Avian Sarcoma Viruses
Alpharetrovirus
Sarcoma, Avian
Sarcoma Viruses, Murine
Cell Transformation, Viral
Sarcoma
Chick Embryo
Avian leukosis virus
Oncogene Protein pp60(v-src)
Sarcoma Viruses, Feline
Quail
Sarcoma, Experimental
Kirsten murine sarcoma virus
Rous sarcoma virus
Defective Viruses
Cell Transformation, Neoplastic
Moloney murine sarcoma virus
Chickens
RNA-Directed DNA Polymerase
Base Sequence
Harvey murine sarcoma virus
Helper Viruses
Retroviridae Proteins
Retroviridae
Integrases
Oncogene Protein v-crk
Sarcoma, Ewing
Nucleic Acid Hybridization
Oncogenes
Virus Replication
Gammaretrovirus
Gene Products, gag
Sarcoma, Kaposi
Sarcoma, Synovial
Genes, src
Receptors, Virus
Avian Leukosis
Sarcoma Virus, Woolly Monkey
Fibroblasts
Protein Kinases
Coturnix
Cells, Cultured
Fusion Proteins, gag-onc
Culture Techniques
Molecular Sequence Data
Virus Integration
DNA Restriction Enzymes
Moloney murine leukemia virus
Ribonuclease T1
Mutation
Repetitive Sequences, Nucleic Acid
Recombination, Genetic
Cloning, Molecular
Amino Acid Sequence
Vaccinia virus
Temperature
Transcription, Genetic
DNA, Circular
Species Specificity
Virus Assembly
Genes
DNA, Recombinant
Simian virus 40
Tyrosine
Transfection
Cell-Free System
Virus Shedding
Phosphotyrosine
Virion
Genes, gag
Phosphorylation
Reticuloendotheliosis virus
DNA
Epsilonretrovirus
Soft Tissue Neoplasms
Nucleic Acid Conformation
Protein Biosynthesis
Sindbis Virus
Leukemia Virus, Feline
Measles virus
Influenza A Virus, H1N1 Subtype
Histiocytic Sarcoma
Binding Sites
Genetic Vectors
Poly A
RNA, Messenger
Rabies virus
Influenza A Virus, H5N1 Subtype
RNA, Transfer
Electrophoresis, Agar Gel
Peptide Fragments
Protein-Tyrosine Kinases
Sarcoma, Myeloid
Influenza A Virus, H3N2 Subtype
Hepatitis B virus
Sarcoma, Endometrial Stromal
West Nile virus
Gene Products, env
Sarcoma, Clear Cell
Parainfluenza Virus 1, Human
Respiratory Syncytial Viruses
Glycoproteins
Vesicular stomatitis Indiana virus
Tumor Virus Infections
Virus Activation
Viral Fusion Proteins
Gene Expression Regulation, Viral
Viral Plaque Assay
Cell Fusion
Virus Latency
RNA Splicing
Cercopithecus aethiops
Hemagglutinin Glycoproteins, Influenza Virus
Clone Cells
Viral Envelope Proteins
Electrophoresis, Polyacrylamide Gel
Neutralization Tests
Leukemia Virus, Murine
Plasmids
Vero Cells
Membrane Fusion
Simian immunodeficiency virus
Retroviridae Proteins, Oncogenic
Cytopathogenic Effect, Viral
Inhibition of the rous sarcoma virus long terminal repeat-driven transcription by in vitro methylation: different sensitivity in permissive chicken cells versus mammalian cells. (1/1585)
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)HMG protein family members stimulate human immunodeficiency virus type 1 and avian sarcoma virus concerted DNA integration in vitro. (2/1585)
We have reconstituted concerted human immunodeficiency virus type 1 (HIV-1) integration in vitro with specially designed mini-donor HIV-1 DNA, a supercoiled plasmid acceptor, purified bacterium-derived HIV-1 integrase (IN), and host HMG protein family members. This system is comparable to one previously described for avian sarcoma virus (ASV) (A. Aiyar et al., J. Virol. 70:3571-3580, 1996) that was stimulated by the presence of HMG-1. Sequence analyses of individual HIV-1 integrants showed loss of 2 bp from the ends of the donor DNA and almost exclusive 5-bp duplications of the acceptor DNA at the site of integration. All of the integrants sequenced were inserted into different sites in the acceptor. These are the features associated with integration of viral DNA in vivo. We have used the ASV and HIV-1 reconstituted systems to compare the mechanism of concerted DNA integration and examine the role of different HMG proteins in the reaction. Of the three HMG proteins examined, HMG-1, HMG-2, and HMG-I(Y), the products formed in the presence of HMG-I(Y) for both systems most closely match those observed in vivo. Further analysis of HMG-I(Y) mutants demonstrates that the stimulation of integration requires an HMG-I(Y) domain involved in DNA binding. While complexes containing HMG-I(Y), ASV IN, and donor DNA can be detected in gel shift experiments, coprecipitation experiments failed to demonstrate stable interactions between HMG-I(Y) and ASV IN or between HMG-I(Y) and HIV-1 IN. (+info)Protective effects of type I and type II interferons toward Rous sarcoma virus-induced tumors in chickens. (3/1585)
Growth of tumors induced by Rous sarcoma virus (RSV) is controlled by alleles at the major histocompatibility complex locus in chickens, indicating that immunological host defense mechanisms play a major role. We show here that the resistance phenotype of CB regressor chickens can be partially reverted by treating the animals with a monoclonal antibody that neutralizes the major serotype of chicken type I interferon, ChIFN-alpha. Injection of recombinant ChIFN-alpha into susceptible CC progressor chickens resulted in a dose-dependent inhibition of RSV-induced tumor development. This treatment was not effective, however, in CC chickens challenged with a DNA construct expressing the v-src oncogene, suggesting that the beneficial effect of type I interferon in this system resulted from its intrinsic antiviral activity and probably not from indirect immunmodulatory effects. By contrast, recombinant chicken interferon-gamma strongly inhibited tumor growth when given to CC chickens that were challenged with the v-src oncogene, indicating that the two cytokines target different steps of tumor development. (+info)The role of overlapping U1 and U11 5' splice site sequences in a negative regulator of splicing. (4/1585)
