A replication-defective murine sarcoma virus (SARCOMA VIRUSES, MURINE) capable of transforming mouse lymphoid cells and producing erythroid leukemia after superinfection with murine leukemia viruses (LEUKEMIA VIRUS, MURINE). It has also been found to transform cultured human fibroblasts, rat liver epithelial cells, and rat adrenocortical cells.
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).
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.
A replication-defective murine sarcoma virus (SARCOMA VIRUSES, MURINE) isolated from a rhabdomyosarcoma by Moloney in 1966.
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.
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 replication-defective mouse sarcoma virus (SARCOMA VIRUSES, MURINE) first described by J.J. Harvey in 1964.
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.
Group of alpharetroviruses (ALPHARETROVIRUS) producing sarcomata and other tumors in chickens and other fowl and also in pigeons, ducks, and RATS.
The functional hereditary units of VIRUSES.
Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, Ki-ras, rasK) murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras genes have been detected in human, avian, murine, and non-vertebrate genomes. The closely related N-ras gene has been detected in human neuroblastoma and sarcoma cell lines. All genes of the family have a similar exon-intron structure and each encodes a p21 protein.
Experimentally induced neoplasms of CONNECTIVE TISSUE in animals to provide a model for studying human SARCOMA.
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.
Established cell cultures that have the potential to propagate indefinitely.
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.
A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant.
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.
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.

Glucose regulates protein catabolism in ras-transformed fibroblasts through a lysosomal-dependent proteolytic pathway. (1/106)

Transformed cells are exposed to heterogeneous microenvironments, including low D-glucose (Glc) concentrations inside tumours. The regulation of protein turnover is commonly impaired in many types of transformed cells, but the role of Glc in this regulation is unknown. In the present study we demonstrate that Glc controls protein turnover in ras-transformed fibroblasts (KBALB). The regulation by Glc of protein breakdown was correlated with modifications in the levels of lysosomal cathepsins B, L and D, while autophagic sequestration and non-lysosomal proteolytic systems (m- and mu-calpains and the zeta-subunit of the proteasome) remained unaffected. Lactacystin, a selective inhibitor of the proteasome, depressed proteolysis, but did not prevent its regulation by Glc. The sole inhibition of the cysteine endopeptidases (cathepsins B and L, and calpains) by E-64d [(2S,3S)-trans-epoxysuccinyl-L-leucylamido-3-methylbutane ethyl ester] was also not sufficient to alter the effect of Glc on proteolysis. The Glc-dependent increase in proteolysis was, however, prevented after optimal inhibition of lysosomal cysteine and aspartic endopeptidases by methylamine. We conclude that, in transformed cells, Glc plays a critical role in the regulation of protein turnover and that the lysosomal proteolytic capacity is mainly responsible for the control of intracellular proteolysis by Glc.  (+info)

Thyroid cell transformation requires the expression of the HMGA1 proteins. (2/106)

Elevated expression of HMGA1 and HMGA2 proteins is correlated with a highly malignant phenotype in several human tumors. We previously demonstrated that the block of HMGA2 protein synthesis prevented rat thyroid cell transformation by murine retroviruses. Suppression of HMGA2 synthesis was associated with lack of induction of HMGA1 proteins suggesting that both HMGA1 and HMGA2 play a role in the process of neoplastic transformation. To determine the role of the HMGA1 gene in thyroid cell transformation, we blocked HMGA1 protein synthesis by an antisense methodology. Here we report that transfection of an HMGA1 cDNA antisense construct into a normal rat thyroid cell line (FRTL-5 Cl2), followed by infection with Kirsten murine sarcoma virus (KiMSV), generated a transformed cell line that expresses high levels of the v-ras-Ki oncogene and that does not require thyroid-stimulating hormones for growth. However, this cell line does not show the malignant phenotype, i.e., it neither grows in soft agar nor induces tumors after injection in athymic mice. Moreover, the lack of the neoplastic phenotype in the virus-infected thyroid cells carrying the HMGA1 antisense construct correlates with the absence of induction of AP-1 transcriptional activity.  (+info)

Oncogenic ras induces an inhibitor of double-stranded RNA-dependent eukaryotic initiation factor 2 alpha-kinase activation. (3/106)

