A genus of the family RETROVIRIDAE with type C morphology, that causes malignant and other diseases in wild birds and domestic fowl.
A condition characterized by the abnormal presence of ERYTHROBLASTS in the circulation of the FETUS or NEWBORNS. It is a disorder due to BLOOD GROUP INCOMPATIBILITY, such as the maternal alloimmunization by fetal antigen RH FACTORS leading to HEMOLYSIS of ERYTHROCYTES, hemolytic anemia (ANEMIA, HEMOLYTIC), general edema (HYDROPS FETALIS), and SEVERE JAUNDICE IN NEWBORN.
A group of transmissible viral diseases of chickens and turkeys. Liver tumors are found in most forms, but tumors can be found elsewhere.
The type species of ALPHARETROVIRUS producing latent or manifest lymphoid leukosis in fowl.
Transforming proteins encoded by erbB oncogenes from the avian erythroblastosis virus. The protein is a truncated form of the EGF receptor (RECEPTOR, EPIDERMAL GROWTH FACTOR) whose kinase domain is constitutively activated by deletion of the ligand-binding domain.
Transforming proteins encoded by erbA oncogenes from the avian erythroblastosis virus. They are truncated versions of c-erbA, the thyroid hormone receptor (RECEPTORS, THYROID HORMONE) that have retained both the DNA-binding and hormone-binding domains. Mutations in the hormone-binding domains abolish the transcriptional activation function. v-erbA acts as a dominant repressor of c-erbA, inducing transformation by disinhibiting proliferation.
Immature, nucleated ERYTHROCYTES occupying the stage of ERYTHROPOIESIS that follows formation of ERYTHROID PRECURSOR CELLS and precedes formation of RETICULOCYTES. The normal series is called normoblasts. Cells called MEGALOBLASTS are a pathologic series of erythroblasts.
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.
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.
Common name for the species Gallus gallus, the domestic fowl, in the family Phasianidae, order GALLIFORMES. It is descended from the red jungle fowl of SOUTHEAST ASIA.
Retroviral proteins that have the ability to transform cells. They can induce sarcomas, leukemias, lymphomas, and mammary carcinomas. Not all retroviral proteins are oncogenic.
An ets proto-oncogene expressed primarily in adult LYMPHOID TISSUE; BRAIN; and VASCULAR ENDOTHELIAL CELLS.
A myeloproliferative disorder characterized by neoplastic proliferation of erythroblastic and myeloblastic elements with atypical erythroblasts and myeloblasts in the peripheral blood.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
Strains of MURINE LEUKEMIA VIRUS that are replication-defective and rapidly transforming. The envelope gene plays an essential role in initiating erythroleukemia (LEUKEMIA, ERYTHROBLASTIC, ACUTE), manifested by splenic foci, SPLENOMEGALY, and POLYCYTHEMIA. Spleen focus-forming viruses are generated by recombination with endogenous retroviral sequences.
A ubiquitously expressed ets proto-oncogene protein that may play a role in regulation of CELL PROLIFERATION and CELL DIFFERENTIATION.
The developmental entity of a fertilized chicken egg (ZYGOTE). The developmental process begins about 24 h before the egg is laid at the BLASTODISC, a small whitish spot on the surface of the EGG YOLK. After 21 days of incubation, the embryo is fully developed before hatching.
The functional hereditary units of VIRUSES.
Proteins from the family Retroviridae. The most frequently encountered member of this family is the Rous sarcoma virus protein.
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 strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) producing leukemia of the reticulum-cell type with massive infiltration of liver, spleen, and bone marrow. It infects DBA/2 and Swiss mice.
Widely used technique which exploits the ability of complementary sequences in single-stranded DNAs or RNAs to pair with each other to form a double helix. Hybridization can take place between two complimentary DNA sequences, between a single-stranded DNA and a complementary RNA, or between two RNA sequences. The technique is used to detect and isolate specific sequences, measure homology, or define other characteristics of one or both strands. (Kendrew, Encyclopedia of Molecular Biology, 1994, p503)
Products of viral oncogenes, most commonly retroviral oncogenes. They usually have transforming and often protein kinase activities.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Specific high affinity binding proteins for THYROID HORMONES in target cells. They are usually found in the nucleus and regulate DNA transcription. These receptors are activated by hormones that leads to transcription, cell differentiation, and growth suppression. Thyroid hormone receptors are encoded by two genes (GENES, ERBA): erbA-alpha and erbA-beta for alpha and beta thyroid hormone receptors, respectively.
Proteins found in any species of virus.
Normal cellular genes homologous to viral oncogenes. The products of proto-oncogenes are important regulators of biological processes and appear to be involved in the events that serve to maintain the ordered procession through the cell cycle. Proto-oncogenes have names of the form c-onc.
A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A cell surface receptor involved in regulation of cell growth and differentiation. It is specific for EPIDERMAL GROWTH FACTOR and EGF-related peptides including TRANSFORMING GROWTH FACTOR ALPHA; AMPHIREGULIN; and HEPARIN-BINDING EGF-LIKE GROWTH FACTOR. The binding of ligand to the receptor causes activation of its intrinsic tyrosine kinase activity and rapid internalization of the receptor-ligand complex into the cell.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Established cell cultures that have the potential to propagate indefinitely.
Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
The sum of the weight of all the atoms in a molecule.
Ribonucleic acid that makes up the genetic material of viruses.
Deoxyribonucleic acid that makes up the genetic material of viruses.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.

Serum malondialdehyde concentration in babies with hyperbilirubinaemia. (1/148)

AIM: To determine lipid peroxide concentrations in the first 10 days of life. METHODS: Malondialdehyde concentrations were investigated in neonates with or without hyperbilirubinaemia during the first 10 days of life. RESULTS: Serum malondialdehyde concentrations were higher in infants with hyperbilirubinaemia than in controls. A positive correlation was found between malondialdehyde and bilirubin concentrations in the study group. When the study group was categorised according to the presence of haemolysis, a significant correlation was found between malondialdehyde and bilirubin concentrations in those infants with hyperbilirubinaemia due to haemolysis. There was no such correlation in those without haemolysis. CONCLUSION: Exchange transfusion rapidly produces variable changes in pro-oxidant and antioxidant plasma concentrations in neonates, which may be responsible for free radical metabolism. The fall in malondialdehyde concentration is probably directly related to its exogenous removal by exchange transfusion.  (+info)

Perinatal management of fetal hemolytic disease due to Rh incompatibility combined with fetal alloimmune thrombocytopenia due to HPA-5b incompatibility. (2/148)