Splicing of Rous sarcoma virus RNA is regulated in part by a cis-acting intronic RNA element called the negative regulator of splicing (NRS). An NRS mutant affecting nt 916-923 disrupts U11 snRNP binding and reduces NRS activity (Gontarek et al., 1993, Genes & Dev 7:1926-1936). However, we observed that a U15' splice site-like sequence, which overlapped the U11 site, was also disrupted by this mutation. To determine whether the U1 or the U11 site was essential for NRS activity, we analyzed twelve additional mutants involving nt 915-926. All mutations that disrupted the potential base pairing between U1 snRNA and the NRS reduced NRS activity, including single point mutations at nt 915, 916, and 919. The point mutation at nt 919 was partially suppressed by a compensatory base change mutation in U1 snRNA. In contrast, a mutation which strengthened the potential base pairing between the U1 site and the NRS increased NRS activity. Surprisingly, mutations that specifically targeted the U115' splice site consensus sequence increased the levels of unspliced RNA, suggesting U11 binding plays an antagonistic role to NRS activity. We propose that U1 snRNP binding to the NRS inhibits splicing and is regulated by U11 snRNP binding to the overlapping sequence. Competition between U1 and U11 snRNPs would result in the appropriate balance of spliced to unspliced RNAs for optimal viral replication. Further, a virus mutated in the U1/U11 region of the NRS was found to have delayed replication. (+info)Transgenic mice ubiquitously expressing human placental alkaline phosphatase (PLAP): an additional reporter gene for use in tandem with beta-galactosidase (lacZ). (5/1585)
A fundamental keystone of developmental biology has been the growing use of reporter genes in model transgenic systems. Their use has greatly facilitated investigations of cell lineage and cell fate in addition to aiding experiments aimed at determining patterns of gene expression, gene interaction and gene regulation. Through construction of transgenic mice, ubiquitously expressing human placental alkaline phosphatase (PLAP), we demonstrate the suitability of PLAP as a reporter gene for use in conjunction with, or as an alternative to, beta-galactosidase (lacZ). Our findings demonstrate that over-expression of PLAP has no adverse effects on mouse development or viability, despite a widespread pattern of expression. This technology provides a simple yet effective mechanism based on eukaryotic reporter gene technology to facilitate the identification of transgenic cells within complex in vivo systems. (+info)A mutant form of the rho protein can restore stress fibers and adhesion plaques in v-src transformed fibroblasts. (6/1585)
The organization of polymerized actin in the mammalian cell is regulated by several members of the rho family. Three rho proteins, cdc42, rac and rho act in a cascade to organize the intracellular actin cytoskeleton. Rho proteins are involved in the formation of actin stress fibers and adhesion plaques in fibroblasts. During transformation of mammalian cells by oncogenes the cytoskeleton is rearranged and stress fibers and adhesion plaques are disintegrated. In this paper we investigate the function of the rho protein in RR1022 rat fibroblasts transformed by the Rous sarcoma virus. Two activated mutants of the rho protein, rho G14V and rho Q63L, and a dominant negative mutant, rho N1171, were stably transfected into RR1022 cells. The resulting cell lines were analysed for the organization of polymerized actin and adhesion plaques. Cells expressing rho Q63L, but not rho wt, rho G14V or rho N1171, showed an altered morphology. These cells displayed a flat, fibroblast like shape when compared with the RR1022 ancestor cells. Immunofluorescence analyses revealed that actin stress fibers and adhesion plaques were rearranged in these cells. We conclude from these data that an active rho protein can restore elements of the actin cytoskeleton in transformed cells by overriding the tyrosine kinase phosphorylation induced by the pp60(v-src). (+info)Molecular dynamics studies on the HIV-1 integrase catalytic domain. (7/1585)
The HIV-1 integrase, which is essential for viral replication, catalyzes the insertion of viral DNA into the host chromosome, thereby recruiting host cell machinery into making viral proteins. It represents the third main HIV enzyme target for inhibitor design, the first two being the reverse transcriptase and the protease. Two 1-ns molecular dynamics simulations have been carried out on completely hydrated models of the HIV-1 integrase catalytic domain, one with no metal ions and another with one magnesium ion in the catalytic site. The simulations predict that the region of the active site that is missing in the published crystal structures has (at the time of this work) more secondary structure than previously thought. The flexibility of this region has been discussed with respect to the mechanistic function of the enzyme. The results of these simulations will be used as part of inhibitor design projects directed against the catalytic domain of the enzyme. (+info)Biodegradable alginate microspheres as a delivery system for naked DNA. (8/1585)
Sodium alginate is a naturally occurring polysaccharide that can easily be polymerized into a solid matrix to form microspheres. These biodegradable microspheres were used to encapsulate plasmid DNA containing the bacterial beta-galactosidase (LacZ) gene under the control of either the cytomegalovirus (CMV) immediate-early promoter or the Rous sarcoma virus (RSV) early promoter. Mice inoculated orally with microspheres containing plasmid DNA expressed LacZ in the intestine, spleen and liver. Inoculation of mice with microspheres containing both the plasmid DNA and bovine adenovirus type 3 (BAd3) resulted in a significant increase in LacZ expression compared to those inoculated with microspheres containing only the plasmid DNA. Our results suggest that adenoviruses are capable of augumenting transgene expression by plasmid DNA both in vitro and in vivo. (+info)Incidence- Avian sarcoma is a relatively rare disease, although it is one of the most common types of cancer to affect psittacines (parrots and other similar birds). It primarily affects macaws, cockatoos, African greys, and amazons.