The interferon-inducible 68-kDa dsRNA-dependent eIF2 alpha-kinase (dsI) is a potent cellular antiviral enzyme which is activated by autophosphorylation in response to double-stranded RNA (dsRNA). Activated dsI has also been implicated as a second messenger for gene induction by platelet-derived growth factor (PDGF) and interferon (IFN). We have shown previously that introduction of a transforming ras gene into BALB/c-3T3 fibroblasts blocks induction of responsive genes by PDGF and IFN. We therefore investigated the effect of transforming ras genes on dsI activity in these cells. We report here that dsRNA-mediated activation of dsI is blocked in v-ras-containing cells in a manner specific to ras and not attributable to the transformed phenotype since: 1) a dexamethasone-inducible v-Ha-ras gene produced the effect within 18 h of induction; 2) morphologic reversion of ras-transformed cells with cAMP or the Krev-1 gene restored potential for dsI activation; and 3) transformation by v-mos or v-abl had no effect on dsI activation. Latent dsI levels were unaffected by v-ras. A heat-sensitive dsI inhibitory activity could be demonstrated in v-ras-containing cells which functioned in trans when mixed with untransformed cell extracts prior to stimulation with dsRNA. The inhibitory activity, which was destroyed by phenol-chloroform extraction, did not bind dsRNA.  (+info)

Reversal of divergent differentiation by ras oncogene-mediated transformation. (4/106)

In embryogenesis, ovarian surface epithelial cells and ovarian granulosa cells arise through divergent differentiation from a common mesenchymal precursor, the urogenital ridge. In the adult rat, ovarian surface epithelial cells are nonsteroidogenic and keratin positive, while ovarian granulosa cells are steroidogenic and keratin negative. In culture, Kirsten murine sarcoma virus-transformed, tumorigenic ovarian surface epithelial cells continued to express keratin but also became steroidogenic. Transformed ovarian granulosa cells remained steroidogenic but also acquired keratins. Mesodermally derived cells from other sources did not show these differentiation-related changes in response to transformation. The results suggest that v-ras oncogenes may cause the reversion of adult, developmentally related cells to the phenotype of a common, multipotential precursor. They also demonstrate the capacity of v-ras to either induce or reduce the same differentiated characteristic, depending on the developmental history of the target cells.  (+info)

Differential processing of osteopontin transcripts in rat kidney- and osteoblast-derived cell lines. (5/106)

Using immunoprecipitation and tryptic peptide microsequencing we confirmed the identity of normal rat kidney (NRK) cell-secreted 69-kDa major phosphoprotein as osteopontin (OP). We then immunoselected a 1.4-kilobase pair (kb) OP cDNA from a lambda gt11 library prepared from Kirsten sarcoma virus-transformed NRK (KNRK) cellular mRNA, using rabbit anti-69-kDa OP serum. Sequence analysis of this cDNA revealed the presence of a 52-nucleotide-long insert in the 5'-noncoding region, which was absent in OP cDNA cloned from the cDNA library of ROS 17/2.8 rat osteosarcoma cells. The insert sequence is flanked by putative intron splice junctions and is located 15-nucleotide upstream of the translational initiation site. An insert-specific 30-mer oligonucleotide probe hybridized to a single 1.5-kb RNA species from both NRK and KNRK cells, but not from ROS 17/2.8 cells. However, Southern analysis showed the presence of this insert sequence in the genomic DNA of both NRK and ROS 17/2.8 cells. Furthermore, PCR amplification of the insert-containing region using genomic DNAs from both NRK and ROS 17/2.8 cells gave products of identical size and sequence. Since OP is a single copy gene, these data provide strong evidence for differential cell type-specific processing of OP transcripts. In addition, we demonstrate that, in contrast to most transformed cells, levels of OP expression are significantly reduced in KNRK cells as compared to NRK cells.  (+info)

Senescence as a mode of tumor suppression. (6/106)

Two independent lines of experimental evidence are presented in support of the hypothesis that senescence is a normal mechanism of tumor suppression, a homeostatic device designed through evolution to limit cell proliferation irreversibly and thereby to protect the organism against cancer. One set of experiments uses normal human foreskin fibroblasts, transfected at early passage with SV40 DNA and subsequently infected with the K-ras virus. If the cells are immortal prior to infection, they become tumorigenic and make large tumors in nude mice, whereas if they are not immortal, though expressing SV40 T-antigen, they make tiny tumors that senesce in the test mouse after as many doublings as similar cells make in culture. This result demonstrates that immortalization is essential for progressive tumor growth in vivo. The second set of experiments demonstrate that normal human mammary epithelial cells can be immortalized by transfection with viral DNA from human papilloma virus 16 or 18, although these viruses have not been associated with breast cancer. The effective immortalization and other premalignant changes induced by human papilloma virus transfection are accompanied by chromosome changes that may contribute to the partially transformed phenotypes. None of the cloned or pooled transfectants have been tumorigenic in the nude mouse assay. Here, too, immortalization is experimentally separable from tumor-forming ability.  (+info)

Identification and molecular cloning of a novel mouse mucosal mast cell serine protease. (7/106)

