetically transformed cells and individual organisms.
Fusion of somatic cells in vitro or in vivo, which results in somatic cell hybridization.
An encapsulated lymphatic organ through which venous blood filters.
An endogenous GAMMARETROVIRUS from the germ line of mice but isolated from humans. It has close similarity to xenotropic MURINE LEUKEMIA VIRUS.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
The spatial arrangement of the atoms of a nucleic acid or polynucleotide that results in its characteristic 3-dimensional shape.
Polymers made up of a few (2-20) nucleotides. In molecular genetics, they refer to a short sequence synthesized to match a region where a mutation is known to occur, and then used as a probe (OLIGONUCLEOTIDE PROBES). (Dorland, 28th ed)
A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.
Process of generating a genetic MUTATION. It may occur spontaneously or be induced by MUTAGENS.
A group of genetically identical cells all descended from a single common ancestral cell by mitosis in eukaryotes or by binary fission in prokaryotes. Clone cells also include populations of recombinant DNA molecules all carrying the same inserted sequence. (From King & Stansfield, Dictionary of Genetics, 4th ed)
Leukemia associated with HYPERPLASIA of the lymphoid tissues and increased numbers of circulating malignant LYMPHOCYTES and lymphoblasts.
A family of the order Rodentia containing 250 genera including the two genera Mus (MICE) and Rattus (RATS), from which the laboratory inbred strains are developed. The fifteen subfamilies are SIGMODONTINAE (New World mice and rats), CRICETINAE, Spalacinae, Myospalacinae, Lophiomyinae, ARVICOLINAE, Platacanthomyinae, Nesomyinae, Otomyinae, Rhizomyinae, GERBILLINAE, Dendromurinae, Cricetomyinae, MURINAE (Old World mice and rats), and Hydromyinae.
Mutagenesis where the mutation is caused by the introduction of foreign DNA sequences into a gene or extragenic sequence. This may occur spontaneously in vivo or be experimentally induced in vivo or in vitro. Proviral DNA insertions into or adjacent to a cellular proto-oncogene can interrupt GENETIC TRANSLATION of the coding sequences or interfere with recognition of regulatory elements and cause unregulated expression of the proto-oncogene resulting in tumor formation.
Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
The sum of the weight of all the atoms in a molecule.
A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.
Viruses that produce tumors.
A genus of the family RETROVIRIDAE consisting of non-oncogenic retroviruses that produce multi-organ diseases characterized by long incubation periods and persistent infection. Lentiviruses are unique in that they contain open reading frames (ORFs) between the pol and env genes and in the 3' env region. Five serogroups are recognized, reflecting the mammalian hosts with which they are associated. HIV-1 is the type species.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) isolated from radiation-induced lymphomas in C57BL mice. It is leukemogenic, thymotrophic, can be transmitted vertically, and replicates only in vivo.
A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms.
Refers to animals in the period of time just after birth.
Acquired defect of cellular immunity that occurs in mice infected with mouse leukemia viruses (MuLV). The syndrome shows striking similarities with human AIDS and is characterized by lymphadenopathy, profound immunosuppression, enhanced susceptibility to opportunistic infections, and B-cell lymphomas.
Transcriptional trans-acting proteins of the promoter elements found in the long terminal repeats (LTR) of HUMAN T-LYMPHOTROPIC VIRUS 1 and HUMAN T-LYMPHOTROPIC VIRUS 2. The tax (trans-activator x; x is undefined) proteins act by binding to enhancer elements in the LTR.
The biosynthesis of DNA carried out on a template of RNA.
The type species of VESICULOVIRUS causing a disease symptomatically similar to FOOT-AND-MOUTH DISEASE in cattle, horses, and pigs. It may be transmitted to other species including humans, where it causes influenza-like symptoms.
Experimentally induced neoplasms of CONNECTIVE TISSUE in animals to provide a model for studying human SARCOMA.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
A group of deoxyribonucleotides (up to 12) in which the phosphate residues of each deoxyribonucleotide act as bridges in forming diester linkages between the deoxyribose moieties.
Actual loss of portion of a chromosome.
The adherence and merging of cell membranes, intracellular membranes, or artificial membranes to each other or to viruses, parasites, or interstitial particles through a variety of chemical and physical processes.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Group of alpharetroviruses (ALPHARETROVIRUS) producing sarcomata and other tumors in chickens and other fowl and also in pigeons, ducks, and RATS.
Progenitor cells from which all blood cells derive.
The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.
Proteins prepared by recombinant DNA technology.
A single, unpaired primary lymphoid organ situated in the MEDIASTINUM, extending superiorly into the neck to the lower edge of the THYROID GLAND and inferiorly to the fourth costal cartilage. It is necessary for normal development of immunologic function early in life. By puberty, it begins to involute and much of the tissue is replaced by fat.
Retroviral proteins coded by the pol gene. They are usually synthesized as a protein precursor (POLYPROTEINS) and later cleaved into final products that include reverse transcriptase, endonuclease/integrase, and viral protease. Sometimes they are synthesized as a gag-pol fusion protein (FUSION PROTEINS, GAG-POL). pol is short for polymerase, the enzyme class of reverse transcriptase.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
14-carbon saturated monocarboxylic acids.
Techniques and strategies which include the use of coding sequences and other conventional or radical means to transform or modify cells for the purpose of treating or reversing disease conditions.
Proteins found mainly in icosahedral DNA and RNA viruses. They consist of proteins directly associated with the nucleic acid inside the NUCLEOCAPSID.
The small RNA molecules, 73-80 nucleotides long, that function during translation (TRANSLATION, GENETIC) to align AMINO ACIDS at the RIBOSOMES in a sequence determined by the mRNA (RNA, MESSENGER). There are about 30 different transfer RNAs. Each recognizes a specific CODON set on the mRNA through its own ANTICODON and as aminoacyl tRNAs (RNA, TRANSFER, AMINO ACYL), each carries a specific amino acid to the ribosome to add to the elongating peptide chains.
Any of various enzymatically catalyzed post-translational modifications of PEPTIDES or PROTEINS in the cell of origin. These modifications include carboxylation; HYDROXYLATION; ACETYLATION; PHOSPHORYLATION; METHYLATION; GLYCOSYLATION; ubiquitination; oxidation; proteolysis; and crosslinking and result in changes in molecular weight and electrophoretic motility.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
A family of enzymes that catalyze the endonucleolytic cleavage of RNA. It includes EC 3.1.26.-, EC 3.1.27.-, EC 3.1.30.-, and EC 3.1.31.-.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
A phenomenon in which infection by a first virus results in resistance of cells or tissues to infection by a second, unrelated virus.
A true neoplasm composed of a number of different types of tissue, none of which is native to the area in which it occurs. It is composed of tissues that are derived from three germinal layers, the endoderm, mesoderm, and ectoderm. They are classified histologically as mature (benign) or immature (malignant). (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1642)
A class of enzymes that inactivate aminocyclitol-aminoglycoside antibiotics (AMINOGLYCOSIDES) by regiospecific PHOSPHORYLATION of the 3' and/or 5' hydroxyl.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
Any of the covalently closed DNA molecules found in bacteria, many viruses, mitochondria, plastids, and plasmids. Small, polydisperse circular DNA's have also been observed in a number of eukaryotic organisms and are suggested to have homology with chromosomal DNA and the capacity to be inserted into, and excised from, chromosomal DNA. It is a fragment of DNA formed by a process of looping out and deletion, containing a constant region of the mu heavy chain and the 3'-part of the mu switch region. Circular DNA is a normal product of rearrangement among gene segments encoding the variable regions of immunoglobulin light and heavy chains, as well as the T-cell receptor. (Riger et al., Glossary of Genetics, 5th ed & Segen, Dictionary of Modern Medicine, 1992)
The type species of ORTHOPOXVIRUS, related to COWPOX VIRUS, but whose true origin is unknown. It has been used as a live vaccine against SMALLPOX. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of VACCINIA VIRUS.
The sequential correspondence of nucleotides in one nucleic acid molecule with those of another nucleic acid molecule. Sequence homology is an indication of the genetic relatedness of different organisms and gene function.
Transforming proteins encoded by the abl oncogenes. Oncogenic transformation of c-abl to v-abl occurs by insertional activation that results in deletions of specific N-terminal amino acids.
Enzymes that catalyze the hydrolysis of ester bonds within RNA. EC 3.1.-.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
DNA present in neoplastic tissue.
Any method used for determining the location of and relative distances between genes on a chromosome.
A lymphoid neoplastic disease in cattle caused by the bovine leukemia virus. Enzootic bovine leukosis may take the form of lymphosarcoma, malignant lymphoma, or leukemia but the presence of malignant cells in the blood is not a consistent finding.
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.
Motifs in DNA- and RNA-binding proteins whose amino acids are folded into a single structural unit around a zinc atom. In the classic zinc finger, one zinc atom is bound to two cysteines and two histidines. In between the cysteines and histidines are 12 residues which form a DNA binding fingertip. By variations in the composition of the sequences in the fingertip and the number and spacing of tandem repeats of the motif, zinc fingers can form a large number of different sequence specific binding sites.
The rate dynamics in chemical or physical systems.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
Double-stranded nucleic acid molecules (DNA-DNA or DNA-RNA) which contain regions of nucleotide mismatches (non-complementary). In vivo, these heteroduplexes can result from mutation or genetic recombination; in vitro, they are formed by nucleic acid hybridization. Electron microscopic analysis of the resulting heteroduplexes facilitates the mapping of regions of base sequence homology of nucleic acids.
A polynucleotide consisting essentially of chains with a repeating backbone of phosphate and ribose units to which nitrogenous bases are attached. RNA is unique among biological macromolecules in that it can encode genetic information, serve as an abundant structural component of cells, and also possesses catalytic activity. (Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The type species of ALPHARETROVIRUS producing latent or manifest lymphoid leukosis in fowl.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
A malignant disease of the T-LYMPHOCYTES in the bone marrow, thymus, and/or blood.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A purine or pyrimidine base bonded to a DEOXYRIBOSE containing a bond to a phosphate group.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
A fractionated cell extract that maintains a biological function. A subcellular fraction isolated by ultracentrifugation or other separation techniques must first be isolated so that a process can be studied free from all of the complex side reactions that occur in a cell. The cell-free system is therefore widely used in cell biology. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p166)
The ultimate exclusion of nonsense sequences or intervening sequences (introns) before the final RNA transcript is sent to the cytoplasm.
A family of highly conserved and widely expressed sodium-phosphate cotransporter proteins. They are electrogenic sodium-dependent transporters of phosphate that were originally identified as retroviral receptors in HUMANS and have been described in yeast and many other organisms.
Genes which regulate or circumscribe the activity of other genes; specifically, genes which code for PROTEINS or RNAs which have GENE EXPRESSION REGULATION functions.
An enzyme that catalyzes the acetylation of chloramphenicol to yield chloramphenicol 3-acetate. Since chloramphenicol 3-acetate does not bind to bacterial ribosomes and is not an inhibitor of peptidyltransferase, the enzyme is responsible for the naturally occurring chloramphenicol resistance in bacteria. The enzyme, for which variants are known, is found in both gram-negative and gram-positive bacteria. EC 2.3.1.28.
Leukemia produced by exposure to IONIZING RADIATION or NON-IONIZING RADIATION.
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.
Deletion of sequences of nucleic acids from the genetic material of an individual.
Disruption of the secondary structure of nucleic acids by heat, extreme pH or chemical treatment. Double strand DNA is "melted" by dissociation of the non-covalent hydrogen bonds and hydrophobic interactions. Denatured DNA appears to be a single-stranded flexible structure. The effects of denaturation on RNA are similar though less pronounced and largely reversible.
A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (CODON, TERMINATOR). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, TRANSFER) complementary to all codons. These codons are referred to as unassigned codons (CODONS, NONSENSE).