We report out experience in the perinatal management of a complex case of fetal hemolytic disease primarily due to Rhesus incompatibility combined with fetal alloimmune thrombocytopenia. The lowest fetal hemoglobin and platelet levels were 2.6 g/dl and 13,000/microliter, respectively. Intrauterine treatment consisted of six transfusions of packed red cells into the umbilical vein and one transfusion of platelets. The neonate required four transfusions of packed red cells to correct her hyporegenerative erythropoiesis. Postnatal management also included one platelet transfusion, intravenous immunoglobulins and erythropoietin. Although some degree of fetal thrombocytopenia may invariably be found in fetal red cell incompatibility, other rare causes need to be excluded.  (+info)

A likelihood-based method of identifying contaminated lots of blood product. (3/148)

BACKGROUND: In 1994 a small cluster of hepatitis-C cases in Rhesus-negative women in Ireland prompted a nationwide screening programme for hepatitis-C antibodies in all anti-D recipients. A total of 55 386 women presented for screening and a history of exposure to anti-D was sought from all those testing positive and a sample of those testing negative. The resulting data comprised 620 antibody-positive and 1708 antibody-negative women with known exposure history, and interest was focused on using these data to estimate the infectivity of anti-D in the period 1970-1993. METHODS: Any exposure to anti-D provides an opportunity for infection, but the infection status at each exposure time is not observed. Instead, the available data from antibody testing only indicate whether at least one of the exposures resulted in infection. Using a simple Bernoulli model to describe the risk of infection in each year, the absence of information regarding which exposure(s) led to infection fits neatly into the framework of 'incomplete data'. Hence the expectation-maximization (EM) algorithm provides estimates of the infectiousness of anti-D in each of the 24 years studied. RESULTS: The analysis highlighted the 1977 anti-D as a source of infection, a fact which was confirmed by laboratory investigation. Other suspect batches were also identified, helping to direct the efforts of laboratory investigators. CONCLUSIONS: We have presented a method to estimate the risk of infection at each exposure time from multiple exposure data. The method can also be used to estimate transmission rates and the risk associated with different sources of infection in a range of infectious disease applications.  (+info)

Noninvasive diagnosis by Doppler ultrasonography of fetal anemia due to maternal red-cell alloimmunization. Collaborative Group for Doppler Assessment of the Blood Velocity in Anemic Fetuses. (4/148)

BACKGROUND: Invasive techniques such as amniocentesis and cordocentesis are used for diagnosis and treatment in fetuses at risk for anemia due to maternal red-cell alloimmunization. The purpose of our study was to determine the value of noninvasive measurements of the velocity of blood flow in the fetal middle cerebral artery for the diagnosis of fetal anemia. METHODS: We measured the hemoglobin concentration in blood obtained by cordocentesis and also the peak velocity of systolic blood flow in the middle cerebral artery in 111 fetuses at risk for anemia due to maternal red-cell alloimmunization. Peak systolic velocity was measured by Doppler velocimetry. To identify the fetuses with anemia, the hemoglobin values of those at risk were compared with the values in 265 normal fetuses. RESULTS: Fetal hemoglobin concentrations increased with increasing gestational age in the 265 normal fetuses. Among the 111 fetuses at risk for anemia, 41 fetuses did not have anemia; 35 had mild anemia; 4 had moderate anemia; and 31, including 12 with hydrops, had severe anemia. The sensitivity of an increased peak velocity of systolic blood flow in the middle cerebral artery for the prediction of moderate or severe anemia was 100 percent either in the presence or in the absence of hydrops (95 percent confidence interval, 86 to 100 percent for the 23 fetuses without hydrops), with a false positive rate of 12 percent. CONCLUSIONS: In fetuses without hydrops that are at risk because of maternal red-cell alloimmunization, moderate and severe anemia can be detected noninvasively by Doppler ultrasonography on the basis of an increase in the peak velocity of systolic blood flow in the middle cerebral artery.  (+info)

Hemolytic disease of the newborn due to anti S antibodies. (5/148)

We report a case of hemolytic disease in a newborn due to anti S antibodies. Baby R was born at term to an O+ mother whose antibody screen was positive for phenotype big S. Cord blood eluate revealed anti-S RBC; antigen: RBC typing for S- was positive. Physical examination of baby was unremarkable. The infant's HCT was 44.2 at 6 hours of age. At 48 hours, the HCT decreased to 33.5, bilirubin peaked to 5.4, retic had peaked to 6.8. By seven days, all these values reverted to the normal, and baby has remained asymptomatic.  (+info)

Middle cerebral artery peak systolic velocity in the prediction of fetal anemia. (6/148)

OBJECTIVE: The fetal middle cerebral artery peak systolic velocity (MCA PSV) has been suggested as a potential test to predict the fetal hematocrit level. We tested the hypothesis that a low fetal hematocrit is associated with an increase in MCA PSV in a prospective study of normal and alloimmunized pregnancies. METHODS: Fetal hematocrit and MCA PSV were obtained in 26 alloimmunized fetuses, immediately before their first fetal blood transfusions between 15 and 35 weeks. Results were compared with the MCA PSVs from 170 control fetuses not at risk of alloimmune anemia between 13 and 37 weeks. RESULTS: In control fetuses, PSV varied with gestation (PSV = 0.56 - 0.032 GA + 0.00086 GA2, where GA is gestational age; R2 = 0.41). The correlation between PSV and hematocrit Z scores (Pearson correlation coefficient r = -0.69) was highly significant (P = 0.0001). Using a PSV > 1 SD, the sensitivity of the test in predicting a fetal hematocrit < 2 SD below the mean was only 64% but the specificity was 100%. However, the sensitivity of the test in predicting a fetal hematocrit < 3 SD and < 4 SD rose to 73% and 83%, while the specificity was still good (93% and 80% respectively). CONCLUSIONS: MCA PSV and fetal hematocrit are highly significantly correlated. The sensitivity of the test was good and the high positive predictive value indicates that the presence of a raised PSV (defined as > 1 SD) is a strong indicator of fetal anemia. In conclusion, MCA PSV is a useful test in clinical practice for the detection of fetal anemia.  (+info)

Early neonatal hypocalcaemia. (7/148)

In our hospital early neonatal hypocalcaemia is now the major cause of low serum calcium in the neonatal period. Over a 2-year period, only 2 cases of hypocalcaemic convulsions were seen in a total of 8700 deliveries, though 51 infants had early neonatal hypocalcaemia. All sick low birth-weight infants should have daily serum calcium estimations carried out. Calcium supplements should be considered if symptoms of hypocalcaemia are present.  (+info)

Identification of alloreactive T-cell epitopes on the Rhesus D protein. (8/148)