A novel 28,000 Mr serine protease, designated mouse mast cell protease-2 (MMCP-2), that is stored in the secretory granules of Kirsten sarcoma virus-immortalized mouse mast cells (KiSV-MC) has been identified and its NH2-terminal amino acid sequence has been determined. Analysis of a 953-base pair cDNA that encodes MMCP-2 revealed that this serine protease is a basically charged protein, possessing the histidine-aspartic acid-serine charge relay system that is characteristic of other serine proteases. DNA blot analysis using the full-length MMCP-2 cDNA indicated the existence of a family of highly related serine protease genes in the mouse genome. When the same DNA blot was probed with the 149-base pair KpnI----3' fragment of the cDNA, the probe hybridized to a single DNA fragment, thereby demonstrating that this 3' fragment could be used as a gene-specific probe. The presence of high levels of the MMCP-2 mRNA transcript in the intestines of nematode-infected mice, and its absence in mouse bone marrow-derived mast cells and peritoneal cavity-derived connective tissue mast cells, suggest that this member of the mouse mast cell protease family is preferentially expressed late in the differentiation of mucosal mast cells.  (+info)

Alkalinization of the lysosomes is correlated with ras transformation of murine and human fibroblasts. (8/106)

The pH of the intralysosomal compartment of fibroblasts in culture was monitored by measuring the fluorescence emission intensity at 530 nm of fluid phase pinocytosed fluorescein-conjugated dextrans (FITC-dextrans) excited at 488 and 457 nm. Following the procedure of Ohkuma and Poole (Ohkuma, S., and Poole, B. (1978) Proc. Natl. Acad. Sci. U. S. A. (1978) 75, 3327-3331), a relationship was established between the fluorescence emission intensity of the FITC-dextrans and pH. This correlation was used to determine the intralysosomal apparent pH (pHapp) of a series of fibroblast cultures. The mean intralysosomal pHapp values of nontransformed mouse 3T3 fibroblasts and an infinite life-span human fibroblast cell strain, designated MSU-1.1, was 5.0. In distinction that of 3T3 fibroblasts transformed to the malignant state by Kirsten murine sarcoma virus and MSU-1.1 cells transformed by transfection of the v-Ki-ras or T24 H-ras oncogene was 6.1. These measurements suggest that ras transformation results in a significant perturbation of lysosomal pH.  (+info)

The Kirsten murine sarcoma virus (KiMSV) is a type of retrovirus that can cause tumors in mice. It was first discovered in 1968 by Charlotte Kirsten and her colleagues. KiMSV is a complex retrovirus, which means that it contains additional genes beyond the standard gag, pol, and env genes found in simple retroviruses.

In particular, KiMSV contains an oncogene called v-Ki-ras, which encodes a protein that can transform cells and lead to cancer. This oncogene is derived from the host cell's c-Ki-ras gene, which is involved in normal cell signaling pathways. When the viral oncogene is expressed in infected cells, it can cause uncontrolled cell growth and division, leading to the formation of tumors.

KiMSV primarily causes fibrosarcomas, a type of cancer that arises from connective tissue cells called fibroblasts. However, it has also been shown to induce other types of tumors in mice, including leukemias and lymphomas.

While KiMSV is not known to infect humans or cause disease in humans, the study of this virus and its oncogene have provided important insights into the mechanisms of cancer development and progression. The v-Ki-ras oncogene, for example, has been found to be mutated and activated in many human cancers, including lung, colon, and pancreatic cancers.

Sarcoma viruses, murine, are a group of RNA viruses that primarily affect mice and other rodents. They are classified as type C retroviruses, which means they contain an envelope, have reverse transcriptase enzyme activity, and replicate through a DNA intermediate.

The murine sarcoma viruses (MSVs) are associated with the development of various types of tumors in mice, particularly fibrosarcomas, which are malignant tumors that originate from fibroblasts, the cells that produce collagen and other fibers in connective tissue.

The MSVs are closely related to the murine leukemia viruses (MLVs), and together they form a complex called the murine leukemia virus-related viruses (MLVRVs). The MLVRVs can undergo recombination events, leading to the generation of new viral variants with altered biological properties.

The MSVs are important tools in cancer research because they can transform normal cells into tumor cells in vitro and in vivo. The study of these viruses has contributed significantly to our understanding of the molecular mechanisms underlying cancer development and progression.

A gammaretrovirus is a type of retrovirus, which is a virus that contains RNA as its genetic material and uses the reverse transcriptase enzyme to produce DNA from its RNA genome. Gammaretroviruses are enveloped viruses, meaning they have a lipid membrane derived from the host cell. They are also classified as simple retroviruses because their genome only contains the genes gag, pol, and env.

Gammaretroviruses are known to cause diseases in animals, including leukemias and immunodeficiencies. One example of a gammaretrovirus is the feline leukemia virus (FeLV), which can cause a variety of symptoms in cats, including anemia, lymphoma, and immune suppression.

Gammaretroviruses have also been implicated in some human diseases, although they are not thought to be major causes of human disease. For example, the human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that is closely related to gammaretroviruses and can cause adult T-cell leukemia/lymphoma and tropical spastic paraparesis/ HTLV-associated myelopathy (TSP/HAM).