Causes - Avian sarcoma is caused by a virus called polyomavirus, which is thought to be transmitted through the droppings of infected birds. This virus was first identified in the 1970s and has since been found to cause this disease in many species of parrots.
Symptoms - The symptoms of avian sarcoma can vary depending on the location of the tumor, but they may include swelling or lumps near the site of the tumor, difficulty eating, weight loss, and lethargy. As the disease progresses, it can spread to other parts of the body and cause further symptoms such as difficulty walking or standing, and difficulty breathing.
Diagnosis - The diagnosis of avian sarcoma is typically made through a combination of physical examination, radiographs (x-rays), and biopsy.
Treatment - There are several treatment options for avian sarcoma including surgery, chemotherapy, and radiation therapy. The most effective treatment will depend on the size, location, and stage of the tumor. Surgery may be possible to remove the tumor, but in some cases, the tumor may have spread too far for this to be an option. Chemotherapy can be used to shrink the tumor before surgery or to treat the disease if surgery is not possible. Radiation therapy may also be used to treat the disease.
Prognosis - The prognosis for avian sarcoma is generally poor, as the disease tends to progress quickly and spread to other parts of the body. However, with early diagnosis and appropriate treatment, some birds can survive for several years or even be cured. It's important to note that the prognosis will depend on the size, location, and stage of the tumor at the time of diagnosis.
Prevention - There is no known prevention for avian sarcoma, but regular veterinary check-ups can help with early detection and treatment. It's also important to keep your bird in a safe environment, free from hazards such as toxins and infectious diseases, which can increase the risk of developing cancer.
It is important to note that avian sarcoma is a rare disease and not all birds will develop it. If you suspect your bird has avian sarcoma, it's important to seek veterinary care as soon as possible for proper diagnosis and treatment.
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.
Sarcomas can arise in any part of the body, but they are most common in the arms and legs. They can also occur in the abdomen, chest, or head and neck. There are many different types of sarcoma, each with its own unique characteristics and treatment options.
The causes of sarcoma are not fully understood, but genetic mutations, exposure to radiation, and certain chemicals have been linked to an increased risk of developing the disease. Sarcomas can be challenging to diagnose and treat, as they often grow slowly and may not cause symptoms until they are advanced.
Treatment for sarcoma typically involves a combination of surgery, radiation therapy, and chemotherapy. The specific treatment plan will depend on the type of sarcoma, its location, and the stage of the disease. In some cases, amputation may be necessary to remove the tumor.
Prognosis for sarcoma varies depending on the type of cancer, the size and location of the tumor, and the stage of the disease. In general, the prognosis is best for patients with early-stage sarcoma that is confined to a small area and has not spread to other parts of the body.
Overall, sarcoma is a rare and complex form of cancer that requires specialized treatment and care. While the prognosis can vary depending on the specific type of cancer and the stage of the disease, advances in medical technology and treatment options have improved outcomes for many patients with sarcoma.
Example sentence: The patient was diagnosed with experimental sarcoma and underwent a novel chemotherapy regimen that included a targeted therapy drug.
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
Ewing's sarcoma is a rare and aggressive type of cancer that affects the bones and soft tissues of the body. It primarily occurs in the pelvis, spine, and limbs. This malignancy usually develops in children and young adults between the ages of 10 and 30.
Ewing's sarcoma is caused by a genetic mutation in the EWS gene, which is responsible for regulating cell growth and division. The mutated gene leads to uncontrollable cell proliferation, resulting in the formation of a tumor.
The symptoms of Ewing's sarcoma vary depending on the location of the tumor but can include pain, swelling, limited mobility, and broken bones. Diagnosis is usually made through a combination of imaging tests such as X-rays, CT scans, and PET scans, along with a biopsy to confirm the presence of cancer cells.