Although considerable effort has been devoted to characterizing alloantibodies specific for the Rhesus D (RhD) blood group antigen, virtually nothing is known about the helper response that drives their production. Therefore, the aim of this study was to map alloreactive T-cell epitopes on the RhD protein. Peripheral blood mononuclear cells (PBMCs) were obtained from 22 RhD-negative volunteers in whom anti-D alloantibodies had developed after deliberate immunization or RhD-incompatible pregnancy. The PBMCs were stimulated with a panel of up to 68 overlapping synthetic 15-mer peptides spanning the complete sequence of the RhD protein. One or more peptides elicited proliferative responses by PBMCs from all 22 of the alloimmune volunteers but from only 2 of 8 alloantibody-negative control donors. Proliferation of PBMCs from the alloimmune donors was mediated by major histocompatibility complex class II-restricted T cells expressing the CD45RO marker of previous activation or memory. The number of peptides that induced proliferative responses was unrelated to either the frequency of, or time since, exposure to RhD-positive red blood cells, but it correlated strongly (R(s) = 0.75; P <.003) with the level of anti-D antibodies in deliberately immunized donors. The patterns of stimulatory peptides varied among alloimmune volunteers, but particular sequences were commonly recognized, with 4 peptides each eliciting a response in more than 50% of these donors. Identification of such peptides containing dominant alloreactive helper epitopes is the first step in the development of improved or new approaches to preventing hemolytic disease of the newborn that are based on modulating the T-cell response to the RhD protein.  (+info)

An alpharetrovirus is a type of retrovirus, which is a group of viruses that integrate their genetic material into the DNA of the host cell. Alpharetroviruses are characterized by their ability to cause persistent infections and are associated with various diseases in animals. One well-known example of an alpharetrovirus is the Rous sarcoma virus (RSV), which was the first retrovirus to be discovered and is known to cause cancer in chickens.

Alpharetroviruses have a complex structure, consisting of an outer envelope that contains glycoprotein spikes, and an inner core that contains the viral RNA genome and associated enzymes. The viral RNA genome contains three main genes: gag, pol, and env, which encode for the structural proteins, enzymes, and envelope proteins of the virus, respectively.

Alpharetroviruses are transmitted through various routes, including horizontal transmission (from host to host) and vertical transmission (from parent to offspring). They can cause a range of diseases, depending on the specific virus and the host species. In addition to RSV, other examples of alpharetroviruses include the avian leukosis virus, which causes tumors and immunosuppression in birds, and the Jaagsiekte sheep retrovirus, which causes a wasting disease in sheep.

It's worth noting that while alpharetroviruses are associated with diseases in animals, there are no known alpharetroviruses that infect humans. However, understanding the biology and behavior of these viruses in animal hosts can provide valuable insights into retroviral replication and pathogenesis, which may have implications for human health.

Erythroblastosis, fetal is a medical condition that occurs in the fetus or newborn when there is an incompatibility between the fetal and maternal blood types, specifically related to the Rh factor or ABO blood group system. This incompatibility leads to the destruction of the fetal red blood cells by the mother's immune system, resulting in the release of bilirubin, which can cause jaundice, anemia, and other complications.

In cases where the mother is Rh negative and the fetus is Rh positive, the mother may develop antibodies against the Rh factor during pregnancy or after delivery, leading to hemolysis (breakdown) of the fetal red blood cells in subsequent pregnancies if preventive measures are not taken. This is known as hemolytic disease of the newborn (HDN).

Similarly, incompatibility between the ABO blood groups can also lead to HDN, although it is generally less severe than Rh incompatibility. In this case, the mother's immune system produces antibodies against the fetal red blood cells, leading to their destruction and subsequent complications.

Fetal erythroblastosis is a serious condition that can lead to significant morbidity and mortality if left untreated. Treatment options include intrauterine transfusions, phototherapy, and exchange transfusions in severe cases. Preventive measures such as Rh immune globulin (RhIG) injections can help prevent the development of antibodies in Rh-negative mothers, reducing the risk of HDN in subsequent pregnancies.

Avian leukosis is a group of viral diseases that primarily affect chickens and other birds. It is caused by retroviruses known as avian leukosis viruses (ALVs) and leads to a variety of clinical signs, including immunosuppression, growth retardation, and the development of tumors in various organs. The disease can be transmitted both horizontally (through direct contact with infected birds or their secretions) and vertically (from infected hens to their offspring through the egg).

There are several subgroups of ALVs, each associated with specific types of tumors and clinical manifestations. For example:

1. ALV-J (Japanese strain): This subgroup is responsible for myelocytomatosis, a condition characterized by the proliferation of immature blood cells in the bone marrow, leading to anemia, leukopenia, and enlarged spleens and livers.
2. ALV-A, ALV-B, and ALV-C (American strains): These subgroups are associated with various types of lymphoid tumors, such as B-cell and T-cell lymphomas, which can affect the bursa of Fabricius, thymus, spleen, and other organs.
3. ALV-E (European strain): This subgroup is linked to erythroblastosis, a condition in which there is an excessive proliferation of red blood cell precursors, resulting in the formation of tumors in the bone marrow and other organs.

Avian leukosis poses significant economic challenges for the poultry industry due to its impact on growth, feed conversion efficiency, and mortality rates. Additionally, some countries have regulations in place to prevent the spread of avian leukosis viruses through the trade of infected birds or their products. Prevention measures include strict biosecurity protocols, vaccination programs, and rigorous screening and eradication strategies for infected flocks.

Avian leukosis virus (ALV) is a type of retrovirus that primarily affects chickens and other birds. It is responsible for a group of diseases known as avian leukosis, which includes various types of tumors and immunosuppressive conditions. The virus is transmitted horizontally through the shedder's dander, feathers, and vertical transmission through infected eggs.

There are several subgroups of ALV (A, B, C, D, E, and J), each with different host ranges and pathogenicity. Some strains can cause rapid death in young chickens, while others may take years to develop clinical signs. The most common form of the disease is neoplastic, characterized by the development of various types of tumors such as lymphomas, myelomas, and sarcomas.

Avian leukosis virus infection can have significant economic impacts on the poultry industry due to decreased growth rates, increased mortality, and condemnation of infected birds at processing. Control measures include eradication programs, biosecurity practices, vaccination, and breeding for genetic resistance.

The oncogene proteins v-erbB are derived from the erbB oncogene, which is a retroviral oncogene first discovered in avian erythroblastosis viruses (AEV). The erbB oncogene is homologous to the human epidermal growth factor receptor 2 (HER2/erbB-2) gene, which encodes a transmembrane tyrosine kinase receptor involved in cell proliferation and differentiation.

The v-erbB oncogene protein is a truncated and mutated version of the normal EGFR/erbB-1 receptor, which has lost its extracellular ligand-binding domain and gained constitutive tyrosine kinase activity. This results in uncontrolled cell growth and division, leading to the development of cancer.

The v-erbB oncogene protein has been extensively studied as a model system for understanding the molecular mechanisms of oncogenesis and has provided valuable insights into the regulation of cell growth and differentiation. Additionally, the study of v-erbB and other oncogenes has led to the development of targeted cancer therapies that inhibit the activity of these aberrant proteins and slow or stop the growth of cancer cells.