It's important to note that the classification of retroviruses has evolved over time, and some viruses that were once classified as gammaretroviruses are now considered to be part of other retrovirus genera.

Moloney murine sarcoma virus (Mo-MSV) is a type of retrovirus, specifically a sarcoma virus that infects mice. It was first discovered and isolated by John Moloney in 1960. Mo-MSV is a horizontally transmitted virus, meaning it is typically spread through the direct transfer of bodily fluids between infected and uninfected hosts.

Mo-MSV is closely related to Moloney leukemia virus (Mo-MLV), and both viruses are often found as co-infections in mice. Mo-MSV is associated with the development of sarcomas, which are malignant tumors that arise from connective tissues such as bone, cartilage, fat, muscle, or fibrous tissue.

The virus contains an RNA genome and integrates its genetic material into the host cell's DNA upon infection. Mo-MSV is capable of transforming cells by introducing oncogenes into the host cell's genome, which can lead to uncontrolled cell growth and ultimately result in cancer formation.

Mo-MSV has been extensively studied as a model system for retroviral infection and tumorigenesis, contributing significantly to our understanding of oncogene function and the molecular mechanisms underlying cancer development.

Cell transformation, viral refers to the process by which a virus causes normal cells to become cancerous or tumorigenic. This occurs when the genetic material of the virus integrates into the DNA of the host cell and alters its regulation, leading to uncontrolled cell growth and division. Some viruses known to cause cell transformation include human papillomavirus (HPV), hepatitis B virus (HBV), and certain types of herpesviruses.

Neoplastic cell transformation is a process in which a normal cell undergoes genetic alterations that cause it to become cancerous or malignant. This process involves changes in the cell's DNA that result in uncontrolled cell growth and division, loss of contact inhibition, and the ability to invade surrounding tissues and metastasize (spread) to other parts of the body.

Neoplastic transformation can occur as a result of various factors, including genetic mutations, exposure to carcinogens, viral infections, chronic inflammation, and aging. These changes can lead to the activation of oncogenes or the inactivation of tumor suppressor genes, which regulate cell growth and division.

The transformation of normal cells into cancerous cells is a complex and multi-step process that involves multiple genetic and epigenetic alterations. It is characterized by several hallmarks, including sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, enabling replicative immortality, induction of angiogenesis, activation of invasion and metastasis, reprogramming of energy metabolism, and evading immune destruction.

Neoplastic cell transformation is a fundamental concept in cancer biology and is critical for understanding the molecular mechanisms underlying cancer development and progression. It also has important implications for cancer diagnosis, prognosis, and treatment, as identifying the specific genetic alterations that underlie neoplastic transformation can help guide targeted therapies and personalized medicine approaches.

Harvey murine sarcoma virus (HMSV) is a type of retrovirus, specifically a sarcoma virus that was first isolated from mice. It is named after J. Harvey, who discovered the virus in 1964. HMSV is closely related to Moloney murine leukemia virus (M-MuLV).

HMSV is a complex retrovirus, which contains several accessory genes that are not required for replication but contribute to viral pathogenesis and oncogenic transformation. The most well-known oncogene carried by HMSV is v-src, which encodes the pp60v-src protein tyrosine kinase. This oncogene was the first cellular oncogene (c-src) to be discovered, and it plays a crucial role in the transformation of cells and the development of sarcomas in infected mice.

HMSV infection typically occurs through the direct introduction of viral particles into susceptible tissues or by the transfer of infected cells. Once inside the host, HMSV integrates its genetic material into the host cell's DNA, leading to the expression of viral genes and the production of new virus particles. The activation of the v-src oncogene results in uncontrolled cell growth and division, ultimately leading to the formation of tumors.

In summary, Harvey murine sarcoma virus is a retrovirus that carries the v-src oncogene, causing uncontrolled cell growth and leading to the development of sarcomas in infected mice.

Oncogenes are genes that have the potential to cause cancer. They can do this by promoting cell growth and division (cellular proliferation), preventing cell death (apoptosis), or enabling cells to invade surrounding tissue and spread to other parts of the body (metastasis). Oncogenes can be formed when normal genes, called proto-oncogenes, are mutated or altered in some way. This can happen as a result of exposure to certain chemicals or radiation, or through inherited genetic mutations. When activated, oncogenes can contribute to the development of cancer by causing cells to divide and grow in an uncontrolled manner.

Avian sarcoma viruses (ASVs) are a group of retroviruses that primarily infect birds and cause various types of tumors, particularly sarcomas. These viruses contain an oncogene, which is a gene that has the ability to transform normal cells into cancerous ones. The oncogene in ASVs is often derived from cellular genes called proto-oncogenes, which are normally involved in regulating cell growth and division.