Suppression of Moloney sarcoma virus immunity following sensitization with attenuated virus. (1/1467)

Murine sarcoma virus (Moloney strain) (MSV-M)-induced tumors are unusual in that they regularly appear less than 2 weeks after virus inoculation, progress for 1 to 2 weeks, and are rejected by normal adult BALB/c mice. Rejectio leaves the animals immune to tumor induction. In the present study, presensitization of normal adult BALB/c mice with attenuated MSV-M resulted in an altered pattern of tumor immunity. Injection of active MSV-M into the presensitized animals resulted in tumor induction and rejection similar to that observed in normal animals, but rejection failed to produce protection against the secondary inoculation with MSV-M. After the second inoculation with active MSV-M, tumors appeared and progressed but ultimately were rejected. Over 80% of the mice died, 25% after the primary challenge and the remainder after the secondary challenge. At death, all mice had histological evidence of leukemia which was the probable cause of death. The animals that died following the secondary challenge also had evidence of disseminated MSV-M. Solid tumor nodules were found in skeletal muscle distant from the original site of inoculation, and active MSV-M was isolated from spleen and lungs. The possibility that the results were produced by specific suppression of MSV-Moloney leukemia virus immunity is discussed.  (+info)

Inhibition of the rous sarcoma virus long terminal repeat-driven transcription by in vitro methylation: different sensitivity in permissive chicken cells versus mammalian cells. (2/1467)

Rous sarcoma virus (RSV) enhancer sequences in the long terminal repeat (LTR) have previously been shown to be sensitive to CpG methylation. We report further that the high density methylation of the RSV LTR-driven chloramphenicol acetyltransferase reporter is needed for full transcriptional inhibition in chicken embryo fibroblasts and for suppression of tumorigenicity of the RSV proviral DNA in chickens. In nonpermissive mammalian cells, however, the low density methylation is sufficient for full inhibition. The time course of inhibition differs strikingly in avian and mammalian cells: although immediately inhibited in mammalian cells, the methylated RSV LTR-driven reporter is fully inhibited with a significant delay after transfection in avian cells. Moreover, transcriptional inhibition can be overridden by transfection with a high dose of the methylated reporter plasmid in chicken cells but not in hamster cells. The LTR, v-src, LTR proviral DNA is easily capable of inducing sarcomas in chickens but not in hamsters. In contrast, Moloney murine leukemia virus LTR-driven v-src induces sarcomas in hamsters with high incidence. Therefore, the repression of integrated RSV proviruses in rodent cells is directed against the LTR.  (+info)

Gene transfer of cytokine inhibitors into human synovial fibroblasts in the SCID mouse model. (3/1467)

OBJECTIVE: To investigate the effects of retrovirus-based gene delivery of inhibitory cytokines and cytokine inhibitors into human synovial fibroblasts in the SCID mouse model of rheumatoid arthritis (RA). METHODS: The MFG vector was used for gene delivery of tumor necrosis factor alpha receptor (TNFalphaR) p55, viral interleukin-10 (IL-10), and murine IL-10 into RA synovial fibroblasts. The effect on invasion of these cells into human articular cartilage and on perichondrocytic cartilage degradation was examined after 60 days of coimplantation into the SCID mouse. RESULTS: TNFalphaR p55 gene transfer showed only a limited effect on inhibition of RA synovial fibroblast invasiveness and cartilage degradation. In contrast, invasion of the RA synovial fibroblasts into the coimplanted cartilage was strongly inhibited by both viral and murine IL-10. Perichondrocytic cartilage degradation was not affected by either form of IL-10. CONCLUSION: The data show that cytokines can be successfully inserted into the genome of human RA synovial fibroblasts using a retroviral vector delivery system, and that the SCID mouse model of human RA is a valuable tool for examining the effects of gene transfer. In addition, inhibition of more than one cytokine pathway may be required to inhibit both synovial- and chondrocyte-mediated cartilage destruction in RA.  (+info)

Development of viral vectors for gene therapy of beta-chain hemoglobinopathies: optimization of a gamma-globin gene expression cassette. (4/1467)

Progress toward gene therapy of beta-chain hemoglobinopathies has been limited in part by poor expression of globin genes in virus vectors. To derive an optimal expression cassette, we systematically analyzed the sequence requirements and relative strengths of the Agamma- and beta-globin promoters, the activities of various erythroid-specific enhancers, and the importance of flanking and intronic sequences. Expression was analyzed by RNase protection after stable plasmid transfection of the murine erythroleukemia cell line, MEL585. Promoter truncation studies showed that the Agamma-globin promoter could be deleted to -159 without affecting expression, while deleting the beta-globin promoter to -127 actually increased expression compared with longer fragments. Expression from the optimal beta-globin gene promoter was consistently higher than that from the optimal Agamma-globin promoter, regardless of the enhancer used. Enhancers tested included a 2.5-kb composite of the beta-globin locus control region (termed a muLCR), a combination of the HS2 and HS3 core elements of the LCR, and the HS-40 core element of the alpha-globin locus. All three enhancers increased expression from the beta-globin gene to roughly the same extent, while the HS-40 element was notably less effective with the Agamma-globin gene. However, the HS-40 element was able to efficiently enhance expression of a Agamma-globin gene linked to the beta-globin promoter. Inclusion of extended 3' sequences from either the beta-globin or the Agamma-globin genes had no significant effect on expression. A 714-bp internal deletion of Agamma-globin intron 2 unexpectedly increased expression more than twofold. With the combination of a -127 beta-globin promoter, an Agamma-globin gene with the internal deletion of intron 2, and a single copy of the HS-40 enhancer, gamma-globin expression averaged 166% of murine alpha-globin mRNA per copy in six pools and 105% in nine clones. When placed in a retrovirus vector, this cassette was also expressed at high levels in MEL585 cells (averaging 75% of murine alpha-globin mRNA per copy) without reducing virus titers. However, recombined provirus or aberrant splicing was observed in 5 of 12 clones, indicating a significant degree of genetic instability. Taken together, these data demonstrate the development of an optimal expression cassette for gamma-globin capable of efficient expression in a retrovirus vector and form the basis for further refinement of vectors containing this cassette.  (+info)

One-day ex vivo culture allows effective gene transfer into human nonobese diabetic/severe combined immune-deficient repopulating cells using high-titer vesicular stomatitis virus G protein pseudotyped retrovirus. (5/1467)

Retrovirus-mediated gene transfer into long-lived human pluripotent hematopoietic stem cells (HSCs) is a widely sought but elusive goal. A major problem is the quiescent nature of most HSCs, with the perceived requirement for ex vivo prestimulation in cytokines to induce stem cell cycling and allow stable gene integration. However, ex vivo culture may impair stem cell function, and could explain the disappointing clinical results in many current gene transfer trials. To address this possibility, we examined the ex vivo survival of nonobese diabetic/severe combined immune-deficient (NOD/SCID) repopulating cells (SRCs) over 3 days. After 1 day of culture, the SRC number and proliferation declined twofold, and was further reduced by day 3; self-renewal was only detectable in noncultured cells. To determine if the period of ex vivo culture could be shortened, we used a vesicular stomatitis virus G protein (VSV-G) pseudotyped retrovirus vector that was concentrated to high titer. The results showed that gene transfer rates were similar without or with 48 hours prestimulation. Thus, the use of high-titer VSV-G pseudotyped retrovirus may minimize the loss of HSCs during culture, because efficient gene transfer can be obtained without the need for extended ex vivo culture.  (+info)

Gene transfer to human pancreatic endocrine cells using viral vectors. (6/1467)