The oncogene proteins v-erbA are a subset of oncogenes that were initially discovered in retroviruses, specifically the avian erythroblastosis virus (AEV). These oncogenes are derived from normal cellular genes called proto-oncogenes, which play crucial roles in various cellular processes such as growth, differentiation, and survival.

The v-erbA oncogene protein is a truncated and mutated version of the thyroid hormone receptor alpha (THRA) gene, which is a nuclear receptor that regulates gene expression in response to thyroid hormones. The v-erbA protein can bind to DNA but cannot interact with thyroid hormones, leading to aberrant regulation of gene expression and uncontrolled cell growth, ultimately resulting in cancer.

In particular, the v-erbA oncogene has been implicated in the development of erythroblastosis, a disease characterized by the proliferation of immature red blood cells, leading to anemia and other symptoms. The activation of the v-erbA oncogene can also contribute to the development of other types of cancer, such as leukemia and lymphoma.

Erythroblasts are immature red blood cells that are produced in the bone marrow. They are also known as normoblasts and are a stage in the development of red blood cells, or erythrocytes. Erythroblasts are larger than mature red blood cells and have a nucleus, which is lost during the maturation process. These cells are responsible for producing hemoglobin, the protein that carries oxygen in the blood. Abnormal increases or decreases in the number of erythroblasts can be indicative of certain medical conditions, such as anemia or leukemia.

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.

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.

"Chickens" is a common term used to refer to the domesticated bird, Gallus gallus domesticus, which is widely raised for its eggs and meat. However, in medical terms, "chickens" is not a standard term with a specific definition. If you have any specific medical concern or question related to chickens, such as food safety or allergies, please provide more details so I can give a more accurate answer.

Retroviridae proteins, oncogenic, refer to the proteins expressed by retroviruses that have the ability to transform normal cells into cancerous ones. These oncogenic proteins are typically encoded by viral genes known as "oncogenes," which are acquired through the process of transduction from the host cell's DNA during retroviral replication.

The most well-known example of an oncogenic retrovirus is the Human T-cell Leukemia Virus Type 1 (HTLV-1), which encodes the Tax and HBZ oncoproteins. These proteins manipulate various cellular signaling pathways, leading to uncontrolled cell growth and malignant transformation.

It is important to note that not all retroviruses are oncogenic, and only a small subset of them have been associated with cancer development in humans or animals.

Proto-oncogene protein c-ets-1 is a transcription factor that regulates gene expression in various cellular processes, including cell growth, differentiation, and apoptosis. It belongs to the ETS family of transcription factors, which are characterized by a highly conserved DNA-binding domain known as the ETS domain. The c-ets-1 protein is encoded by the ETS1 gene located on chromosome 11 in humans.

In normal cells, c-ets-1 plays critical roles in development, tissue repair, and immune function. However, when its expression or activity is dysregulated, it can contribute to tumorigenesis and cancer progression. In particular, c-ets-1 has been implicated in the development of various types of leukemia and solid tumors, such as breast, prostate, and lung cancer.

The activation of c-ets-1 can occur through various mechanisms, including gene amplification, chromosomal translocation, or point mutations. Once activated, c-ets-1 can promote cell proliferation, survival, and migration, while also inhibiting apoptosis. These oncogenic properties make c-ets-1 a potential target for cancer therapy.

Erythroblastic Leukemia, Acute (also known as Acute Erythroid Leukemia or AEL) is a subtype of acute myeloid leukemia (AML), which is a type of cancer affecting the blood and bone marrow. In this condition, there is an overproduction of erythroblasts (immature red blood cells) in the bone marrow, leading to their accumulation and interference with normal blood cell production. This results in a decrease in the number of functional red blood cells, white blood cells, and platelets in the body. Symptoms may include fatigue, weakness, frequent infections, and easy bruising or bleeding. AEL is typically treated with chemotherapy and sometimes requires stem cell transplantation.

Experimental leukemia refers to the stage of research or clinical trials where new therapies, treatments, or diagnostic methods are being studied for leukemia. Leukemia is a type of cancer that affects the blood and bone marrow, leading to an overproduction of abnormal white blood cells.

In the experimental stage, researchers investigate various aspects of leukemia, such as its causes, progression, and potential treatments. They may conduct laboratory studies using cell cultures or animal models to understand the disease better and test new therapeutic approaches. Additionally, clinical trials may be conducted to evaluate the safety and efficacy of novel treatments in human patients with leukemia.

Experimental research in leukemia is crucial for advancing our understanding of the disease and developing more effective treatment strategies. It involves a rigorous and systematic process that adheres to ethical guidelines and scientific standards to ensure the validity and reliability of the findings.

"Spleen Focus-Forming Virus" (SFFV) is not a widely used medical term, but it is a term from the field of virology. SFFV is a type of retrovirus that primarily infects mice and causes erythroleukemia, a cancer of the blood-forming organs. The virus is called "Spleen Focus-Forming" because when it infects mice, it initially replicates in the spleen and forms distinct foci or clusters of infected cells.

The virus contains an oncogene called v-abl, which is a cancer-causing gene that contributes to the development of leukemia in infected animals. SFFV is closely related to another retrovirus called Friend Virus (FV), and together they are referred to as the FV complex. These viruses have been extensively studied as models for retroviral-induced leukemogenesis and have provided valuable insights into the mechanisms of cancer development.

Proto-oncogene protein c-ets-2 is a transcription factor that regulates gene expression in various cellular processes, including cell growth, differentiation, and apoptosis. It belongs to the ETS family of transcription factors, which are characterized by a highly conserved DNA-binding domain known as the ETS domain. The c-ets-2 protein binds to specific DNA sequences called ETS response elements (EREs) in the promoter regions of target genes and regulates their expression.

Proto-oncogenes are normal genes that can become oncogenes when they are mutated or overexpressed, leading to uncontrolled cell growth and cancer. The c-ets-2 gene can be activated by various mechanisms, including chromosomal translocations, gene amplification, and point mutations, resulting in the production of abnormal c-ets-2 proteins that contribute to tumorigenesis.

Abnormal expression or activity of c-ets-2 has been implicated in several types of cancer, such as leukemia, breast cancer, and prostate cancer. Therefore, understanding the role of c-ets-2 in cellular processes and its dysregulation in cancer can provide insights into the development of novel therapeutic strategies for cancer treatment.

A chick embryo refers to the developing organism that arises from a fertilized chicken egg. It is often used as a model system in biological research, particularly during the stages of development when many of its organs and systems are forming and can be easily observed and manipulated. The study of chick embryos has contributed significantly to our understanding of various aspects of developmental biology, including gastrulation, neurulation, organogenesis, and pattern formation. Researchers may use various techniques to observe and manipulate the chick embryo, such as surgical alterations, cell labeling, and exposure to drugs or other agents.