ASVs can be divided into two main types: non-defective and defective. Non-defective ASVs contain a complete set of viral genes that allow them to replicate independently, while defective ASVs lack some of the necessary viral genes and require assistance from other viruses to replicate.

One well-known example of an avian sarcoma virus is the Rous sarcoma virus (RSV), which was first discovered in chickens by Peyton Rous in 1910. RSV causes a highly malignant form of sarcoma in chickens and has been extensively studied as a model system for cancer research. The oncogene in RSV is called v-src, which is derived from the normal cellular gene c-src.

Avian sarcoma viruses have contributed significantly to our understanding of the molecular mechanisms underlying cancer development and have provided valuable insights into the role of oncogenes in tumorigenesis.

Viral genes refer to the genetic material present in viruses that contains the information necessary for their replication and the production of viral proteins. In DNA viruses, the genetic material is composed of double-stranded or single-stranded DNA, while in RNA viruses, it is composed of single-stranded or double-stranded RNA.

Viral genes can be classified into three categories: early, late, and structural. Early genes encode proteins involved in the replication of the viral genome, modulation of host cell processes, and regulation of viral gene expression. Late genes encode structural proteins that make up the viral capsid or envelope. Some viruses also have structural genes that are expressed throughout their replication cycle.

Understanding the genetic makeup of viruses is crucial for developing antiviral therapies and vaccines. By targeting specific viral genes, researchers can develop drugs that inhibit viral replication and reduce the severity of viral infections. Additionally, knowledge of viral gene sequences can inform the development of vaccines that stimulate an immune response to specific viral proteins.

Ras genes are a group of genes that encode for proteins involved in cell signaling pathways that regulate cell growth, differentiation, and survival. Mutations in Ras genes have been associated with various types of cancer, as well as other diseases such as developmental disorders and autoimmune diseases. The Ras protein family includes H-Ras, K-Ras, and N-Ras, which are activated by growth factor receptors and other signals to activate downstream effectors involved in cell proliferation and survival. Abnormal activation of Ras signaling due to mutations or dysregulation can contribute to tumor development and progression.

I'm sorry for any confusion, but "Sarcoma, Experimental" is not a recognized medical term or definition. Sarcomas are a type of cancer that develop in the body's connective tissues, such as bones, muscles, tendons, cartilage, and fat. There are many different types of sarcomas, classified based on the specific type of tissue they originate from.

Experimental, on the other hand, refers to something that is being tested or tried out for the first time, typically as part of a scientific experiment or clinical trial. In the context of cancer treatment, an experimental therapy might refer to a new drug, procedure, or device that is still being studied in clinical trials to determine its safety and effectiveness.

Therefore, "Sarcoma, Experimental" could potentially refer to a clinical trial or research study involving a new treatment for sarcoma, but it would not be a medical definition in and of itself. If you have any specific questions about sarcomas or experimental treatments, I would recommend consulting with a healthcare professional or medical researcher for more accurate information.

The Moloney murine leukemia virus (Mo-MLV) is a type of retrovirus, specifically a gammaretrovirus, that is commonly found in mice. It was first discovered and isolated by John Moloney in 1960. Mo-MLV is known to cause various types of cancerous conditions, particularly leukemia, in susceptible mouse strains.

Mo-MLV has a single-stranded RNA genome that is reverse transcribed into double-stranded DNA upon infection of the host cell. This viral DNA then integrates into the host's genome and utilizes the host's cellular machinery to produce new virus particles. The Mo-MLV genome encodes for several viral proteins, including gag (group-specific antigen), pol (polymerase), and env (envelope) proteins, which are essential for the replication cycle of the virus.

Mo-MLV is widely used in laboratory research as a model retrovirus to study various aspects of viral replication, gene therapy, and oncogenesis. It has also been engineered as a vector for gene delivery applications due to its ability to efficiently integrate into the host genome and deliver large DNA sequences. However, it is important to note that Mo-MLV and other retroviruses have the potential to cause insertional mutagenesis, which can lead to unintended genetic alterations and adverse effects in some cases.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

Helper viruses, also known as "auxiliary" or "satellite" viruses, are defective viruses that depend on the assistance of a second virus, called a helper virus, to complete their replication cycle. They lack certain genes that are essential for replication, and therefore require the helper virus to provide these functions.

Helper viruses are often found in cases of dual infection, where both the helper virus and the dependent virus infect the same cell. The helper virus provides the necessary enzymes and proteins for the helper virus to replicate, package its genome into new virions, and bud off from the host cell.

One example of a helper virus is the hepatitis B virus (HBV), which can serve as a helper virus for hepatitis D virus (HDV) infection. HDV is a defective RNA virus that requires the HBV surface antigen to form an envelope around its nucleocapsid and be transmitted to other cells. In the absence of HBV, HDV cannot replicate or cause disease.