Treatment for Ewing's sarcoma typically involves a combination of surgery, chemotherapy, and radiation therapy. Surgery is used to remove the tumor and any affected tissue, while chemotherapy and radiation therapy are used to kill any remaining cancer cells. The prognosis for Ewing's sarcoma varies depending on the stage and location of the cancer but can be improved with early diagnosis and appropriate treatment.
A rare and aggressive type of cancer that affects the connective tissue cells of the body, including blood vessels, lymph nodes, and soft tissue. It is caused by the human herpesvirus 8 (HHV-8) and is more common in people with weakened immune systems, such as those with HIV/AIDS.
Symptoms:
* Painless lumps or lesions on the skin or mouth
* Fatigue
* Weight loss
* Night sweats
Diagnosis:
* Biopsy of affected tissue
* Imaging tests, such as CT scans or MRI
Treatment:
* Chemotherapy to shrink the tumors
* Radiation therapy to kill cancer cells
* Surgery to remove the affected tissue
Prognosis:
* Poor, especially in people with HIV/AIDS
Etymology:
* Named after the Hungarian-born Jewish doctor, Georg Kaposi, who first described the condition in 1872.
There are several types of avian leukosis, including:
* B-cell leukemia/lymphoma: This type of cancer affects the B cells, a type of white blood cell that produces antibodies to fight infection.
* T-cell leukemia/lymphoma: This type of cancer affects the T cells, a type of white blood cell that helps coordinate the immune response.
* Myeloid leukemia/lymphoma: This type of cancer affects the myeloid cells, a type of white blood cell that produces antibodies to fight infection.
* Hair follicle leukosis: This type of cancer affects the hair follicles and can cause excessive feather growth or loss.
The symptoms of avian leukosis can vary depending on the type of cancer and the severity of the disease. Some common symptoms include:
* Swollen lymph nodes
* Weight loss
* Lethargy
* Loss of appetite
* Swelling of the abdomen or limbs
* Excessive feather growth or loss
* Pale or enlarged liver and spleen
Avian leukosis is diagnosed through a combination of physical examination, blood tests, and biopsies. Treatment options are limited, and the disease is often fatal. However, some birds may be able to manage the symptoms with supportive care, such as antibiotics, anti-inflammatory medications, and nutritional support.
Prevention is key in managing avian leukosis. Vaccination against ALV is available for certain types of birds, and good husbandry practices, such as providing clean water, a balanced diet, and proper housing, can help reduce the risk of transmission. Additionally, separating infected birds from healthy ones can help prevent the spread of the disease.
It's important to note that avian leukosis is not transmissible to humans or other animals, and it is not a reportable disease in most jurisdictions. However, if you suspect that your bird has avian leukosis, it is important to seek veterinary care as soon as possible to determine the best course of treatment and provide appropriate supportive care.
The term "Sarcoma 180" was coined by a German surgeon named Otto Kunkel in the early 20th century. He described this type of cancer as a highly malignant tumor that grows slowly but is resistant to treatment with surgery, radiation therapy, and chemotherapy.
The exact cause of Sarcoma 180 is not known, but it is believed to be linked to genetic mutations and exposure to certain chemicals or radiation. The disease typically affects middle-aged adults and is more common in men than women.
The symptoms of Sarcoma 180 can vary depending on the location of the tumor, but they may include pain, swelling, redness, and limited mobility in the affected area. If left untreated, the cancer can spread to other parts of the body and be fatal.
Treatment for Sarcoma 180 usually involves a combination of surgery, radiation therapy, and chemotherapy. In some cases, amputation of the affected limb may be necessary. The prognosis for this disease is generally poor, with a five-year survival rate of less than 50%.
In summary, Sarcoma 180 is a rare and aggressive form of cancer that affects connective tissue and has a poor prognosis. It is important for medical professionals to be aware of this condition and its symptoms in order to provide proper diagnosis and treatment.
1. Common cold: A viral infection that affects the upper respiratory tract and causes symptoms such as sneezing, running nose, coughing, and mild fever.
2. Influenza (flu): A viral infection that can cause severe respiratory illness, including pneumonia, bronchitis, and sinus and ear infections.
3. Measles: A highly contagious viral infection that causes fever, rashes, coughing, and redness of the eyes.
4. Rubella (German measles): A mild viral infection that can cause fever, rashes, headache, and swollen lymph nodes.
5. Chickenpox: A highly contagious viral infection that causes fever, itching, and a characteristic rash of small blisters on the skin.
6. Herpes simplex virus (HSV): A viral infection that can cause genital herpes, cold sores, or other skin lesions.
7. Human immunodeficiency virus (HIV): A viral infection that attacks the immune system and can lead to acquired immunodeficiency syndrome (AIDS).
8. Hepatitis B: A viral infection that affects the liver, causing inflammation and damage to liver cells.
9. Hepatitis C: Another viral infection that affects the liver, often leading to chronic liver disease and liver cancer.
10. Ebola: A deadly viral infection that causes fever, vomiting, diarrhea, and internal bleeding.
11. SARS (severe acute respiratory syndrome): A viral infection that can cause severe respiratory illness, including pneumonia and respiratory failure.