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.

Retroviridae is a family of viruses that includes HIV (Human Immunodeficiency Virus). Retroviridae proteins refer to the various structural and functional proteins that are encoded by the retroviral genome. These proteins can be categorized into three main groups:

1. Group-specific antigen (Gag) proteins: These proteins make up the viral matrix, capsid, and nucleocapsid. They are involved in the assembly of new virus particles.

2. Polymerase (Pol) proteins: These proteins include the reverse transcriptase, integrase, and protease enzymes. Reverse transcriptase is responsible for converting the viral RNA genome into DNA, which can then be integrated into the host cell's genome by the integrase enzyme. The protease enzyme is involved in processing the polyprotein precursors of Gag and Pol into their mature forms.

3. Envelope (Env) proteins: These proteins are responsible for the attachment and fusion of the virus to the host cell membrane. They are synthesized as a precursor protein, which is then cleaved by a host cell protease to form two distinct proteins - the surface unit (SU) and the transmembrane unit (TM). The SU protein contains the receptor-binding domain, while the TM protein forms the transmembrane anchor.

Retroviral proteins play crucial roles in various stages of the viral life cycle, including entry, reverse transcription, integration, transcription, translation, assembly, and release. Understanding the functions of these proteins is essential for developing effective antiretroviral therapies and vaccines against retroviral infections.

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.

Friend murine leukemia virus (F-MuLV) is a type of retrovirus that specifically infects mice. It was first discovered by Charlotte Friend in the 1950s and has since been widely used as a model system to study retroviral pathogenesis, oncogenesis, and immune responses.

F-MuLV is a complex retrovirus that contains several accessory genes, including gag, pol, env, and others. The virus can cause leukemia and other malignancies in susceptible mice, particularly when it is transmitted from mother to offspring through the milk.

The virus is also known to induce immunosuppression, which makes infected mice more susceptible to other infections and diseases. F-MuLV has been used extensively in laboratory research to investigate various aspects of retroviral biology, including viral entry, replication, gene expression, and host immune responses.

It is important to note that Friend murine leukemia virus only infects mice and is not known to cause any disease in humans or other animals.

Nucleic acid hybridization is a process in molecular biology where two single-stranded nucleic acids (DNA, RNA) with complementary sequences pair together to form a double-stranded molecule through hydrogen bonding. The strands can be from the same type of nucleic acid or different types (i.e., DNA-RNA or DNA-cDNA). This process is commonly used in various laboratory techniques, such as Southern blotting, Northern blotting, polymerase chain reaction (PCR), and microarray analysis, to detect, isolate, and analyze specific nucleic acid sequences. The hybridization temperature and conditions are critical to ensure the specificity of the interaction between the two strands.

Oncogene proteins, viral, are cancer-causing proteins that are encoded by the genetic material (DNA or RNA) of certain viruses. These viral oncogenes can be acquired through infection with retroviruses, such as human immunodeficiency virus (HIV), human T-cell leukemia virus (HTLV), and certain types of papillomaviruses and polyomaviruses.

When these viruses infect host cells, they can integrate their genetic material into the host cell's genome, leading to the expression of viral oncogenes. These oncogenes may then cause uncontrolled cell growth and division, ultimately resulting in the formation of tumors or cancers. The process by which viruses contribute to cancer development is complex and involves multiple steps, including the alteration of signaling pathways that regulate cell proliferation, differentiation, and survival.

Examples of viral oncogenes include the v-src gene found in the Rous sarcoma virus (RSV), which causes chicken sarcoma, and the E6 and E7 genes found in human papillomaviruses (HPVs), which are associated with cervical cancer and other anogenital cancers. Understanding viral oncogenes and their mechanisms of action is crucial for developing effective strategies to prevent and treat virus-associated cancers.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Thyroid hormone receptors (THRs) are nuclear receptor proteins that bind to thyroid hormones, triiodothyronine (T3) and thyroxine (T4), and regulate gene transcription in target cells. These receptors play a crucial role in the development, growth, and metabolism of an organism by mediating the actions of thyroid hormones. THRs are encoded by genes THRA and THRB, which give rise to two major isoforms: TRα1 and TRβ1. Additionally, alternative splicing results in other isoforms with distinct tissue distributions and functions. THRs function as heterodimers with retinoid X receptors (RXRs) and bind to thyroid hormone response elements (TREs) in the regulatory regions of target genes. The binding of T3 or T4 to THRs triggers a conformational change, which leads to recruitment of coactivators or corepressors, ultimately resulting in activation or repression of gene transcription.

Viral proteins are the proteins that are encoded by the viral genome and are essential for the viral life cycle. These proteins can be structural or non-structural and play various roles in the virus's replication, infection, and assembly process. Structural proteins make up the physical structure of the virus, including the capsid (the protein shell that surrounds the viral genome) and any envelope proteins (that may be present on enveloped viruses). Non-structural proteins are involved in the replication of the viral genome and modulation of the host cell environment to favor viral replication. Overall, a thorough understanding of viral proteins is crucial for developing antiviral therapies and vaccines.

Proto-oncogenes are normal genes that are present in all cells and play crucial roles in regulating cell growth, division, and death. They code for proteins that are involved in signal transduction pathways that control various cellular processes such as proliferation, differentiation, and survival. When these genes undergo mutations or are activated abnormally, they can become oncogenes, which have the potential to cause uncontrolled cell growth and lead to cancer. Oncogenes can contribute to tumor formation through various mechanisms, including promoting cell division, inhibiting programmed cell death (apoptosis), and stimulating blood vessel growth (angiogenesis).

A gene is a specific sequence of nucleotides in DNA that carries genetic information. Genes are the fundamental units of heredity and are responsible for the development and function of all living organisms. They code for proteins or RNA molecules, which carry out various functions within cells and are essential for the structure, function, and regulation of the body's tissues and organs.

Each gene has a specific location on a chromosome, and each person inherits two copies of every gene, one from each parent. Variations in the sequence of nucleotides in a gene can lead to differences in traits between individuals, including physical characteristics, susceptibility to disease, and responses to environmental factors.

Medical genetics is the study of genes and their role in health and disease. It involves understanding how genes contribute to the development and progression of various medical conditions, as well as identifying genetic risk factors and developing strategies for prevention, diagnosis, and treatment.

Fibroblasts are specialized cells that play a critical role in the body's immune response and wound healing process. They are responsible for producing and maintaining the extracellular matrix (ECM), which is the non-cellular component present within all tissues and organs, providing structural support and biochemical signals for surrounding cells.

Fibroblasts produce various ECM proteins such as collagens, elastin, fibronectin, and laminins, forming a complex network of fibers that give tissues their strength and flexibility. They also help in the regulation of tissue homeostasis by controlling the turnover of ECM components through the process of remodeling.