We have studied the factors that influence the efficiency of infection of human fetal and adult pancreatic endocrine cells with adenovirus, murine retrovirus, and lentivirus vectors all expressing the green fluorescent protein (Ad-GFP, MLV-GFP, and Lenti-GFP, respectively). Adenoviral but not retroviral vectors efficiently infected intact pancreatic islets and fetal islet-like cell clusters (ICCs) in suspension. When islets and ICCs were plated in monolayer culture, infection efficiency with all three viral vectors increased. Ad-GFP infected 90-95% of the cells, whereas infection with MLV-GFP and Lenti-GFP increased only slightly. Both exposure to hepatocyte growth factor/scatter factor (HGF/SF) and dispersion of the cells by removal from the culture dish and replating had substantial positive effects on the efficiency of infection with retroviral vectors. Studies of virus entry and cell replication revealed that cell dispersion and stimulation by HGF/SF may be acting through both mechanisms to increase the efficiency of retrovirus-mediated gene transfer. Although HGF/SF and cell dispersion increased the efficiency of infection with MLV-GFP, only rare cells with weak staining for insulin were infected, whereas approximately 25% of beta-cells were infected with Lenti-GFP. We conclude that adenovirus is the most potent vector for ex vivo overexpression of foreign genes in adult endocrine pancreatic cells and is the best vector for applications where high-level but transient expression is desired. Under the optimal conditions of cell dispersion plus HGF/SF, infection with MLV and lentiviral vectors is reasonably efficient and stable, but only lentiviral vectors efficiently infect pancreatic beta-cells.  (+info)

Transplantation of transduced nonhuman primate CD34+ cells using a gibbon ape leukemia virus vector: restricted expression of the gibbon ape leukemia virus receptor to a subset of CD34+ cells. (7/1467)

The transduction efficiencies of immunoselected rhesus macaque (Macaca mulatta) CD34+ cells and colony-forming progenitor cells based on polymerase chain reaction (PCR) analysis were comparable for an amphotropic Moloney murine leukemia virus (MLV) retroviral vector and a retroviral vector derived from the gibbon ape leukemia virus (GaLV) packaging cell line, PG13. On performing autologous transplantation studies using immunoselected CD34+ cells transduced with the GaLV envelope (env) retroviral vector, less than 1% of peripheral blood (PB) contained provirus. This was true whether bone marrow (BM) or cytokine-mobilized PB immunoselected CD34+ cells were reinfused. This level of marking was evident in two animals whose platelet counts never fell below 50,000/microliter and whose leukocyte counts had recovered by days 8 and 10 after having received 1.7 x 10(7) or greater of cytokine-mobilized CD34+ PB cells/kg. Reverse transcriptase(RT)-PCR analysis of CD34+ subsets for both the GaLV and amphotropic receptor were performed. The expression of the GaLV receptor was determined to be restricted to CD34+ Thy-1+ cells, and both CD34+ CD38+ and CD34+ CD38dim cells, while the amphotropic receptor was present on all CD34+ cell subsets examined. Our findings suggest that, in rhesus macaques, PG13-derived retroviral vectors may only be able to transduce a subset of CD34+ cells as only CD34+ Thy-1+ cells express the GaLV receptor.  (+info)

Retrovirus integration site Mintb encoding the mouse homolog of hnRNP U. (8/1467)

Retroviral genes are not usually expressed in mouse embryonal carcinoma (EC) cells, but they are readily expressed upon differentiation of these cells. We previously reported the isolation of EC cell lines that express a neomycin resistance (neo) gene introduced by a recombinant transducing Moloney murine leukemia virus from specific integration sites, Minta, Mintb, Mintc, or Mintd. In some of these clones, the entire 5' long terminal repeat (LTR) was deleted, and the neo gene was expressed by read-through transcription from upstream cellular promoters in a "promoter-trap" fashion. One such promoter ("promoter B" at the Mintb locus) was found in a CpG island, associated with an upstream enhancer ("enhancer B"). Although enhancer B caused expression of the neo gene in the transductant EC cell line, no endogenous transcription from promoter B was detected in the parental EC or NIH3T3 cells. In contrast, we found a strong counter-flow endogenous transcription unit ("R" for reverse), which apparently interfered with transcription from promoter B. Promoter R turned out to have a bidirectional activity in transfection assays. In normal tissues, promoter R activates gene R, which encodes an 800-residue protein that is highly homologous to the rat and human heterogeneous nuclear ribonucleoprotein U (hnRNP U). Northern and in situ hybridization analyses revealed that gene R was abundantly expressed in the testis, especially in the pachytene spermatocytes and round spermatids.  (+info)

Examples of experimental leukemias include:

1. X-linked agammaglobulinemia (XLA): A rare inherited disorder that leads to a lack of antibody production and an increased risk of infections.
2. Diamond-Blackfan anemia (DBA): A rare inherited disorder characterized by a failure of red blood cells to mature in the bone marrow.
3. Fanconi anemia: A rare inherited disorder that leads to a defect in DNA repair and an increased risk of cancer, particularly leukemia.
4. Ataxia-telangiectasia (AT): A rare inherited disorder characterized by progressive loss of coordination, balance, and speech, as well as an increased risk of cancer, particularly lymphoma.
5. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21, which increases the risk of developing leukemia, particularly acute myeloid leukemia (AML).

These experimental leukemias are often used in research studies to better understand the biology of leukemia and to develop new treatments.

1. HIV (Human Immunodeficiency Virus): This is a virus that attacks the body's immune system, making it difficult to fight off infections and diseases. HIV is a type of retrovirus that can lead to AIDS (Acquired Immunodeficiency Syndrome).
2. HTLV-1 (Human T-lymphotropic virus type 1): This is a virus that affects the immune system and can lead to diseases such as adult T-cell leukemia/lymphoma and myelopathy.
3. HBV (Hepatitis B Virus): This is a virus that attacks the liver and can cause inflammation, scarring, and cirrhosis.
4. HCV (Hepatitis C Virus): This is a virus that attacks the liver and can cause inflammation, scarring, and cirrhosis.
5. FeLV (Feline Leukemia Virus): This is a virus that affects cats and can cause a variety of diseases, including leukemia and lymphoma.
6. FIV (Feline Immunodeficiency Virus): This is a virus that affects cats and can weaken their immune system, making them more susceptible to other infections and diseases.
7. Bovine Immunodeficiency Virus (BIV): This is a virus that affects cattle and can cause a variety of diseases, including leukemia and lymphoma.
8. Equine Infectious Anemia Virus (EIAV): This is a virus that affects horses and can cause a variety of diseases, including anemia and swelling of the lymph nodes.

Retroviridae infections are typically diagnosed through blood tests that detect the presence of antibodies or genetic material from the virus. Treatment options vary depending on the specific virus and the severity of the infection, but may include antiretroviral medications, immune-suppressive drugs, and supportive care such as blood transfusions or antibiotics for secondary infections.

It is important to note that retroviruses can be transmitted through contact with infected bodily fluids, such as blood, semen, and breast milk. Therefore, it is important to take precautions such as using condoms, gloves, and other protective measures when dealing with infected individuals or animals. Additionally, it is important to maintain good hygiene practices, such as washing hands regularly, to reduce the risk of transmission.

There are several different types of preleukemia, including:

1. Myelodysplastic syndrome (MDS): A condition where there is a defect in the development of immature blood cells in the bone marrow, leading to an overproduction of blasts and a decrease in the number of healthy red blood cells, white blood cells, and platelets.
2. Myeloproliferative neoplasms (MPNs): A group of conditions characterized by an overproduction of one or more types of blood cells, including red blood cells, white blood cells, and platelets. MPNs can progress to leukemia over time.
3. Chronic myelogenous leukemia (CML): A type of leukemia that develops from a preleukemic condition called chronic myeloid leukemia. CML is characterized by the presence of a genetic abnormality known as the Philadelphia chromosome, which leads to an overproduction of white blood cells.
4. Acute myeloid leukemia (AML): A type of leukemia that can develop from preleukemic conditions such as MDS and MPNs. AML is characterized by the rapid growth of immature white blood cells in the bone marrow, which can crowd out healthy cells and lead to a decrease in the number of normal red blood cells, white blood cells, and platelets.

Preleukemia can be difficult to diagnose, as it often does not have clear symptoms in its early stages. However, doctors may use a variety of tests, including blood tests and bone marrow biopsies, to detect abnormalities in the blood or bone marrow that could indicate preleukemia.

Treatment for preleukemia depends on the specific type of condition and its severity. Some common treatments include:

1. Chemotherapy: A type of cancer treatment that uses drugs to kill cancer cells. Chemotherapy may be used to treat preleukemia, particularly in cases where there are abnormalities in the blood or bone marrow.
2. Blood transfusions: Transfusions of healthy red blood cells, platelets, or plasma may be given to patients with preleukemia who have low levels of these cells.
3. Supportive care: Patients with preleukemia may require supportive care, such as antibiotics or other medications, to manage symptoms and prevent complications.
4. Stem cell transplantation: In some cases, stem cell transplantation may be recommended for patients with preleukemia who have a high risk of developing acute leukemia. This involves replacing the patient's defective bone marrow stem cells with healthy ones from a donor.

Overall, early detection and treatment of preleukemia can improve outcomes and reduce the risk of developing acute leukemia. If you have been diagnosed with preleukemia or are experiencing symptoms that may indicate preleukemia, it is important to discuss your treatment options with your healthcare provider.

There are several different types of tumor viruses, including:

1. Human papillomavirus (HPV): This virus is responsible for causing cervical cancer and other types of cancer, such as anal, vulvar, vaginal, and penile cancer.
2. Hepatitis B virus (HBV): This virus can cause liver cancer, known as hepatocellular carcinoma (HCC).
3. Human immunodeficiency virus (HIV): This virus can increase the risk of developing certain types of cancer, such as Kaposi's sarcoma and lymphoma.
4. Epstein-Barr virus (EBV): This virus has been linked to the development of Burkitt lymphoma and Hodgkin's lymphoma.
5. Merkel cell polyomavirus (MCPyV): This virus is responsible for causing Merkel cell carcinoma, a rare type of skin cancer.
6. Human T-lymphotropic virus (HTLV-1): This virus has been linked to the development of adult T-cell leukemia/lymphoma (ATLL).

Tumor virus infections can be diagnosed through a variety of methods, including blood tests, imaging studies, and biopsies. Treatment for these infections often involves antiviral medications, chemotherapy, and surgery. In some cases, tumors may also be removed through radiation therapy.

It's important to note that not all tumors or cancers are caused by viruses, and that many other factors, such as genetics and environmental exposures, can also play a role in the development of cancer. However, for those tumor virus infections that are caused by a specific virus, early diagnosis and treatment can improve outcomes and reduce the risk of complications.