12. West Nile virus: A viral infection that can cause fever, headache, and muscle pain, as well as more severe symptoms such as meningitis or encephalitis.
Viral infections can be spread through contact with an infected person or contaminated surfaces, objects, or insects such as mosquitoes. Prevention strategies include:
1. Practicing good hygiene, such as washing hands frequently and thoroughly.
2. Avoiding close contact with people who are sick.
3. Covering the mouth and nose when coughing or sneezing.
4. Avoiding sharing personal items such as towels or utensils.
5. Using condoms or other barrier methods during sexual activity.
6. Getting vaccinated against certain viral infections, such as HPV and hepatitis B.
7. Using insect repellents to prevent mosquito bites.
8. Screening blood products and organs for certain viruses before transfusion or transplantation.
Treatment for viral infections depends on the specific virus and the severity of the illness. Antiviral medications may be used to reduce the replication of the virus and alleviate symptoms. In severe cases, hospitalization may be necessary to provide supportive care such as intravenous fluids, oxygen therapy, or mechanical ventilation.
Prevention is key in avoiding viral infections, so taking the necessary precautions and practicing good hygiene can go a long way in protecting oneself and others from these common and potentially debilitating illnesses.
Examples of soft tissue neoplasms include:
1. Lipoma: a benign tumor composed of fat cells.
2. Fibroma: a benign tumor composed of fibrous tissue.
3. Leiomyoma: a benign tumor composed of smooth muscle tissue.
4. Synovial sarcoma: a malignant tumor that arises in the soft tissues surrounding joints.
5. Rhabdomyosarcoma: a malignant tumor that arises in the skeletal muscles.
6. Neurofibroma: a benign tumor that arises in the nerve tissue.
Soft tissue neoplasms can occur in various parts of the body, including the extremities (arms and legs), trunk, and head and neck. They can be diagnosed through a combination of imaging studies such as X-rays, CT scans, MRI scans, and biopsy.
Treatment for soft tissue neoplasms depends on the type, size, location, and aggressiveness of the tumor, as well as the patient's overall health. Benign tumors may not require treatment, while malignant tumors may be treated with surgery, radiation therapy, or chemotherapy.
Symptoms of histiocytic sarcoma may include swelling or lumps in the neck, underarm, or groin area, as well as fatigue, fever, and weight loss. The diagnosis is usually made through a combination of physical examination, imaging tests (such as CT scans or MRI), and biopsy. Treatment typically involves a combination of surgery, chemotherapy, and radiation therapy, and may vary depending on the location and extent of the cancer.
Histiocytic sarcoma is rare, accounting for only about 1-2% of all childhood cancers. While it is generally considered to be a more aggressive form of cancer, the prognosis has improved significantly in recent years with advances in treatment and surgical techniques. With appropriate treatment, many children with histiocytic sarcoma can achieve long-term survival and a good quality of life.
Symptoms of myeloid sarcoma may include:
* Painless lumps or swelling in the skin, often on the arms, legs, or trunk
* Fever
* Fatigue
* Night sweats
* Weight loss
* Bone pain
Myeloid sarcoma is diagnosed through a combination of physical examination, imaging tests such as CT scans and PET scans, and blood tests. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and relieve symptoms. In some cases, bone marrow transplantation may be recommended.
Myeloid sarcoma is a type of cancer that arises from immature myeloid cells in the bone marrow. It is a rare and aggressive form of cancer that can occur at any age but is more common in adults. Symptoms include painless lumps or swelling in the skin, fever, fatigue, night sweats, weight loss, and bone pain. Diagnosis is made through a combination of physical examination, imaging tests such as CT scans and PET scans, and blood tests. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and relieve symptoms, with bone marrow transplantation sometimes being recommended.
There are several subtypes of myeloid sarcoma, including:
* Acute myeloid leukemia (AML) with myeloid sarcomatous differentiation
* Chronic myeloid leukemia (CML) with myeloid sarcomatous differentiation
* Myelodysplastic syndrome (MDS) with myeloid sarcomatous differentiation
Myeloid sarcoma is often associated with genetic mutations, such as the FLT3 and NPM1 genes. These mutations can lead to uncontrolled cell growth and the development of cancer. Treatment for myeloid sarcoma can be challenging, as it can be difficult to distinguish from other types of cancer and may require a combination of chemotherapy, radiation therapy, and bone marrow transplantation.
Prognosis for myeloid sarcoma varies depending on the subtype, but in general, the prognosis is poor. The 5-year survival rate for all subtypes of myeloid sarcoma is less than 30%, and the disease can be difficult to treat. However, with early diagnosis and appropriate treatment, some patients with myeloid sarcoma can achieve long-term survival.
Overall, myeloid sarcoma is a rare and aggressive form of cancer that requires prompt and accurate diagnosis and treatment. Further research is needed to improve our understanding of this disease and to develop more effective treatment strategies.
The symptoms of sarcoma, endometrial stromal can include abnormal vaginal bleeding, pelvic pain, and a mass in the pelvis. The tumor can be small or large, and it may or may not have spread to other parts of the body (metastasized) at the time of diagnosis.