In response to injury or infection, fibroblasts become activated and start to proliferate rapidly, migrating towards the site of damage. Here, they participate in the inflammatory response, releasing cytokines and chemokines that attract immune cells to the area. Additionally, they deposit new ECM components to help repair the damaged tissue and restore its functionality.

Dysregulation of fibroblast activity has been implicated in several pathological conditions, including fibrosis (excessive scarring), cancer (where they can contribute to tumor growth and progression), and autoimmune diseases (such as rheumatoid arthritis).

The Epidermal Growth Factor Receptor (EGFR) is a type of receptor found on the surface of many cells in the body, including those of the epidermis or outer layer of the skin. It is a transmembrane protein that has an extracellular ligand-binding domain and an intracellular tyrosine kinase domain.

EGFR plays a crucial role in various cellular processes such as proliferation, differentiation, migration, and survival. When EGF (Epidermal Growth Factor) or other ligands bind to the extracellular domain of EGFR, it causes the receptor to dimerize and activate its intrinsic tyrosine kinase activity. This leads to the autophosphorylation of specific tyrosine residues on the receptor, which in turn recruits and activates various downstream signaling molecules, resulting in a cascade of intracellular signaling events that ultimately regulate gene expression and cell behavior.

Abnormal activation of EGFR has been implicated in several human diseases, including cancer. Overexpression or mutation of EGFR can lead to uncontrolled cell growth and division, angiogenesis, and metastasis, making it an important target for cancer therapy.

Genetic transcription is the process by which the information in a strand of DNA is used to create a complementary RNA molecule. This process is the first step in gene expression, where the genetic code in DNA is converted into a form that can be used to produce proteins or functional RNAs.

During transcription, an enzyme called RNA polymerase binds to the DNA template strand and reads the sequence of nucleotide bases. As it moves along the template, it adds complementary RNA nucleotides to the growing RNA chain, creating a single-stranded RNA molecule that is complementary to the DNA template strand. Once transcription is complete, the RNA molecule may undergo further processing before it can be translated into protein or perform its functional role in the cell.

Transcription can be either "constitutive" or "regulated." Constitutive transcription occurs at a relatively constant rate and produces essential proteins that are required for basic cellular functions. Regulated transcription, on the other hand, is subject to control by various intracellular and extracellular signals, allowing cells to respond to changing environmental conditions or developmental cues.

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.

Protein-Tyrosine Kinases (PTKs) are a type of enzyme that plays a crucial role in various cellular functions, including signal transduction, cell growth, differentiation, and metabolism. They catalyze the transfer of a phosphate group from ATP to the tyrosine residues of proteins, thereby modifying their activity, localization, or interaction with other molecules.

PTKs can be divided into two main categories: receptor tyrosine kinases (RTKs) and non-receptor tyrosine kinases (NRTKs). RTKs are transmembrane proteins that become activated upon binding to specific ligands, such as growth factors or hormones. NRTKs, on the other hand, are intracellular enzymes that can be activated by various signals, including receptor-mediated signaling and intracellular messengers.

Dysregulation of PTK activity has been implicated in several diseases, such as cancer, diabetes, and inflammatory disorders. Therefore, PTKs are important targets for drug development and therapy.

Molecular cloning is a laboratory technique used to create multiple copies of a specific DNA sequence. This process involves several steps:

1. Isolation: The first step in molecular cloning is to isolate the DNA sequence of interest from the rest of the genomic DNA. This can be done using various methods such as PCR (polymerase chain reaction), restriction enzymes, or hybridization.
2. Vector construction: Once the DNA sequence of interest has been isolated, it must be inserted into a vector, which is a small circular DNA molecule that can replicate independently in a host cell. Common vectors used in molecular cloning include plasmids and phages.
3. Transformation: The constructed vector is then introduced into a host cell, usually a bacterial or yeast cell, through a process called transformation. This can be done using various methods such as electroporation or chemical transformation.
4. Selection: After transformation, the host cells are grown in selective media that allow only those cells containing the vector to grow. This ensures that the DNA sequence of interest has been successfully cloned into the vector.
5. Amplification: Once the host cells have been selected, they can be grown in large quantities to amplify the number of copies of the cloned DNA sequence.

Molecular cloning is a powerful tool in molecular biology and has numerous applications, including the production of recombinant proteins, gene therapy, functional analysis of genes, and genetic engineering.

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

Molecular weight, also known as molecular mass, is the mass of a molecule. It is expressed in units of atomic mass units (amu) or daltons (Da). Molecular weight is calculated by adding up the atomic weights of each atom in a molecule. It is a useful property in chemistry and biology, as it can be used to determine the concentration of a substance in a solution, or to calculate the amount of a substance that will react with another in a chemical reaction.

A viral RNA (ribonucleic acid) is the genetic material found in certain types of viruses, as opposed to viruses that contain DNA (deoxyribonucleic acid). These viruses are known as RNA viruses. The RNA can be single-stranded or double-stranded and can exist as several different forms, such as positive-sense, negative-sense, or ambisense RNA. Upon infecting a host cell, the viral RNA uses the host's cellular machinery to translate the genetic information into proteins, leading to the production of new virus particles and the continuation of the viral life cycle. Examples of human diseases caused by RNA viruses include influenza, COVID-19 (SARS-CoV-2), hepatitis C, and polio.

Viral DNA refers to the genetic material present in viruses that consist of DNA as their core component. Deoxyribonucleic acid (DNA) is one of the two types of nucleic acids that are responsible for storing and transmitting genetic information in living organisms. Viruses are infectious agents much smaller than bacteria that can only replicate inside the cells of other organisms, called hosts.

Viral DNA can be double-stranded (dsDNA) or single-stranded (ssDNA), depending on the type of virus. Double-stranded DNA viruses have a genome made up of two complementary strands of DNA, while single-stranded DNA viruses contain only one strand of DNA.

Examples of dsDNA viruses include Adenoviruses, Herpesviruses, and Poxviruses, while ssDNA viruses include Parvoviruses and Circoviruses. Viral DNA plays a crucial role in the replication cycle of the virus, encoding for various proteins necessary for its multiplication and survival within the host cell.

Transfection is a term used in molecular biology that refers to the process of deliberately introducing foreign genetic material (DNA, RNA or artificial gene constructs) into cells. This is typically done using chemical or physical methods, such as lipofection or electroporation. Transfection is widely used in research and medical settings for various purposes, including studying gene function, producing proteins, developing gene therapies, and creating genetically modified organisms. It's important to note that transfection is different from transduction, which is the process of introducing genetic material into cells using viruses as vectors.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Proto-oncogene proteins are normal cellular proteins that play crucial roles in various cellular processes, such as signal transduction, cell cycle regulation, and apoptosis (programmed cell death). They are involved in the regulation of cell growth, differentiation, and survival under physiological conditions.