Overall, tumor virus infections are a complex and diverse group of conditions, and further research is needed to better understand their causes and develop effective treatments.

There are several different types of leukemia, including:

1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.

Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.

1. Activation of oncogenes: Some viruses contain genes that code for proteins that can activate existing oncogenes in the host cell, leading to uncontrolled cell growth.
2. Inactivation of tumor suppressor genes: Other viruses may contain genes that inhibit the expression of tumor suppressor genes, allowing cells to grow and divide uncontrollably.
3. Insertional mutagenesis: Some viruses can insert their own DNA into the host cell's genome, leading to disruptions in normal cellular function and potentially causing cancer.
4. Epigenetic changes: Viral infection can also cause epigenetic changes, such as DNA methylation or histone modification, that can lead to the silencing of tumor suppressor genes and the activation of oncogenes.

Viral cell transformation is a key factor in the development of many types of cancer, including cervical cancer caused by human papillomavirus (HPV), and liver cancer caused by hepatitis B virus (HBV). In addition, some viruses are specifically known to cause cancer, such as Kaposi's sarcoma-associated herpesvirus (KSHV) and Merkel cell polyomavirus (MCV).

Early detection and treatment of viral infections can help prevent the development of cancer. Vaccines are also available for some viruses that are known to cause cancer, such as HPV and hepatitis B. Additionally, antiviral therapy can be used to treat existing infections and may help reduce the risk of cancer development.

A thymus neoplasm is a type of cancer that originates in the thymus gland, which is located in the chest behind the sternum and is responsible for the development and maturation of T-lymphocytes (T-cells) of the immune system.

Types of Thymus Neoplasms

There are several types of thymus neoplasms, including:

1. Thymoma: A slow-growing tumor that is usually benign but can sometimes be malignant.
2. Thymic carcinoma: A more aggressive type of cancer that is less common than thymoma.
3. Thymic lymphoma: A type of cancer that arises from the T-cells in the thymus gland and can be either B-cell or T-cell derived.

Symptoms of Thymus Neoplasms

The symptoms of thymus neoplasms can vary depending on the location and size of the tumor, but they may include:

1. Chest pain or discomfort
2. Coughing or shortness of breath
3. Fatigue or fever
4. Swelling in the neck or face
5. Weight loss or loss of appetite

Diagnosis of Thymus Neoplasms

The diagnosis of a thymus neoplasm typically involves a combination of imaging tests such as chest X-rays, computed tomography (CT) scans, and positron emission tomography (PET) scans, as well as a biopsy to confirm the presence of cancer cells.

Treatment of Thymus Neoplasms

The treatment of thymus neoplasms depends on the type and stage of the cancer, but may include:

1. Surgery to remove the tumor
2. Radiation therapy to kill any remaining cancer cells
3. Chemotherapy to destroy cancer cells
4. Targeted therapy to specific molecules involved in the growth and progression of the cancer.

Prognosis of Thymus Neoplasms

The prognosis for thymus neoplasms depends on the type and stage of the cancer at the time of diagnosis. In general, the earlier the cancer is detected and treated, the better the prognosis.

Prevention of Thymus Neoplasms

There is no known way to prevent thymus neoplasms, as they are rare and can occur in people of all ages. However, early detection and treatment of the cancer can improve the chances of a successful outcome.

Current Research on Thymus Neoplasms

Researchers are currently studying new treatments for thymus neoplasms, such as targeted therapies and immunotherapy, which use the body's own immune system to fight cancer. Additionally, researchers are working to develop better diagnostic tests to detect thymus neoplasms at an earlier stage, when they are more treatable.

Conclusion

Thymus neoplasms are rare and complex cancers that require specialized care and treatment. While the prognosis for these cancers can be challenging, advances in diagnosis and treatment have improved outcomes for many patients. Researchers continue to study new treatments and diagnostic tools to improve the chances of a successful outcome for those affected by thymus neoplasms.

There are several types of lymphoma, including:

1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.

The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching

Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.

Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.

AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.

There are several subtypes of AML, including:

1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.

The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:

* Fatigue
* Weakness
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Headache
* Confusion or seizures

AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:

1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.

Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:

1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.

It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.

1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.

Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.

Thymoma can be broadly classified into two main types:

1. Benign thymoma: This type of thymoma is non-cancerous and does not spread to other parts of the body. It is usually small in size and may not cause any symptoms.
2. Malignant thymoma: This type of thymoma is cancerous and can spread to other parts of the body, including the lungs, liver, and bone marrow. Malignant thymomas are more aggressive than benign thymomas and can be life-threatening if not treated promptly.

The exact cause of thymoma is not known, but it is believed to arise from abnormal cell growth in the thymus gland. Some risk factors that may increase the likelihood of developing thymoma include:

1. Genetic mutations: Certain genetic mutations, such as those affecting the TREX1 gene, can increase the risk of developing thymoma.
2. Radiation exposure: Exposure to radiation, such as from radiation therapy, may increase the risk of developing thymoma.
3. Thymic hyperplasia: Enlargement of the thymus gland, known as thymic hyperplasia, may increase the risk of developing thymoma.

The symptoms of thymoma can vary depending on the size and location of the tumor. Some common symptoms include:

1. Chest pain or discomfort
2. Shortness of breath
3. Coughing
4. Fatigue
5. Weight loss
6. Fever
7. Night sweats
8. Pain in the arm or shoulder

Thymoma is diagnosed through a combination of imaging tests, such as computed tomography (CT) scans and magnetic resonance imaging (MRI), and biopsy, which involves removing a sample of tissue from the thymus gland for examination under a microscope. Treatment options for thymoma depend on the stage and aggressiveness of the tumor, and may include:

1. Surgery: Removing the tumor through surgery is often the first line of treatment for thymoma.
2. Radiation therapy: High-energy beams can be used to kill cancer cells and shrink the tumor.
3. Chemotherapy: Drugs can be used to kill cancer cells and shrink the tumor.
4. Targeted therapy: Drugs that target specific molecules involved in the growth and spread of cancer cells can be used to treat thymoma.
5. Immunotherapy: Treatments that use the body's immune system to fight cancer, such as checkpoint inhibitors, can be effective for some people with thymoma.

Overall, the prognosis for thymoma is generally good, with a 5-year survival rate of about 70% for people with localized disease. However, the prognosis can vary depending on the stage and aggressiveness of the tumor, as well as the effectiveness of treatment.

* Peripheral T-cell lymphoma (PTCL): This is a rare type of T-cell lymphoma that can develop in the skin, lymph nodes, or other organs.
* Cutaneous T-cell lymphoma (CTCL): This is a type of PTCL that affects the skin and can cause lesions, rashes, and other skin changes.
* Anaplastic large cell lymphoma (ALCL): This is a rare subtype of PTCL that can develop in the lymph nodes, spleen, or bone marrow.
* Adult T-cell leukemia/lymphoma (ATLL): This is a rare and aggressive subtype of PTCL that is caused by the human T-lymphotropic virus type 1 (HTLV-1).

Symptoms of T-cell lymphoma can include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Skin lesions or rashes

Treatment options for T-cell lymphoma depend on the subtype and stage of the cancer, but may include:

* Chemotherapy
* Radiation therapy
* Immunotherapy
* Targeted therapy

Prognosis for T-cell lymphoma varies depending on the subtype and stage of the cancer, but in general, the prognosis for PTCL is poorer than for other types of non-Hodgkin lymphoma. However, with prompt and appropriate treatment, many people with T-cell lymphoma can achieve long-term remission or even be cured.

Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.

Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.

In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.

It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.

See also: Cancer, Tumor

Word count: 190

Erythroleukemia typically affects adults in their 50s and 60s, although it can occur at any age. Symptoms may include fever, night sweats, weight loss, and fatigue. The cancer cells can spread to other parts of the body, including the spleen, liver, and lymph nodes.

Erythroleukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore normal blood cell production. In some cases, a bone marrow transplant may be necessary. The prognosis for erythroleukemia is generally poor, with a five-year survival rate of about 20%.

Erythroleukemia is classified as an acute leukemia, meaning it progresses rapidly and can lead to life-threatening complications if left untreated. It is important for patients to receive prompt and appropriate treatment to improve their chances of survival and quality of life.

In LLCB, the B cells undergo a mutation that causes them to become cancerous and multiply rapidly. This can lead to an overproduction of these cells in the bone marrow, causing the bone marrow to become crowded and unable to produce healthy red blood cells, platelets, and white blood cells.

LLCB is typically a slow-growing cancer, and it can take years for symptoms to develop. However, as the cancer progresses, it can lead to a range of symptoms including fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes.

LLCB is typically diagnosed through a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as X-rays or CT scans. Treatment options for LLCB include chemotherapy, radiation therapy, and in some cases, stem cell transplantation.

Overall, while LLCB is a serious condition, it is typically slow-growing and can be managed with appropriate treatment. With current treatments, many people with LLCB can achieve long-term remission and a good quality of life.

The two main types of lymphoid leukemia are:

1. Acute Lymphoblastic Leukemia (ALL): This type of leukemia is most commonly seen in children, but it can also occur in adults. It is characterized by a rapid increase in the number of immature white blood cells in the blood and bone marrow.
2. Chronic Lymphocytic Leukemia (CLL): This type of leukemia usually affects older adults and is characterized by the gradual buildup of abnormal white blood cells in the blood, bone marrow, and lymph nodes.

Symptoms of lymphoid leukemia include fatigue, fever, night sweats, weight loss, and swollen lymph nodes. Treatment options for lymphoid leukemia can vary depending on the type of cancer and the severity of symptoms, but may include chemotherapy, radiation therapy, or bone marrow transplantation.

The term "Murine" refers to the fact that the condition occurs in mice and other rodents. "Acquired Immunodeficiency Syndrome" (AIDS) is a similar condition in humans caused by HIV. The similarity between MAIDS and AIDS lies in their shared origins as retroviral infections, but there are significant differences in the viruses themselves and the symptoms they cause.

Example sentence: The patient was diagnosed with experimental sarcoma and underwent a novel chemotherapy regimen that included a targeted therapy drug.