The exact cause of sarcoma, endometrial stromal is not known, but there are several risk factors that have been associated with an increased risk of developing this type of cancer. These include:
* Previous radiation therapy to the pelvis
* Family history of uterine cancer
* Early onset of menstruation (before age 12) or late menopause (after age 55)
* Never being pregnant or having few or no full-term pregnancies
* Obesity
* Use of tamoxifen, a medication used to treat certain types of breast cancer
To diagnose sarcoma, endometrial stromal, a doctor may perform a physical exam, take a medical history, and use one or more of the following tests:
* Pelvic exam: The doctor will insert a speculum into the vagina to examine the cervix and uterus for any abnormalities.
* Imaging tests: Such as ultrasound, CT scan, or MRI to look for any tumors in the pelvis.
* Biopsy: A sample of tissue is taken from the suspected tumor and examined under a microscope for cancer cells.
* Endometrial biopsy: A sample of tissue is taken from the lining of the uterus to check for any abnormalities.
Treatment for sarcoma, endometrial stromal usually involves a combination of surgery and hormone therapy. The specific treatment plan will depend on the stage and location of the cancer, as well as the patient's overall health. Some common treatments include:
* Surgery: To remove the tumor and any affected tissues.
* Hysterectomy: Removal of the uterus is often necessary to treat sarcoma, endometrial stromal.
* Radiation therapy: Use of high-energy beams to kill cancer cells.
* Chemotherapy: Use of drugs to kill cancer cells.
It's important for women to talk to their doctor about their risk factors and any symptoms they may be experiencing, so that they can be monitored closely and receive appropriate treatment if necessary.
Also known as: Clear cell sarcoma, clear cell sarcoma of soft tissue.
Epidemiology: Clear cell sarcoma is a rare cancer, accounting for less than 1% of all adult soft tissue sarcomas. It can occur at any age but is most common in the second to third decade of life. The incidence is approximately 1-2 cases per 1 million people per year.
Clinical features: Clear cell sarcoma typically presents as a painless mass or lump in the soft tissues of the extremities, trunk, or retroperitoneum. It can also occur in the gastrointestinal tract or other organs. The tumor is often firm and well-circumscribed, with a variable size range.
Imaging features: On imaging studies, clear cell sarcoma typically appears as a heterogeneous mass with areas of both bright and isointense signal on T1-weighted MRI sequences, and areas of hyperintensity on T2-weighted MRI sequences. There may be associated calcifications or ossification within the tumor.
Histopathology: The hallmark of clear cell sarcoma is the presence of clear cells, which are cells that have a clear or pale appearance due to the absence of pigment. These cells are often arranged in a pattern of "spindle-shaped" or "stellate" nuclei. Other features include atypical mitoses, increased mitotic activity, and necrosis.
Treatment: The treatment of clear cell sarcoma is generally surgical resection, with or without radiation therapy and/or chemotherapy. The prognosis is generally poor, with a five-year survival rate of approximately 50%.
Differential diagnosis: Clear cell sarcoma must be differentiated from other soft tissue sarcomas, such as liposarcoma, leiomyosarcoma, and synovial sarcoma, as well as from other benign tumors that can occur in the soft tissues, such as lipomas and hemangiomas.
Genetics: Clear cell sarcoma is associated with genetic mutations in the TP53 gene, which is a tumor suppressor gene that regulates cell growth and division. Other genes that may be mutated in clear cell sarcoma include the HEXA, MYC, and PTEN genes.
In summary, clear cell sarcoma is a rare and aggressive soft tissue sarcoma that affects adults and children, typically presenting as a painless mass in the soft tissues of the extremities or trunk. The imaging features are nonspecific, but the presence of clear cells on histopathology is diagnostic. Treatment is generally surgical resection, with or without radiation therapy and/or chemotherapy, and the prognosis is poor. Clear cell sarcoma must be differentiated from other soft tissue sarcomas and benign tumors that can occur in the soft tissues.
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.
The symptoms of Sarcoma, Yoshida can vary depending on the location of the tumor, but may include pain, swelling, and limited mobility in the affected limb. The diagnosis of this condition is based on a combination of imaging studies such as CT or MRI scans, and a biopsy to confirm the presence of cancer cells.
Treatment for Sarcoma, Yoshida usually involves a combination of surgery, chemotherapy, and radiation therapy. The prognosis for this condition is generally poor, with a five-year survival rate of around 30%. However, early detection and aggressive treatment can improve outcomes.
Avian sarcoma leukosis virus
Transcription factor Jun
Rous sarcoma virus
Peter K. Vogt
Long terminal repeat
CRKL
ROS1
Kimberly W. Anderson
Proto-oncogene tyrosine-protein kinase Src
Alpharetrovirus
Adapter molecule crk
Daisy Roulland-Dussoix
Joan Brugge
Anna Marie Skalka
Oncogene
Lck
Chicken as biological research model
Harold E. Varmus
J. Michael Bishop
V-Src
Retrovirus direct repeat 1 (dr1)
Francis Peyton Rous
Raymond L. Erikson
Evžen Korec
Env (gene)
Harry Rubin (virologist)
AP-1 transcription factor
Leucosis
Endogenous retrovirus
Margaret Oakley Dayhoff
List of feline diseases
Murine respirovirus
Duplodnaviria
List of MeSH codes (C04)
Peter Duesberg
List of MeSH codes (B04)
Retroviral matrix protein
Leslie Parent
Zidovudine
Herpes simplex virus
2015 in Taiwan
Biology
List of MeSH codes (C22)
Format: Text / Subject: Hepatitis B virus - Harold Varmus - Profiles in Science Search Results
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Avian Leukosis Virus Subgroup J in Layer Chickens, China - Volume 16, Number 10-October 2010 - Emerging Infectious Diseases...