Understanding the role of helper viruses in viral infections is important for developing effective treatments and vaccines against viral diseases.

Sarcoma is a type of cancer that develops from certain types of connective tissue (such as muscle, fat, fibrous tissue, blood vessels, or nerves) found throughout the body. It can occur in any part of the body, but it most commonly occurs in the arms, legs, chest, and abdomen.

Sarcomas are classified into two main groups: bone sarcomas and soft tissue sarcomas. Bone sarcomas develop in the bones, while soft tissue sarcomas develop in the soft tissues of the body, such as muscles, tendons, ligaments, fat, blood vessels, and nerves.

Sarcomas can be further classified into many subtypes based on their specific characteristics, such as the type of tissue they originate from, their genetic makeup, and their appearance under a microscope. The different subtypes of sarcoma have varying symptoms, prognoses, and treatment options.

Overall, sarcomas are relatively rare cancers, accounting for less than 1% of all cancer diagnoses in the United States each year. However, they can be aggressive and may require intensive treatment, such as surgery, radiation therapy, and chemotherapy.

Medical Definition:

Murine leukemia virus (MLV) is a type of retrovirus that primarily infects and causes various types of malignancies such as leukemias and lymphomas in mice. It is a complex genus of viruses, with many strains showing different pathogenic properties.

MLV contains two identical single-stranded RNA genomes and has the ability to reverse transcribe its RNA into DNA upon infection, integrating this proviral DNA into the host cell's genome. This is facilitated by an enzyme called reverse transcriptase, which MLV carries within its viral particle.

The virus can be horizontally transmitted between mice through close contact with infected saliva, urine, or milk. Vertical transmission from mother to offspring can also occur either in-utero or through the ingestion of infected breast milk.

MLV has been extensively studied as a model system for retroviral pathogenesis and tumorigenesis, contributing significantly to our understanding of oncogenes and their role in cancer development. It's important to note that Murine Leukemia Virus does not infect humans.

DNA restriction enzymes, also known as restriction endonucleases, are a type of enzyme that cut double-stranded DNA at specific recognition sites. These enzymes are produced by bacteria and archaea as a defense mechanism against foreign DNA, such as that found in bacteriophages (viruses that infect bacteria).

Restriction enzymes recognize specific sequences of nucleotides (the building blocks of DNA) and cleave the phosphodiester bonds between them. The recognition sites for these enzymes are usually palindromic, meaning that the sequence reads the same in both directions when facing the opposite strands of DNA.

Restriction enzymes are widely used in molecular biology research for various applications such as genetic engineering, genome mapping, and DNA fingerprinting. They allow scientists to cut DNA at specific sites, creating precise fragments that can be manipulated and analyzed. The use of restriction enzymes has been instrumental in the development of recombinant DNA technology and the Human Genome Project.