Some common effects of chromosomal deletions include:

1. Genetic disorders: Chromosomal deletions can lead to a variety of genetic disorders, such as Down syndrome, which is caused by a deletion of a portion of chromosome 21. Other examples include Prader-Willi syndrome (deletion of chromosome 15), and Williams syndrome (deletion of chromosome 7).
2. Birth defects: Chromosomal deletions can increase the risk of birth defects, such as heart defects, cleft palate, and limb abnormalities.
3. Developmental delays: Children with chromosomal deletions may experience developmental delays, learning disabilities, and intellectual disability.
4. Increased cancer risk: Some chromosomal deletions can increase the risk of developing certain types of cancer, such as chronic myelogenous leukemia (CML) and breast cancer.
5. Reproductive problems: Chromosomal deletions can lead to reproductive problems, such as infertility or recurrent miscarriage.

Chromosomal deletions can be diagnosed through a variety of techniques, including karyotyping (examination of the chromosomes), fluorescence in situ hybridization (FISH), and microarray analysis. Treatment options for chromosomal deletions depend on the specific effects of the deletion and may include medication, surgery, or other forms of therapy.

There are several types of teratomas, including:

1. Mature teratoma: This type of teratoma is made up of well-differentiated tissues that resemble normal tissues. It can contain structures such as hair follicles, sweat glands, and sebaceous glands.
2. Immature teratoma: This type of teratoma is made up of poorly differentiated cells that do not resemble normal tissues. It can contain structures such as cartilage, bone, and nervous tissue.
3. Teratoid mesodermal tumor: This type of teratoma arises from the mesoderm, which is one of the three primary layers of cells in the embryo. It can contain structures such as muscle, bone, and connective tissue.
4. Teratoid endodermal tumor: This type of teratoma arises from the endoderm, which is another primary layer of cells in the embryo. It can contain structures such as glandular tissue and epithelial tissue.

Teratomas are usually benign, but they can sometimes be malignant. Malignant teratomas can spread to other parts of the body and cause serious complications. The treatment of teratomas depends on their type, size, and location, as well as the patient's overall health. Treatment options can include surgery, chemotherapy, and radiation therapy.

In summary, a teratoma is a type of tumor that contains abnormal cells that grow and multiply in an uncontrolled manner, often forming masses or lumps. There are several types of teratomas, and they can occur in various parts of the body. Treatment options depend on the type, size, location, and patient's overall health.

Symptoms of EBL can vary widely and may include:

* Swollen lymph nodes
* Chronic diarrhea
* Weight loss
* Anemia
* Lethargy
* Enlarged spleen and liver
* Neoplastic diseases such as lymphosarcoma, leukemia, or other types of cancer.

EBL is usually diagnosed through a combination of physical examination, blood tests, and biopsies. There is no cure for EBL, and treatment is primarily focused on managing symptoms and preventing the spread of the disease.

Prevention of EBL includes:

* Testing herds for BLV regularly
* Avoiding close contact between animals
* Practicing good hygiene and sanitation
* Implementing strict biosecurity measures
* Eliminating infected animals from the herd

It is important to note that EBL is not a reportable disease in all countries, and testing for BLV may not be mandatory in all regions. However, it is still important for farmers and veterinarians to be aware of the risk of EBL and take appropriate measures to prevent its spread.

The BCR-ABL gene is a fusion gene that is present in the majority of cases of CML. It is created by the translocation of two genes, called BCR and ABL, which leads to the production of a constitutively active tyrosine kinase protein that promotes the growth and proliferation of abnormal white blood cells.

There are three main phases of CML, each with distinct clinical and laboratory features:

1. Chronic phase: This is the earliest phase of CML, where patients may be asymptomatic or have mild symptoms such as fatigue, night sweats, and splenomegaly (enlargement of the spleen). The peripheral blood count typically shows a high number of blasts in the blood, but the bone marrow is still functional.
2. Accelerated phase: In this phase, the disease progresses to a higher number of blasts in the blood and bone marrow, with evidence of more aggressive disease. Patients may experience symptoms such as fever, weight loss, and pain in the joints or abdomen.
3. Blast phase: This is the most advanced phase of CML, where there is a high number of blasts in the blood and bone marrow, with significant loss of function of the bone marrow. Patients are often symptomatic and may have evidence of spread of the disease to other organs, such as the liver or spleen.

Treatment for CML typically involves targeted therapy with drugs that inhibit the activity of the BCR-ABL protein, such as imatinib (Gleevec), dasatinib (Sprycel), or nilotinib (Tasigna). These drugs can slow or stop the progression of the disease, and may also produce a complete cytogenetic response, which is defined as the absence of all Ph+ metaphases in the bone marrow. However, these drugs are not curative and may have significant side effects. Allogenic hematopoietic stem cell transplantation (HSCT) is also a potential treatment option for CML, but it carries significant risks and is usually reserved for patients who are in the blast phase of the disease or have failed other treatments.

In summary, the clinical course of CML can be divided into three phases based on the number of blasts in the blood and bone marrow, and treatment options vary depending on the phase of the disease. It is important for patients with CML to receive regular monitoring and follow-up care to assess their response to treatment and detect any signs of disease progression.

The symptoms of T-cell leukemia can vary depending on the severity of the disease, but they may include:

* Fatigue
* Weakness
* Frequent infections
* Easy bruising or bleeding
* Swollen lymph nodes
* Pain in the bones or joints
* Headaches
* Confusion or seizures (in severe cases)

T-cell leukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore the body's normal production of blood cells. In some cases, bone marrow transplantation may be recommended.

The prognosis for T-cell leukemia varies depending on the patient's age and overall health, as well as the aggressiveness of the disease. However, with current treatments, the 5-year survival rate is around 70% for children and adolescents, and around 40% for adults.

It's important to note that T-cell leukemia is relatively rare compared to other types of leukemia, such as acute myeloid leukemia (AML) or chronic lymphocytic leukemia (CLL). However, it can be a very aggressive and difficult-to-treat form of cancer, and patients with T-cell leukemia often require intensive treatment and close follow-up care.

Radiation-induced leukemia is a rare but potentially fatal condition that occurs when a person is exposed to high levels of ionizing radiation, such as from nuclear fallout or radiation therapy. The radiation damages the DNA in the stem cells of the bone marrow, leading to mutations that can cause the development of cancer.

There are two main types of radiation-induced leukemia: acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). AML is the more common type and typically occurs within 1-5 years after exposure to high levels of radiation. CML can take up to 10 years or more to develop.

Symptoms of radiation-induced leukemia can include fatigue, fever, night sweats, weight loss, and easy bruising or bleeding. Treatment typically involves chemotherapy and/or bone marrow transplantation. The prognosis for radiation-induced leukemia is generally poor, with a 5-year survival rate of less than 50%.

Prevention is key to avoiding radiation-induced leukemia. People who work with or are exposed to high levels of radiation, such as nuclear power plant workers, should take precautions to minimize their exposure and undergo regular medical checkups to monitor their health. Additionally, people who have undergone radiation therapy for cancer should be closely monitored by their healthcare providers for any signs of leukemia or other radiation-related side effects.