When proto-oncogene proteins undergo mutations or aberrations in their expression levels, they can transform into oncogenic forms, leading to uncontrolled cell growth and division. These altered proteins are then referred to as oncogene products or oncoproteins. Oncogenic mutations can occur due to various factors, including genetic predisposition, environmental exposures, and aging.

Examples of proto-oncogene proteins include:

1. Ras proteins: Involved in signal transduction pathways that regulate cell growth and differentiation. Activating mutations in Ras genes are found in various human cancers.
2. Myc proteins: Regulate gene expression related to cell cycle progression, apoptosis, and metabolism. Overexpression of Myc proteins is associated with several types of cancer.
3. EGFR (Epidermal Growth Factor Receptor): A transmembrane receptor tyrosine kinase that regulates cell proliferation, survival, and differentiation. Mutations or overexpression of EGFR are linked to various malignancies, such as lung cancer and glioblastoma.
4. Src family kinases: Intracellular tyrosine kinases that regulate signal transduction pathways involved in cell proliferation, survival, and migration. Dysregulation of Src family kinases is implicated in several types of cancer.
5. Abl kinases: Cytoplasmic tyrosine kinases that regulate various cellular processes, including cell growth, differentiation, and stress responses. Aberrant activation of Abl kinases, as seen in chronic myelogenous leukemia (CML), leads to uncontrolled cell proliferation.

Understanding the roles of proto-oncogene proteins and their dysregulation in cancer development is essential for developing targeted cancer therapies that aim to inhibit or modulate these aberrant signaling pathways.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Cell differentiation is the process by which a less specialized cell, or stem cell, becomes a more specialized cell type with specific functions and structures. This process involves changes in gene expression, which are regulated by various intracellular signaling pathways and transcription factors. Differentiation results in the development of distinct cell types that make up tissues and organs in multicellular organisms. It is a crucial aspect of embryonic development, tissue repair, and maintenance of homeostasis in the body.