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Association of p60<sup>c-src</sup> with polyoma virus middle-T antigen abrogating mitosis-specific...
Molecular and immunohistochemical analysis of signaling adaptor protein Crk in human cancers<...
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Isotype: MIgG2c, MIgM, Recommended Applications: ELISA
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MeSH Browser
Leukosis2
- In recent years, cases of avian leukosis virus subgroup J (ALV-J) infection and tumors in commercial layer chickens and breeders of egg-type chickens have been emerging in the People's Republic of China. (cdc.gov)
- Roxadustat The avian sarcoma and leukosis pathogen (ASLV) is a superb model for research of viral entrance, as its envelope glycoprotein (Env) needs two consecutive sets off, binding to cognate receptors and acidic pH, to mediate membrane fusion (27,C29). (bioerc-iend.org)
Oncogene product2
- Middle-T associates with and thereby activates p60 c-src , a cellular tyrosine kinase homologous to the oncogene product of Rous sarcoma virus 2,3 . (elsevierpure.com)
- ROS1 was first discovered as the oncogene product of an avian sarcoma RNA tumor virus [77]. (ebrary.net)
CT101
- Because Crk was originally isolated as an avian sarcoma virus CT10 encoding oncoprotein v-Crk, we examined a potential role for c-Crk in the carcinogenesis of human cancers. (elsevier.com)
Influenza viruses2
RECEPTORS1
- Enveloped viruses infect host cells by fusing their membranes with those of the host cell, an activity mediated by viral glycoproteins upon binding to cognate host receptors or getting into acidic intracellular compartments. (bioerc-iend.org)
Retroviruses1
- These include the retroviruses avian leucosis/sarcoma viruses (ALSV) and reticuloendothesiosis viruses (REV), and the herpesvirus Marek's disease virus (MDV). (cdc.gov)
Viral6
- showed that influenza virus (IAV) hemagglutinin (HA) triggers intracellular [Ca 2+ ] oscillations that are required for viral infection [ 16 ] . (encyclopedia.pub)
- In the production of viral vaccines on a commercial scale, the virus of concern must be reproduced in large quantities. (currenthealthscenario.com)
- Viruses cannot survive or reproduce without being introduced into cells that nourish them, which enables the viral reproductive activity. (currenthealthscenario.com)
- One of the most prominent is a pestivirus called bovine viral diarrhea virus (2). (currenthealthscenario.com)
- agents most frequently detected in CCL's [continuous cell lines] have been bovine viral diarrhea virus and mycoplasma. (currenthealthscenario.com)
- To day, however, just a few research have directly analyzed the link between your pH in virus-carrying endosomes as well as the performance/kinetics of following viral fusion (12,C15). (bioerc-iend.org)
Infection1
- Can this virus cause infection or disease in humans? (currenthealthscenario.com)
Oncogenes1
- Many species contain oncogenes and cause leukemias and sarcomas. (nih.gov)
Tumor Virus Infections1
- Tumor virus infections. (lookformedical.com)
Sequences2
Oncogenic viruses3
- Cancer risk in workers exposed to oncogenic viruses. (cdc.gov)
- Infections produced by oncogenic viruses . (lookformedical.com)
- The infections caused by DNA viruses are less numerous but more diverse than those caused by the RNA oncogenic viruses . (lookformedical.com)
Poultry2
- It has been shown that poultry workers and subjects in the general population are also commonly infected with these viruses. (cdc.gov)
- Human exposure to these viruses occur occupationally (workers in poultry slaughtering/processing plants and poultry farm s, egg candlers, veterinarians, cooks, laboratory workers, etc. (cdc.gov)
H5N11
- This has been driven by fears arising from the rapid emergence, spread and public health impact of several recent outbreaks, such as the international spread of severe acute respiratory syndrome coronavirus (SARS-CoV) (2003), the potential of avian influenza H5N1 to emerge as a highly lethal pandemic as increasing numbers of human cases are reported (2003 and continuing), and the very rapid global spread of pandemic H1N1 influenza in 2009-2010. (who.int)
ALPHARETROVIRUS2
- Grupo de ALPHARETROVIRUS que producen sarcomas y otros tumores en pollos y otras aves de corral, así como en palomas, patos y RATAS. (bvsalud.org)
- Group of alpharetroviruses (ALPHARETROVIRUS) producing sarcomata and other tumors in chickens and other fowl and also in pigeons, ducks, and RATS. (bvsalud.org)
Subtype1
- A subtype of INFLUENZA A VIRUS with the surface proteins hemagglutinin 1 and neuraminidase 1. (lookformedical.com)
Chickens1
- Certain viruses naturally infect and cause cancer in chickens and turkeys. (cdc.gov)
Parasitic2
- Viruses parasitic on plants higher than bacteria. (lookformedical.com)
- In that sense all viruses can be considered parasitic on other cells. (currenthealthscenario.com)
Species3
- The type species of ORTHOPOXVIRUS, related to COWPOX VIRUS , but whose true origin is unknown. (lookformedical.com)