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"NMR structure of the 101-nucleotide core encapsidation signal of the Moloney murine leukemia virus". Journal of Molecular ... The Friend virus (FV) is a strain of murine leukemia virus. The Friend virus has been used for both immunotherapy and vaccines ... The murine leukemia viruses (MLVs or MuLVs) are retroviruses named for their ability to cause cancer in murine (mouse) hosts. ... The murine leukemia viruses are group/type VI retroviruses belonging to the gammaretroviral genus of the Retroviridae family. ...
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"Proviral Integration Site for Moloney Murine Leukemia Virus (PIM) Kinases Promote Human T Helper 1 Cell Differentiation". The ... PIM2 or Proviral Integrations of Moloney virus 2 is serine/threonine kinase that has roles in cell growth, proliferation, ... "Increased Expression of the hPim-2 Gene In Human Chronic lymphocytic Leukemia and Non-Hodgkin Lymphoma". Leukemia & Lymphoma. ... The studies showed higher levels of expression in NHL over normal lymphocytes as well as in chronic lymphocytic leukemia over ...
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... such as Moloney murine leukemia virus (MoMLV), feline leukemia virus (FLV), and feline sarcoma virus (FESV). This family also ... "Atomic resolution structure of Moloney murine leukemia virus matrix protein and its relationship to other retroviral matrix ... Matrix proteins are also components of beta-retroviruses such as Mason-Pfizer monkey virus (MPMV) and mouse mammary tumor virus ... Stansell E, Tytler E, Walter MR, Hunter E (May 2004). "An early stage of Mason-Pfizer monkey virus budding is regulated by the ...
A highly efficient helper virus commonly used when growing A-MuLV in vitro is Moloney murine leukemia virus (M-MuLV). It causes ... Shields A, Rosenberg N, Baltimore D (1979). "Virus production by Abelson murine leukemia virus-transformed lymphoid cells". J. ... The Abelson murine leukemia virus (Ab-MLV or A-MuLV) is a retrovirus (Class VI) used to induce malignant transformation of ... The Abelson murine leukemia virus is named for the American pediatrician Herbert T. Abelson, who together with Louise S ...
In the first system, a wild-type Moloney Murine Leukemia Virus (M-MLV) reverse transcriptase was fused to the Cas9 H840A ... A fusion protein consisting of a Cas9 H840A nickase fused to a Moloney Murine Leukemia Virus (M-MLV) reverse transcriptase. ... The target organism can then be transduced by the virus to synthesize the base editor in vivo. Common laboratory vectors of ... so proposed human therapies often centered around adeno-associated virus (AAV) because AAV infections are largely asymptomatic ...
... purified as a sequence-specific DNA-binding protein that regulated the disease specificity of the Moloney murine Leukemia virus ... a protein that binds the conserved core site in murine leukemia virus enhancers". Mol Cell Biol. 12 (1): 89-102. doi:10.1128/ ... "Cloning and characterization of subunits of the T-cell receptor and murine leukemia virus enhancer core-binding factor". Mol ... Perry C, Eldor A, Soreq H (March 2002). "Runx1/AML1 in leukemia: disrupted association with diverse protein partners". Leukemia ...
A few examples of the virus are Moloney murine leukemia virus, xenotropic MuLB-related virus, feline leukemia virus, and feline ... Example species are the murine leukemia virus and the feline leukemia virus. They cause various sarcomas, leukemias and immune ... over 50 human cancer cell lines that were claimed to be linked to murine leukemia virus-related virus or murine leukemia virus ... One specific gammaretrovirus that is commonly used as a retroviral vector is the Moloney murine leukemia virus. A specific ...
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"Oligomerization and transport of the envelope protein of Moloney murine leukemia virus-TB and of ts1, a neurovirulent ... For the virus to penetrate the cytosol of a host cell, a low pH is necessary. The env gene of Murine Leukemia Virus (MLV) codes ... The Env proteins of the Avian Sarcoma and Leukosis virus (ASLV) and the Murine Leukemia Virus (MLV) are both trimers of SU-TM ... This membrane receptor was isolated from Rauscher murine leukemia virus (R-MuLV). The retroviral protein env has been captured ...
The main use of BOSC 23 is the production of recombinant retroviruses; it stably expresses Moloney murine leukemia virus ... The cell line does not produce detectable replication-competent virus, an important safety feature.[citation needed] BOSC 23 ...
M-MLV reverse transcriptase from the Moloney murine leukemia virus is a single 75 kDa monomer. AMV reverse transcriptase from ... murine leukemia virus and again Rous sarcoma virus. For their achievements, they shared the 1975 Nobel Prize in Physiology or ... Biology portal Viruses portal cDNA library DNA polymerase msDNA Reverse transcribing virus RNA polymerase Telomerase ... ISBN 978-0-87969-382-4. Bernstein A, Weiss R, Tooze J (1985). "RNA tumor viruses". Molecular Biology of Tumor Viruses (2nd ed ...
The earliest retroviral vectors were based on the Moloney murine leukemia virus (MMLV) which when pseudotyped with GaLV ... "The receptors for gibbon ape leukemia virus and amphotropic murine leukemia virus are not downregulated in productively ... "Gibbon ape leukemia virus-Hall's Island: new strain of gibbon ape leukemia virus". Journal of Virology. 29 (1): 395-400. doi: ... J, McKee; N, Clark; F, Shapter; G, Simmons (April 2017). "A New Look at the Origins of Gibbon Ape Leukemia Virus". Virus Genes ...
... has been seen to demonstrate antiviral activity against a number of viruses including Moloney murine leukemia virus, ... Rauscher murine leukemia virus, and the human immunodeficiency virus. Its effects against the proliferation of viruses is ... Myricetin was identified as a competitive inhibitor of the reverse transcriptase of Rauscher murine leukemia virus and a ... "Myricetin-induced oxidative stress suppresses murine T lymphocyte activation". Cell Biology International. 42 (8): 1069-1075. ...
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... immunodeficiency virus type 1 and simian immunodeficiency virus and to the p12Gag protein of Moloney murine leukemia virus". ... Mazzé FM, Degrève L (2006). "The role of viral and cellular proteins in the budding of human immunodeficiency virus". Acta ... Unanchored ubiquitin in virus uncoating". Science. 346 (6208): 427-8. doi:10.1126/science.1261509. PMID 25342790. S2CID ...
... as it was the locus most frequently activated by the Moloney murine leukemia virus. Subsequently, the oncogene has been ... a Potent and Selective Proviral Insertion Site of Moloney Murine Leukemia (PIM) 1, 2, and 3 Kinase Inhibitor in Clinical Trials ... Human, murine and rat Pim-1 contain 313 amino acids, and have a 94 - 97% amino acid identity. The active site of the protein, ... The pim-1 oncogene was first described in relation to murine T-cell lymphomas, ...
... immunodeficiency virus type 1 and simian immunodeficiency virus and to the p12Gag protein of Moloney murine leukemia virus". ... Mazzé FM, Degrève L (2006). "The role of viral and cellular proteins in the budding of human immunodeficiency virus". Acta ... Gottwein E, Kräusslich HG (Jul 2005). "Analysis of human immunodeficiency virus type 1 Gag ubiquitination". Journal of Virology ...
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... moloney murine leukemia virus MeSH B04.820.650.375.525.750 - radiation leukemia virus MeSH B04.820.650.375.525.770 - rauscher ... leukemia virus, feline MeSH B04.820.650.375.510 - leukemia virus, gibbon ape MeSH B04.820.650.375.525 - leukemia virus, murine ... moloney murine leukemia virus MeSH B04.909.574.807.375.525.750 - radiation leukemia virus MeSH B04.909.574.807.375.525.770 - ... moloney murine leukemia virus MeSH B04.909.777.731.375.525.750 - radiation leukemia virus MeSH B04.909.777.731.375.525.770 - ...
"Murine leukemia virus reverse transcriptase: structural comparison with HIV-1 reverse transcriptase". Virus Research. 134 (1-2 ... "Insight into the mechanism of the stabilization of moloney murine leukaemia virus reverse transcriptase by eliminating RNase H ... Retroviral RT proteins from HIV-1 and murine leukemia virus are the best-studied members of the family. Retroviral RT is ... Pathogenic examples include human immunodeficiency virus and hepatitis B virus, respectively. Both encode large multifunctional ...
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Moloney murine leukemia virus retroviral vector pLXSHD, complete sequence Moloney murine leukemia virus retroviral vector ... Moloney murine leukemia virus retroviral vector pLXSHD, complete sequence. GenBank: M64753.1. FASTA Graphics ...
Moloney murine leukemia virus Gag polyprotein Antibody (HRP). 20-abx109167 Abbexa * EUR 493.20 ... Virus mutation evaluation additional revealed the presence of HPV16 and HPV58 sublineages related to probably excessive ... Description: Recombinant Sindbis virus Structural polyprotein,partial expressed in in vitro E.coli expression system ... Description: Recombinant Sindbis virus Structural polyprotein,partial expressed in in vitro E.coli expression system ...
LAP2alpha and BAF collaborate to organize the Moloney murine leukemia virus preintegration complex.. Suzuki Y, Yang H, Craigie ... autointegration factor blocks autointegration and stimulates intermolecular integration of Moloney murine leukemia virus ... Viruses (2010 Dec) 2:2777-81. Abstract/Full Text. Nucleoprotein intermediates in HIV-1 DNA integration visualized by atomic ... Assembly of prototype foamy virus strand transfer complexes on product DNA bypassing catalysis of integration.. Yin Z, ...
Moloney murine leukemia virus; Plasmids; Polymerase Chain Reaction/methods*; Promoter Regions (Genetics)*; Rats; Recombinant ...
Oncogenesis by Moloney murine leukemia virus.. Tsichlis PN. Anticancer Res; 1987; 7(2):171-80. PubMed ID: 3592629. [TBL] ... 7. Moloney murine leukemia virus infection accelerates lymphomagenesis in E mu-bcl-2 transgenic mice.. Shinto Y; Morimoto M; ... Mml1, a new common integration site in murine leukemia virus-induced promonocytic leukemias maps to mouse chromosome 10. ... sites in the enhancer of T-lymphomagenic SL3-3 murine leukemia virus unmasks a significant potential for myeloid leukemia ...
... or stem cell maintaining conditions revealed the development of DOX-dependent acute myeloid leukaemia in a murine ... of multiple genes by provirus integration in the Mlvi-4 locus in T-cell lymphomas induced by Moloney murine leukemia virus. J. ... Identification and characterization of leukemia stem cells in murine MLL-AF9 acute myeloid leukemia. Cancer Cell 10, 257-268 ( ... 6 ng/mL of murine interleukin 3 (mIL3); 10 ng/mL of human interleukin 6 (hIL6); 20 ng/mL of murine stem cell factor (mSCF) (all ...