Kirsten WH, Schauf V, McCoy J (1970). "Properties of a murine sarcoma virus". Bibliotheca Haematologica. International ... the Harvey sarcoma virus and Kirsten sarcoma virus, by Edward M. Scolnick and colleagues at the National Institutes of Health ( ... "Human genome contains four genes homologous to transforming genes of Harvey and Kirsten murine sarcoma viruses". Proceedings of ... Ras, from "Rat sarcoma virus", is a family of related proteins that are expressed in all animal cell lineages and organs. All ...
"Nucleotide sequence of the oncogene encoding the p21 transforming protein of Kirsten murine sarcoma virus". Science. 217 (4563 ... KRAS (Kirsten rat sarcoma virus) is a gene that provides instructions for making a protein called K-Ras, a part of the RAS/MAPK ... It is called KRAS because it was first identified as a viral oncogene in the Kirsten RAt Sarcoma virus. The oncogene identified ... "A Phase I/II Study Administering Peripheral Blood Lymphocytes Transduced With a Murine T-Cell Receptor Recognizing the G12D ...
... harvey murine sarcoma virus MeSH B04.265.600.500 - kirsten murine sarcoma virus MeSH B04.265.600.600 - moloney murine sarcoma ... murine MeSH B04.820.650.375.860.400 - harvey murine sarcoma virus MeSH B04.820.650.375.860.500 - kirsten murine sarcoma virus ... harvey murine sarcoma virus MeSH B04.909.574.807.375.860.500 - kirsten murine sarcoma virus MeSH B04.909.574.807.375.860.600 - ... harvey murine sarcoma virus MeSH B04.909.777.731.375.860.500 - kirsten murine sarcoma virus MeSH B04.909.777.731.375.860.600 - ...
2020 also known as Kirsten Mouse Sarcoma Virus and Kirsten Murine Sarcoma Virus 30 Years Later, WHK Program Remains a Singular ... the Kirsten Rat Sarcoma Virus, and consequently of the KRAS oncogene. Werner H. Kirsten was born in Leipzig in 1925. He ... 963 NCI's Werner Kirsten Is Mourned, in the NIH Record; published February 2, 1993; p 8 "Werner H. Kirsten Student Internship ... Kirsten was married to Inger Nielsen, with whom he had three sons, Christian, Olaf and Thomas. He died age 67 on December 24, ...
... communis Kinglevirus lutadaptatum Kirikabuvirus NV3 Kirnavirus lutenecus Kirovvirus kirov Kirsten murine sarcoma virus ... virus A Potato virus H Potato virus M Potato virus P Potato virus S Potato virus T Potato virus V Potato virus X Potato virus Y ... sarcoma virus Garlic common latent virus Garlic dwarf virus Garlic mite-borne filamentous virus Garlic virus A Garlic virus B ... A Grapevine virus B Grapevine virus D Grapevine virus E Grapevine virus F Grapevine virus G Grapevine virus H Grapevine virus I ...
Kirsten WH, Schauf V, McCoy J (1970). "Properties of a murine sarcoma virus". Bibliotheca Haematologica. International ... the Harvey sarcoma virus and Kirsten sarcoma virus, by Edward M. Scolnick and colleagues at the National Institutes of Health ( ... "Human genome contains four genes homologous to transforming genes of Harvey and Kirsten murine sarcoma viruses". Proceedings of ... Ras, from "Rat sarcoma virus", is a family of related proteins that are expressed in all animal cell lineages and organs. All ...
Identification of a sarcoma virus-coded phosphoprotein in nonproducer cells transformed by Kirsten or Harvey murine sarcoma ... Human genome contains four genes homologous to transforming genes of Harvey and Kirsten murine sarcoma viruses ... Nucleotide Sequence of the Oncogene Encoding the p21 Transforming Protein of Kirsten Murine Sarcoma Virus ... The p21 src genes of Harvey and Kirsten sarcoma viruses originate from divergent members of a family of normal vertebrate genes ...
Kirsten Sarcoma Virus use Kirsten murine sarcoma virus. Kirsten murine sarcoma virus ...
Kirsten Sarcoma Virus use Kirsten murine sarcoma virus. Kirsten murine sarcoma virus ...
Kirsten Sarcoma Virus use Kirsten murine sarcoma virus. Kirsten murine sarcoma virus ...
Kirsten Sarcoma Virus use Kirsten murine sarcoma virus. Kirsten murine sarcoma virus ...
Kirsten Sarcoma Virus use Kirsten murine sarcoma virus. Kirsten murine sarcoma virus ...
Kirsten Sarcoma Virus use Kirsten murine sarcoma virus. Kirsten murine sarcoma virus ...
Isolation and characterization of kirsten murine sarcoma virus‐transformed mouse keratinocytes resistant to transforming growth ... Murine leukaemia C-type virus associated with functional murine carcinomas of endocrine origin. (1971). (12) ... Complexity and abundance of murine leukemia virus-related nuclear and messenger RNA sequences in mouse embryo cell lines which ... Equivalent expression of endogenous murine leukemia virus-related genes in C3H/10T1/2 cells and chemically transformed ...
Rat sequences of the Kirsten and Harvey murine sarcoma virus genomes: nature, origin, and expression in rat tumor RNA. J Virol ... with the definition of the oncogenic sequences of the Kirsten and Harvey strains of murine sarcoma virus[1]. The human homologs ... Nucleotide sequence of the oncogene encoding the p21 transforming protein of Kirsten murine sarcoma virus. Science 1982;217:937 ... HRAS and KRAS are homologs to the Harvey and Kirsten murine oncogenes, respectively, while NRAS was identified in a human ...
... by transformation using Kirsten murine sarcoma virus (Ki-MSV). The cells exhibit a high saturation density, a high plating ... This cell line was derived from the HOS cell line (TE-85) by transformation using Kirsten murine sarcoma virus (Ki-MSV). The ... The cells are useful producing MSV pseudotypes with various ecotropic and xenotropic murine leukemia viruses. Cells carry the ... Other downstream applications of Accutase treatment include analysis of cell surface markers, virus growth assay, cell ...