- Proteins found in any species of virus. (lookformedical.com)
- There is now heightened concern that this virus and others can cross species lines, creating new strains as they adapt to their new hosts, and this would include passage of the virus to and from humans. (currenthealthscenario.com)
Strain1
- Whether the human strain of BVDV causes overt illness is uncertain, because physicians may be uninformed and not even be looking for this virus. (currenthealthscenario.com)
Genome4
- Two critical pieces of evidence are needed to incriminate these viruses as causing cancer in humans: 1) laboratory demonstration of ALSV integrated within the human genome, and 2) epidemiologic evidence of excess cancer occurrence in human exposed to these viruses. (cdc.gov)
- Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. (lookformedical.com)
- Comparative genomic analysis reveals an 'open' pan-genome of African swine fever virus. (cdc.gov)
- Whole genome sequencing and genetic variations in several dengue virus type 1 strains from unusual dengue epidemic of 2017 in Vietnam. (cdc.gov)
19991
- Examples of the former include Sin Nombre virus, which first came to light in 1993 as the cause of Hantavirus pulmonary syndrome in the Four Corners area of the United States of America, and Nipah virus, which was first isolated in 1999 as a cause of acute neurological disease in peninsular Malaysia. (who.int)
Bovine3
- This product can carry many types of bovine blood-borne viruses, and is one of the primary sources of vaccine contaminants. (currenthealthscenario.com)
- The viruses and other agents that can contaminate bovine calf serum are numerous. (currenthealthscenario.com)
- and finally, �In conclusion, most commercially available bovine sera are contaminated with BVDV and, although there is no evidence that the virus is infectious, bovine sera should be screened for this virus�for the development or production of vaccine. (currenthealthscenario.com)
Bacteria1
- This summary, while making no claim of being a complete review of the subject, will point out sufficient examples and illustrations of contamination with bacteria, viruses, and their components, so as to enable the reader to make a more informed decision regarding accepting a vaccination (or forcing others to receive one). (currenthealthscenario.com)
Humans1
- However, in spite of the scientific evidence accumulated thus far, definitive proof that can confirm beyond any doubt that these viruses cause cancer in humans is currently lacking. (cdc.gov)
Commonly1
- Living cell types commonly used to reproduce viruses in the lab include monkey kidney cells, chicken embryos, as well as other animal and human cells. (currenthealthscenario.com)
Infectious1
- Virus shedding is an important means of vertical transmission (INFECTIOUS DISEASE TRANSMISSION, VERTICAL). (lookformedical.com)
Genetic4
- Viruses whose genetic material is RNA. (lookformedical.com)
- Ribonucleic acid that makes up the genetic material of viruses. (lookformedical.com)
- Others, called SATELLITE VIRUSES , are able to replicate only when their genetic defect is complemented by a helper virus. (lookformedical.com)
- Genetic characterization of influenza A(H3N2) viruses circulating in coastal Kenya, 2009-2017. (cdc.gov)
Diseases3
- Virus diseases caused by the RETROVIRIDAE . (lookformedical.com)
- A general term for diseases produced by viruses. (lookformedical.com)
- Virus diseases caused by the ORTHOMYXOVIRIDAE . (lookformedical.com)
Molecular1
- 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. (lookformedical.com)
BREAST1
- Treatments that deliver drugs to the neighborhood of cancer cells in nanoscale capsules have recently become available for breast and ovarian cancers and for Kaposi's sarcoma. (siliconinvestor.com)
Entry1
- Ebola virus (EBOV) also requires Ca 2+ channels for its entry into host cells. (encyclopedia.pub)
Recent1
- More recent evidence highlights how viruses can regulate and/or depend on the ion channels expressed by host cells, highlighting them as new host targets for therapeutic intervention (reviewed by Hover et al. (encyclopedia.pub)
Cell2
- Collectively, these outcomes highlight the part of cell-extrinsic and cell-intrinsic elements in regulating Roxadustat the effectiveness and kinetics of computer virus access and fusion with focus on cells. (bioerc-iend.org)
- It really is therefore most likely that cell type-dependent rules of endosomal pH modulates the effectiveness and kinetics of computer virus fusion. (bioerc-iend.org)
Human immun1
- The design of immunogens susceptible to elicit potent and broadly neutralizing antibodies against the human immunodeficiency virus type 1 (HIV-1) remains a veritable challenge in the course of vaccine development. (bvsalud.org)
Process1
- Process of growing viruses in live animals, plants, or cultured cells. (lookformedical.com)
Cells2
Activity1
- Substances elaborated by viruses that have antigenic activity. (lookformedical.com)
Results1
- Results showed that the predominant virus in the samples was ALV-J. (cdc.gov)