RetrovirusesAntiviral agentsMouse leukemia virusesRetroviruses--GeneticsBiochemistry 2. Domain structure of the Moloney murine ... 1. Structure of a cloned circular Moloney murine leukemia virus DNA molecule containing an inverted segment: implications for ... Mouse leukemia virusesRetroviruses--GeneticsRecombinant proteinsBiochemistryInsertional mutagenesis 3. Host factors regulating ... leukemia virus reverse transcriptase: mutational analysis and separate expression of the DNA polymerase and RNase H activities ...
Tanese, N. and Goff, S.P. (1988) Domain structure of the Moloney murine leukemia virus reverse transcriptase: Mutational ... and Moloney murine leukemia virus (M-MLV or MuLV). Genetic engineering and development of proprietary RT-enhancing buffers have ... Temin, H. and Mizutani, S. (1970) RNA-dependent DNA polymerase in virions of Rous sarcoma virus. Nature 226, 1211-3. ... Baltimore, D. (1970) RNA-dependent DNA polymerase in virions of RNA tumour viruses. Nature 226, 1209-11. ...
Moloney murine leukemia virus Preferred Concept UI. M0014001. Registry Number. txid11801. Scope Note. A strain of Murine ... or LEUKEMIA (IM) (for spontaneous leukemia). Scope Note. A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising ... Moloney Leukemia Virus Registry Number. txid11801. Public MeSH Note. 2002; see MOLONEY LEUKEMIA VIRUS 1985-2001, see MOLONEY ... Leukemia Virus, Murine [B04.613.807.375.525] * Abelson murine leukemia virus [B04.613.807.375.525.020] ...
Escherichia coli DNA polymerase III epsilon subunit increases Moloney murine leukemia virus reverse transcriptase fidelity and ... Mutations within conserved motifs in the 3-5 exonuclease domain of herpes simplex virus DNA polymerase. Hall, J.D., Orth, K.L ... Mutations within conserved motifs in the 3-5 exonuclease domain of herpes simplex virus DNA polymerase [5]. ...
From 500 to 1000 ng total RNA were reverse transcribed using 400 units of Moloney Murine Leukemia Virus Reverse Transcriptase ( ...
In contrast, an intact 7b gene may be necessary for in vivo virus infection and replication. Persistent infection with FCoV in ... a cheetah population results in continued virus circulation and may lead to a quasispecies of virus variants. ... which are believed to play a role in virulence of this virus. Sample Population-Biologic samples collected during a 4-year ... reverse transcription was performed with Moloney murine leukemia virus reverse transcriptase according to the manufacturers ...
Host Cell Cathepsins Potentiate Moloney Murine Leukemia Virus Infection. Journal of Virology, 81: 10506-10514 4. Albritton, ... 9. Khanna M, KUMAR PANKAJ, Chhabra SK, Chugh P, Prasad AK (2001). Evaluation of influenza virus detection by Direct enzyme ... Effect of Quercetin on lipid peroxidation and changes in lung morphology in experimental influenza virus infection. ... Effect of Quercetin supplementation on alterations in antioxidant defenses in lung after experimental influenza virus infection ...
And then, of course, there was Moloney. I dont set as great a store on his murine leukemia virus as I do on his sarcoma virus ... but Moloney, in doing that with his murine leukemia virus, was getting it to produce leukemia earlier and such stuff, but one ... which would have frozen Moloneys virus. You see, Moloney followed the procedure that Ray Bryan had set up with the Rous virus ... And it wasnt just that he was looking at a murine leukemia, he was also seeing other tumors being produced and it was obvious ...
... transcription factor that was previously shown to bind to specific DNA binding sites in the Moloney murine leukemia virus (Mo- ... ZASC1 knockout mice exhibit an early bone marrow-specific defect in murine leukemia virus replication. (2013) Virology Journal. ... Herpes Simplex Virus Type 2 (HSV-2) infection can result in life-long recurrent genital disease, asymptomatic virus shedding, ... The erbBs were discovered in an avian erythroblastosis tumor virus and exhibited similarities to human EGFR (Yarden and ...
Total RNA was extracted using Trizol reagent and reverse transcribed using Moloney Murine Leukemia Virus reverse transcriptase ... COOH-terminal mutations of the murine CD36 cDNA (Fig. 2 a) were generated by PCR, verified by sequencing, and cloned into the ... COOH-terminal mutations of the murine CD36 cDNA were generated by PCR, verified by sequencing, and used to transfect HEK293T ... COOH-terminal mutations of the murine CD36 cDNA were generated by PCR, verified by sequencing, and used to transfect HEK293T ...
p>Improve cDNA yield using a highly sensitive and efficient Moloney Murine Leukemia Virus reverse transcriptase (MMLV-RT) by ... MMLV-RT (Moloney Murine Leukemia Virus Reverse Transcriptase) is used for cDNA synthesis and subsequent PCR or qPCR in a one- ... Moloney Murine Leukemia Virus Reverse Transcriptase (MMLV RT) is an RNA-dependent DNA polymerase that can be used for cDNA ...
... acids inserted during suppression of UAA and UGA termination codons at the gag-pol junction of Moloney murine leukemia virus. ... Translational readthrough of the murine leukemia virus gag gene amber codon does not require virus-induced alteration of tRNA. ... Replication of Murine Leukemia Virus (MLV). Mechanism of Readthrough Suppression. *Feng Y-X, Yuan H, Rein A, Levin JG. ... Synthesis of murine leukemia virus proteins associated with virions assembled in actinomycin D-treated cells: evidence for ...
Influenza viruses exploit host cell machinery to replicate, resulting in epidemics of respiratory illness. In turn, the host ... influenza A virus A/Udorn/72 (H3N2) [H3(Udorn)], or Moloney murine leukemia virus (MLV). 24 h after infection, cells were ... The IFITM proteins mediate cellular resistance to influenza A H1N1 virus, West Nile virus, and dengue virus Abraham L Brass 1 ... The IFITM proteins mediate cellular resistance to influenza A H1N1 virus, West Nile virus, and dengue virus Abraham L Brass et ...
NMR STRUCTURE OF THE COMPLEX BETWEEN THE ZINC FINGER PROTEIN NCP10 OF MOLONEY MURINE LEUKEMIA VIRUS AND A SEQUENCE OF THE PSI- ... Solution Structure of Human Immunodificiency Virus Type-2 Nucleocapsid Protein. 2exf. Solution structure of the HIV-1 ... NUCLEOCAPSID ZINC FINGERS DETECTED IN RETROVIRUSES: EXAFS STUDIES ON INTACT VIRUSES AND THE SOLUTION-STATE STRUCTURE OF THE ... HIGH-RESOLUTION SOLUTION NMR STRUCTURE OF THE MINIMAL ACTIVE DOMAIN OF THE HUMAN IMMUNODEFICIENCY VIRUS TYPE-2 NUCLEOCAPSID ...
Virus de la leucémie murine de Moloney Entry term(s):. Leukemia Virus, Moloney. Moloney Leukemia Virus. Virus, Moloney Leukemia ... Moloney murine leukemia virus - Preferred Concept UI. M0014001. Scope note. A strain of Murine leukemia virus (LEUKEMIA VIRUS, ... Moloney murine leukemia virus Entry term(s). Leukemia Virus, Moloney Moloney Leukemia Virus Virus, Moloney Leukemia ... virus de la leucemia de Moloney Scope note:. Cepa de virus de la leucemia murina (VIRUS DE LA LEUCEMIA MURINA) que surge ...
Moloney murine leukemia virus B04.613.807.375.525.750 Radiation Leukemia Virus B04.613.807.375.525.770 Rauscher Virus B04.613. ... Leukemia Virus, Murine B04.613.807.375.525.020 Abelson murine leukemia virus B04.613.807.375.525.050 AKR murine leukemia virus ... Leukemia Virus, Murine B04.820.650.375.525.020 Abelson murine leukemia virus B04.820.650.375.525.050 AKR murine leukemia virus ... Moloney murine leukemia virus B04.820.650.375.525.750 Radiation Leukemia Virus B04.820.650.375.525.770 Rauscher Virus B04.820. ...
Moloney murine leukemia virus Preferred Concept UI. M0014001. Registry Number. txid11801. Scope Note. A strain of Murine ... or LEUKEMIA (IM) (for spontaneous leukemia). Scope Note. A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising ... Moloney Leukemia Virus Registry Number. txid11801. Public MeSH Note. 2002; see MOLONEY LEUKEMIA VIRUS 1985-2001, see MOLONEY ... Leukemia Virus, Murine [B04.613.807.375.525] * Abelson murine leukemia virus [B04.613.807.375.525.020] ...
MOLONEY MURINE LEUKEMIA VIRUS ,. CLASSIFICATION. VIRAL PROTEIN/RNA SPACE GROUP:. P 1 ...
Moloney murine leukemia virus. MPC:. Mitochondrial pyruvate carrier. mTOR:. mammalian target of rapamycin ... 7). 3-BrPA might promote the dissociation of -phosphorylated- HK2 from mitochondria in T24, as previously shown in leukemia and ...
BACKGROUND: The Proviral Integration site of Moloney murine leukemia virus (PIM) kinases are implicated in tumorigenesis; the ... and acute myeloid leukemia (AML), only a minority of these patients undergo HCT. Patients with TP53-mutated (TP53MUT) MDS/AML ... acute myeloid leukemia (AML) or MF with suboptimal ruxolitinib response. RESULTS: Parts 1/2 (n = 58): 6 patients experienced ... had acute leukemia, high-risk myelodysplastic syndrome (MDS), MDS/myeloproliferative neoplasm, myelofibrosis (MF), multiple ...
  • By screening a library of unintegrated, circular Moloney murine leukemia virus (M-MuLV) DNA cloned in lambda phage, we found that approximately 20% of the M-MuLV DNA inserts contained internal sequence deletions or inversions. (nih.gov)
  • MMLV (Moloney Murine Leukemia Virus) enzyme which allows fast cDNA synthesis due to its exceptionally strong strand-displacement activity. (medica-tradefair.com)
  • Moloney Murine Leukemia Virus Reverse Transcriptase (MMLV RT) is an RNA-dependent DNA polymerase that can be used for cDNA synthesis and subsequent PCR or qPCR in one-step or two-step RT-PCR or RT-qPCR assays. (meridianbioscience.com)
  • Most investigators employ either avian myeloblastosis virus (AMV) RT or Moloney murine leukemia virus (MMLV) RT to accomplish this. (nih.gov)
  • 9. Recurring proviral integration suggests a role for proto-oncogene activation in thymomas induced with Mo-MuLV-rescued BCR/ABL virus. (nih.gov)
  • 1. Insights into the Interaction Mechanisms of the Proviral Integration Site of Moloney Murine Leukemia Virus (Pim) Kinases with Pan-Pim Inhibitors PIM447 and AZD1208: A Molecular Dynamics Simulation and MM/GBSA Calculation Study. (nih.gov)
  • 13. Integrating molecular dynamics simulation and molecular mechanics/generalized Born surface area calculation into pharmacophore modeling: a case study on the proviral integration site for Moloney murine leukemia virus (Pim)-1 kinase inhibitors. (nih.gov)
  • We identified the proviral integration site for Moloney murine leukemia virus 1 (PIM1) and its target nuclear factor of activated T cells-1 (NFATc1) as putative drivers of the sustained profibrotic gene signatures in injured aged fibroblasts. (jci.org)
  • The Pim kinase family is a group of three serine/threonine kinases encoded by genes that were identified as hotspots for proviral integration of Moloney murine leukemia virus (Pim) in retrovirus-induced lymphomas [ 5 ]. (oncotarget.com)