1984) INTEGRATION OF PROVIRAL DNA IN KIRSTEN MURINE SARCOMA VIRUS-INFECTED MOUSE FIBROBLASTS. JOURNAL OF GENERAL VIROLOGY, 65 ( ... 1984) EXPRESSION OF KIRSTEN MURINE SARCOMA-VIRUS IN TRANSFORMED NONPRODUCER AND REVERTANT NIH 3T3 CELLS - EVIDENCE FOR CELL- ... UNSPECIFIED (1984) ELEVATED EXPRESSION OF THE KRAS ONCOGENE IN KIRSTEN MURINE SARCOMA-VIRUS TRANSFORMED NON-PRODUCED AND ... 1984) GENESIS OF KIRSTEN MURINE SARCOMA-VIRUS - SEQUENCE-ANALYSIS REVEALS RECOMBINATION POINTS AND POTENTIAL LEUKEMOGENIC ...
KNRK, normal rat kidney cell line transformed by Kirsten murine sarcoma virus ...
ras oncogenes were first recognized as the transforming genes of Harvey and Kirsten murine sarcoma viruses (Ha-MSV, Ki-MSV). ... These highly oncogenic retroviruses were generated during passage of murine leukemia viruses through laboratory strains of rats ... 1980). Therefore, it was concluded that the p21 gene was the oncogene of Ha-MSV and Ki-MSV (and other closely related viruses) ... The proteins produced by Ha-MSV and Ki-MSV were identified using antibodies from rats bearing tumors induced by these viruses; ...
Kirsten murine sarcoma virus transformed fetal mouse cells) into embryonic chick heart fragments in vitro [34]. ...
... murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras ... Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, ... murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras ... Retrovirus-associated DNA sequences (src) originally isolated from the Rous sarcoma virus (RSV). The proto-oncogene src (c-src ...
... murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras ... Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, ... 3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.. 4. Lymphomas: These are ... 2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include ...
... murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras ... Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, ... The closely related N-ras gene has been detected in human neuroblastoma and sarcoma cell lines. All genes of the family have a ... genes have been detected in human, avian, murine, and non-vertebrate genomes. ...
... murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras ... Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, ... The closely related N-ras gene has been detected in human neuroblastoma and sarcoma cell lines. All genes of the family have a ... which is a truncated form of the chicken erbB gene found in the avian erythroblastosis virus. Overexpression and amplification ...
Chien, Y.; Lai, M.M. 1980: Virus RNA species in kirsten murine sarcoma virus-transformed mink cells. Journal of General ... Kuwata, T.; Okazaki, T.; Spahn, G.J. 1973: Virogenic properties of AKR mouse sarcoma cells induced by rous sarcoma virus. ... pseudorabies virus, reovirus, respiratory syncytial virus and Semliki Forest virus. Journal of General Virology 26(2): 183-196 ... Lemoine, J. 1979: Virus diseases of fruit trees: Effect of two virus diseases on the growth and branching in pear scion nursery ...
OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ...
OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ...
OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ...
OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ...
OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ...
OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... GASTROENTERITIS VIRUS, PORCINE TRANSMISSIBLE. TRANSMISSIBLE GASTROENTERITIS VIRUS. HARVEY SARCOMA VIRUS. HARVEY MURINE SARCOMA ... OVINE PULMONARY ADENOCARCINOMA VIRUS. KIRSTEN SARCOMA VIRUS. KIRSTEN MURINE SARCOMA VIRUS. LACTATE DEHYDROGENASE VIRUS. LACTATE ...
Kirsten rat sarcoma virus-like oncogene homolog and v-raf murine sarcoma virus-like oncogene homolog B2. The actual insight ... Structural Domains in the Hsv simplex virus Simplex Sort One gD Proteins which Minimize HIV-1 Compound Irritation.. * Post ... scientists need to evaluate the very first periods from the Human immunodeficiency virus check details remedy cascade buy ML ... Many cases regarding serious autochthonous hepatitic E virus (HEV) liver disease are already noted within England, mostly in ...
Devouge, M.W.; Mukherjee, B.B.; Pena, S.D. 1982: Kirsten murine sarcoma virus-coded p21ras may act on multiple targets to ... Kinetin inhibition of the multiplication of tobacco mosaic virus and potato virus x in locally infected leaves of the host ... Butenko, A.M.; Gromashevskii, V.L.; L'vov D.K.; Popov, V.F. 1979: Kisemayo virus a member of the bhanja antigenic group. ... Achilli, G.; Sarasini, A.; Revello, M.G.; Torsellini Gerna, M.; Gerna, G.; Iltis, J.P.; Madden, D.L. 1984: Kinetics of virus ...
In 1963, Jennifer Harvey was studying Moloney murine leukemia virus (MMLV) at the cancer research department of the London ... Harveys discovery led to the naming of the corresponding rat sarcoma oncogene as HRAS, while Kirstens related oncogene was ... Werner Kirsten at the University of Chicago observed similar results working with mouse erythroblastosis virus (MEV) (2). ... In addition to the expected leukemia, the mice that received the plasma developed solid tumors (soft-tissue sarcomas), ...
In 1963, Jennifer Harvey was studying Moloney murine leukemia virus (MMLV) at the cancer research department of the London ... Harveys discovery led to the naming of the corresponding rat sarcoma oncogene as HRAS, while Kirstens related oncogene was ... Werner Kirsten at the University of Chicago observed similar results working with mouse erythroblastosis virus (MEV) (2). ... In addition to the expected leukemia, the mice that received the plasma developed solid tumors (soft-tissue sarcomas), ...

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