  • 2. Activation of multiple genes by provirus integration in the Mlvi-4 locus in T-cell lymphomas induced by Moloney murine leukemia virus. (nih.gov)
  • 3. Activation of the Mlvi-1/mis1/pvt-1 locus in Moloney murine leukemia virus-induced T-cell lymphomas. (nih.gov)
  • 12. Tumor progression in murine leukemia virus-induced T-cell lymphomas: monitoring clonal selections with viral and cellular probes. (nih.gov)
  • 5. Human homologue of Moloney leukemia virus integration-4 locus (MLVI-4), located 20 kilobases 3' of the myc gene, is rearranged in multiple myelomas. (nih.gov)
  • Evaluation of influenza virus detection by Direct enzyme immunoassay (EIA) and conventional methods in asthmatic patients. (webmedcentral.com)
  • 1963 and hepatitis A in 1973, but many of the blood varies according to the isolate and genotype of the samples taken for post transfusion illness tested virus from 3008 to 3037 amino acids (6). (who.int)
  • The need to understand these and other aspects of retroviruses has become more urgent with the dis- covery that AIDS is caused by a retrovirus, the hu- man immunodeficiency virus (HIV). (nih.gov)
  • Although we continue to perform most of these studies with avian and murine retroviruses, we are giving increasing attention to HIV. (nih.gov)
  • The remarkable specificity of virus-host interactions has been known for over twenty years from studies of the polymorphic envelope proteins of avian retroviruses, yet little biochemical information is available about the receptors or about the nature of their interactions with viral envelope glycoproteins. (nih.gov)
  • Assembly of prototype foamy virus strand transfer complexes on product DNA bypassing catalysis of integration. (nih.gov)
  • Scientists found that B-cell-specific Moloney murine leukemia virus integration site 1 ( Bmi-1 ) mRNA levels were elevated in nasopharyngeal carcinoma cell lines. (stemcellsciencenews.com)
  • Chicken DNA was introduced into monkey cells (presumed to lack avian 250 virus receptors) by co-transformation with a selectable marker. (nih.gov)
  • PMID- 214398 TI - Characterization of an adenosine triphosphatase of the avian myeloblastosis virus and the virus-infected myeloblast. (nih.gov)
  • Nile virus (WNV) isolates collected during the summer and years, the virus has traversed North America, presumably fall of 2001 and 2002 indicated genetic variation among from New York City, where it was first isolated during the strains circulating in geographically distinct regions of the summer of 1999 (4-7). (cdc.gov)
  • These results show the geographic clustering of genetically similar WNV iso- deaths attributed to WNV in humans, equines, and birds lates and the possible emergence of a dominant variant cir- documented since the discovery of the virus in North culating across much of the United States during 2002. (cdc.gov)
  • 7. AZD1208, a potent and selective pan-Pim kinase inhibitor, demonstrates efficacy in preclinical models of acute myeloid leukemia. (nih.gov)
  • 10. Identification of N-(4-((1R,3S,5S)-3-Amino-5-methylcyclohexyl)pyridin-3-yl)-6-(2,6-difluorophenyl)-5-fluoropicolinamide (PIM447), a Potent and Selective Proviral Insertion Site of Moloney Murine Leukemia (PIM) 1, 2, and 3 Kinase Inhibitor in Clinical Trials for Hematological Malignancies. (nih.gov)
  • 12. Protein profiling identifies mTOR pathway modulation and cytostatic effects of Pim kinase inhibitor, AZD1208, in acute myeloid leukemia. (nih.gov)
  • Researchers performed a comprehensive evaluation of metabolic adaptation to tyrosine kinase inhibitor treatment and its role in chronic myelogenous leukemia hematopoietic stem and progenitor cell persistence. (stemcellsciencenews.com)
  • Recently, the receptor for ecotropic murine leukemia virus (MLV) was shown to be a very different type of protein, with about fourteen transmembrane domains. (nih.gov)
  • The results obtained from the autointegrated clones were supported by nucleotide sequencing of the host-virus junction of two cloned M-MuLV integrated proviruses obtained from infected rat cells. (nih.gov)
  • A strain of Murine leukemia virus ( LEUKEMIA VIRUS, MURINE ) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. (nih.gov)
  • America from 1999 through 2001 set the stage for the Texas shared the following differences from WN-NY99: five rapid and widespread movement of the virus across the nucleotide mutations and one amino acid substitution. (cdc.gov)
  • The kit Ampli set PML-RARa identifies the translocation t(15;17) associated with acute promyelocytic leukemia (APL). (medica-tradefair.com)
  • be used to reliably and rapidly diagnose Acute Myeloid Leukemia (AML). (medica-tradefair.com)
  • Clonit, Innovation and Passion to serve Acute myeloid leukemia (AML) diagnosis and monitoring. (medica-tradefair.com)
  • significant sensitivity in the detection of the translocations or chromosomal abnormalities in patients with Acute myeloid leukemia (AML). (medica-tradefair.com)
  • 5. The novel combination of dual mTOR inhibitor AZD2014 and pan-PIM inhibitor AZD1208 inhibits growth in acute myeloid leukemia via HSF pathway suppression. (nih.gov)
  • Search, retrieve and analyze Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) sequences in NCBI Virus . (nih.gov)
  • Scientists demonstrated for the first time that ZDHHC21 palmitoyltransferase served as a key regulator of oxidative phosphorylation hyperactivity in acute myeloid leukemia (AML) cells. (stemcellsciencenews.com)
  • The authors characterized stem cell-related gene expression and identified stemness biomarker genes in acute myeloid leukemia. (stemcellsciencenews.com)
  • geographic distribution of the virus was limited to Africa, Phylogenetic comparisons of partial and complete the Middle East, India, and western and central Asia with nucleotide sequences from isolates collected in the north- occasional epidemics in Europe (1,2). (cdc.gov)
  • Moloney murine leukemia virus integrase and reverse transcriptase interact with PML proteins. (nbrp.jp)
  • Pull-down assay and co-immunoprecipitation of cell extracts in which the integrase or reverse transcriptase of Moloney murine leukemia virus was transiently expressed showed that both enzymes interacted with PML proteins. (nbrp.jp)
  • M-MuLV-RH is a genetically modified Moloney Murine Leukemia Virus reverse transcriptase (M-MuLV). (geneon.net)
  • 5. PANKAJ KUMAR, Madhu Khanna, Yogesh tyagi, G Pal, Raj HG, (2005) Effect of Quercetin supplementation on alterations in antioxidant defenses in lung after experimental influenza virus infection. (webmedcentral.com)
  • Effect of Quercetin on lipid peroxidation and changes in lung morphology in experimental influenza virus infection. (webmedcentral.com)
  • Then Groupé, at that time, was interested in the usual influenza viruses, the PR8 virus and such stuff, and this is the reason we had a lot of chicken eggs around. (nih.gov)
  • 16. Robertsonian translocation studies on the significance of trisomy 15 in murine T-cell leukemia. (nih.gov)
  • 20. Leukaemogenesis by the delta Mo + SV Moloney murine leukaemia virus (M-MuLV) variant in E mu pim-1 transgenic mice: high frequency of recombination with a solo endogenous M-MuLV LTR in vivo. (nih.gov)
  • and 5) the regulation of viral gene expression displays many features characteristic of cellular genes and some thus far unique to viruses. (nih.gov)
  • Justification: Hepatitis C virus (HCV) continues to be a major disease burden on the world and Man is the only known natural host of Hepatitis C virus (Chivaliez and Pawlotsky, 2007). (who.int)
  • Results: of the 259 plasma specimens screened for Hepatitis C virus in this study, 20(7.7%) were positive for anti HCV antibodies by ELISA and 16(6.2%) of the antibodies positive specimen were positive for HCV RNA. (who.int)
  • Hepatitis C virus genotype 1b was found in the entire HCV RNA positive sample. (who.int)
  • Conclusions: The findings of 6.2% prevalence of HCV infection based on HCV RNA test confirmed that there is Hepatitis C virus in Kaduna State with genotype 1b as the predominant genotype found in all the three senatorial zones. (who.int)
  • identified the virus to be Hepatitis C virus (2). (who.int)
  • Hepatitis C virus (HCV) is a member of or genome fragment sequencing, genotype specific the family Flaviviridae, placed in a new monotypic amplification of a genomic region or PCR genus Hepacivirus (4, 5). (who.int)
  • PMID- 214407 TI - Antibodies to Herpes simplex virus types 1 and 2 in patients with squamous-cell carcinoma of uterine cervix in India. (nih.gov)
  • AB - Antibody activity to Herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2) was measured by the indirect hemagglutination (IHA) test in sera from 124 women with squamous-cell carcinoma of the uterine cervix, 46 women with non-cervical cancer and 116 matched normal women. (nih.gov)
  • This is an interview of Dr. Robert Manaker, who was Deputy Director of the Viruses Cancer Program, taken on March 9, 1995. (nih.gov)
  • See all publicly available virus sequences in newly designed interface at NCBI Virus and send us your feedback! (nih.gov)
  • PMID- 214405 TI - Long-term T-cell-mediated immunity to Epstein-Barr virus in man. (nih.gov)
  • The results strongly suggest that the regression phenomenon is an in vitro expression of long-term T-cell-mediated immunity to EB virus which the large majority, if not all, infected individuals possess. (nih.gov)
  • Hybridoma cell line 500 expresses monoclonal antibody specific for Moloney murine leukemia virus (MuLV) gp80. (nih.gov)
  • 15. Differential disease restriction of Moloney and Friend murine leukemia viruses by the mouse Rmcf gene is governed by the viral long terminal repeat. (nih.gov)
  • Virus mutation evaluation additional revealed the presence of HPV16 and HPV58 sublineages related to probably excessive oncogenicity. (aabioetica.org)
  • 1. Rearrangement of c-myc, pim-1 and Mlvi-1 and trisomy of chromosome 15 in MCF- and Moloney-MuLV-induced murine T-cell leukemias. (nih.gov)
  • 14. Is trisomy cause or consequence of murine T cell leukemia development? (nih.gov)
  • 19. Trisomy 15 and other nonrandom chromosome changes in Rauscher murine leukemia virus-induced leukemia cell lines. (nih.gov)
  • Host Cell Cathepsins Potentiate Moloney Murine Leukemia Virus Infection. (webmedcentral.com)
  • AB - Peripheral blood mononuclear cells from donors of known serological status with respect to EB virus were exposed to the virus in vitro and then cultured at various cell concentrations. (nih.gov)
  • PMID- 214400 TI - Transmission of Japanese encephalitis virus by Culex bitaeniorhynchus Giles. (nih.gov)
  • I. Complete regression of virus-induced transformation in cultures of seropositive donor leukocytes. (nih.gov)