The risk of fetal injury increases with increasing number of puncture attempts. Maternal and fetal blood cells may mix during ... Nassar GN, Wehbe C (2022). "Erythroblastosis Fetalis". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 30020664. ... Lack of fetal lung maturity increases the risk of infant respiratory distress syndrome. Fetal lung development can be tested by ... Fetal viability after the procedure should be confirmed by observing adequate fetal cardiac activity. The number of needle ...
... fetal erythroblastosis). Infections like chorioamnionitis cause an infection in the maternal blood, commonly leading to ... "Fetal Stroke , Causes of Hypoxic-Ischemic Encephalopathy (HIE)". HIE Help Center. Retrieved 2020-04-06. Roach, E. Steve; Golomb ... Birth trauma and mechanical trauma to the fetal head and neck can cause stroke by damaging arteries: Some children may have ... In addition to vascular damage, trauma to the fetal head from excessive uterine activity, manipulation, pressure, and forceps ...
... known as erythroblastosis fetalis. Another example of a complement dependent type II hypersensitivity reaction is Goodpasture's ... type II hypersensitivity can also occur during the transmission of incompatible maternal antibodies to fetal red blood cells ...
The intensity of this fetal disease ranges from mild to very severe, and fetal death from heart failure (hydrops fetalis) can ... earning these forms of the disease the name erythroblastosis fetalis (British English: erythroblastosis foetalis). HDFN ... Fetal-maternal hemorrhage, which is the movement of fetal blood cells across the placenta, can occur during abortion, ectopic ... Fetal mortality was reduced by 36% in the IVIG and IUT group than in the IUT alone group. IVIG and plasmapheresis together can ...
... erythroblastosis, fetal MeSH C13.703.277.060.480 - hydrops fetalis MeSH C13.703.277.080 - fetal alcohol syndrome MeSH C13.703. ... 277.370 - fetal growth retardation MeSH C13.703.277.390 - fetal hypoxia MeSH C13.703.277.570 - fetal macrosomia MeSH C13.703. ... fetal macrosomia MeSH C13.703.243.300 - fetal resorption MeSH C13.703.277.030 - chorioamnionitis MeSH C13.703.277.060 - ... 277.677 - fetal nutrition disorders MeSH C13.703.277.785 - meconium aspiration syndrome MeSH C13.703.395.124 - eclampsia MeSH ...
... pre-existing maternal antibodies to RhD antigens on fetal red blood cells often leads to erythroblastosis fetalis, a condition ... The dosage of RhIG is calculated from the volume of fetal hemorrhage (in mL). Ex: 50 mL fetal hemorrhage / 30 mL = 1.667 (round ... In rare cases this can cause a baby to have a weakly positive direct antiglobulin test (DAT) due to sensitization of fetal ... This qualitative (not quantitative) test will be positive if fetal D-positive cells are present in the maternal sample, ...
... erythroblastosis, fetal MeSH C15.378.120.413.480 - hydrops fetalis MeSH C15.378.120.413.502 - kernicterus MeSH C15.378.120.780 ...
Though she wanted multiple children, Turner had Rh-negative blood, which caused fetal anemia and made it difficult to carry a ... Turner's blood condition resulted in Cheryl being born with near-fatal erythroblastosis fetalis. Meanwhile, publicity over ...
Therapy for Fetal anemia caused by a parvovirus infection or fetomaternal hemorrhage is fetal blood sampling followed by ... Erythroblastosis fetalis, also known as Rh disease, is the only immune cause of hydrops fetalis. Rh disease is a hemolytic ... Hydrops Fetalis resulting from fetal CPAM can be treated using either a fetal needle drainage of effusion or placement of ... 2004). "Thoracoamniotic shunts: fetal treatment of pleural effusions and congenital cystic adenomatoid malformations". Fetal ...
A Case of Fetal-Induced Graft-versus-Host Disease Fung MK, Grossman BJ, Hillyer CD, Westhoff CM (2014). Technical manual (18th ... or erythroblastosis fetalis in newborns Congenital immunodeficiencies Certain hematologic malignancies (e.g. Hodgkin lymphoma) ... the first case of fetal-induced GvHD was reported in the New England Journal of Medicine. Prevention includes gamma irradiation ...
The immunization may conceivably occur as a result of an accident whereby the fetal cells or their hemoglobin gain entrance to ... Her son suffered from erythroblastosis fetalis (now known as hemolytic disease of the newborn) and died shortly after birth. ... While her description of the general mechanism of HDN was correct, Darrow believed the causative agent was fetal hemoglobin ... The maternal antibody could then cross into the fetal circulation and cause an antigen-antibody reaction resulting in ...
A sample of fetal blood can be taken from the umbilical vein prior to the transfusion. Often, this is all done at the same PUBS ... Levine published his theory that the disease known as erythroblastosis fetalis was due to Rh alloimmunization in 1941 while ... Intraperitoneal transfusion-blood transfused into fetal abdomen Intravascular transfusion-blood transfused into fetal umbilical ... Blood is taken from the mother, and using PCR, can detect fetal DNA. This blood test is non-invasive to the fetus and can help ...
The condition is most commonly caused by inadequate maternal-fetal circulation, with a resultant decrease in fetal growth. ... Syphilis Erythroblastosis fetalis Congenital abnormalities Placental genes Maternal genes: Endothelin-1 over-expression, Leptin ... prenatal alcohol use can result in Fetal alcohol syndrome) IUGR is caused by a variety of factors; these can be fetal, maternal ... Therefore, the fetal heart must work harder to contract during each heartbeat, which leads to an increase in wall stress and ...
Both fetal and adult DS fibroblasts are defective in the removal of 8-OHdG as compared with age-matched cells from control ... Online Mendelian Inheritance in Man (OMIM): V-ETS Avian Erythroblastosis virus E26 Oncogene Homolog 2 - 164740 Sumarsono SH, ... Online Mendelian Inheritance in Man (OMIM): V-ETS AVIAN ERYTHROBLASTOSIS VIRUS E26 ONCOGENE HOMOLOG 2; ETS2 - 164740, located ... Another gene, ETS2 is Avian Erythroblastosis Virus E26 Oncogene Homolog 2. Researchers have "demonstrated that over-expression ...
In cases of fetal distress and major degrees (traditional grade III and IV) a caesarean section is indicated. Caesarean section ... Smoking during pregnancy; cocaine use during pregnancy Women with a large placentae from twins or erythroblastosis are at ... Women may also present as a case of failure of engagement of fetal head. The exact cause of placenta previa is unknown. It is ... Complications for the baby may include fetal growth restriction. Risk factors include pregnancy at an older age and smoking as ...
The fetal skull is usually the largest part of the fetal body and its removal may require mechanical collapse if it is too ... is administered to prevent the risk of developing erythroblastosis fetalis (hemolytic disease of the newborn) in subsequent ... If the fetal presentation is not breech, forceps or manual manipulation can be used to turn it to a breech presentation while ... Fetal injection of digoxin or potassium chloride may be administered at the beginning of the procedure to allow for softening ...
More than two-thirds of fetal hepatic circulation is via the main portal vein, while the remainder is shunted from the left ... It may be used as a site for regular transfusion in cases of erythroblastosis or hemolytic disease. It also provides a route ... The umbilical vein is a vein present during fetal development that carries oxygenated blood from the placenta into the growing ... The unpaired umbilical vein carries oxygen and nutrient rich blood derived from fetal-maternal blood exchange at the chorionic ...
Hemolytic disease of the newborn (also known as HDN or erythroblastosis fetalis) Rh D hemolytic disease of the newborn (also ... Coombs test is used to screen pregnant women for IgG antibodies that are likely to pass through the placenta into the fetal ...
The discovery of cell-free fetal DNA in maternal circulation by Holzgrieve et al. led to the noninvasive genotyping of fetal Rh ... The disorder in the fetus due to Rh D incompatibility is known as erythroblastosis fetalis. Hemolytic comes from two words: " ... Levine P, Burnham L, Katzin E, Vogel P (December 1941). "The role of iso-immunization in the pathogenesis of erythroblastosis ... "hema" (blood) and "lysis" (solution) or breaking down of red blood cells Erythroblastosis refers to the making of immature red ...
Erythroblastosis fetalis and biliary atresia are diseases which may cause teeth to appear green from the deposition of ... and the periodontium must all develop during appropriate stages of fetal development. Primary teeth start to form in the ...
ClinicalTrials.gov: Erythroblastosis, Fetal (National Institutes of Health) * ClinicalTrials.gov: Rh Isoimmunization (National ... Fetal-maternal erythrocyte distribution blood test (Medical Encyclopedia) Also in Spanish * Hemolytic disease of the newborn ( ... Hydrops Fetalis/Erythroblastosis Fetalis (Childrens Hospital and Health System, Inc.) * Red Blood Cell Antibody Screen ( ...
ABO fetal erythroblastosis]. BEAUDRY JL. BEAUDRY JL. Lek Wojsk. 1961 Feb;31:191-219. Lek Wojsk. 1961. PMID: 13688303 French. No ... Fetal erythroblastosis]. BEAUDRY JL. BEAUDRY JL. Lek Wojsk. 1960 Nov;30:478-95. Lek Wojsk. 1960. PMID: 13688304 French. No ...
Hemolytic disease (erythroblastosis fetalis). Maternal-Fetal Medicine: Principles and Practice. 2nd ed. Philadelphia, Pa: WB ... The binding of maternal Rh antibodies produced after sensitization with fetal Rh-positive erythrocytes results in fetal ... The amount of fetal blood necessary to produce Rh incompatibility varies. In one study, less than 1 mL of Rh-positive blood was ... Non-invasive fetal RHD genotyping in the first trimester of pregnancy. Clin Chem Lab Med. 2010 Aug. 48(8):1121-6. [QxMD MEDLINE ...
This absence of fetal movement is significant only in the last few months of pregnancy; before this, failure to note fetal ... Certain abnormalities of the fetus -- including erythroblastosis; severe abnormalities of the heart, kidneys, and nervous ... Fetal death is usually brought to the doctors attention by the womans reporting that she has not felt the fetus move for a ... Today, most doctors choose to induce labor and deliver the fetus as soon as possible after the diagnosis of fetal death. This ...
... www.chw.org/medical-care/fetal-concerns-center/conditions/infant-complications/hydrops-fetalis-erythroblastosis-fetalis. ... Erythroblastosis Fetalis. Erythroblastosis fetalis causes the mothers white blood cells to attack her babys red blood cells ... Teratogens are drugs, chemicals, or even infections that can cause abnormal fetal development. Learn what teratogens to avoid ... Occasionally, a doctor may give the baby blood transfusions (intrauterine fetal blood transfusion) to help increase the chances ...
The risk of fetal injury increases with increasing number of puncture attempts. Maternal and fetal blood cells may mix during ... Nassar GN, Wehbe C (2022). "Erythroblastosis Fetalis". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 30020664. ... Lack of fetal lung maturity increases the risk of infant respiratory distress syndrome. Fetal lung development can be tested by ... Fetal viability after the procedure should be confirmed by observing adequate fetal cardiac activity. The number of needle ...
This condition in the child is called fetal erythroblastosis. Firstborn children are not threatened, because the mothers blood ... Fetal alcohol syndrome (FAS), identified in 1973, is perhaps one of the best known and best documented outcomes of drinking, ... In the past, erythroblastosis was always fatal, but now medical techniques can minimize the harmful effects of Rh ... The antibodies in the mothers blood will then cross the placenta into the fetal bloodstream and attack its Rh-positive red ...
fetal erythroblastosis - (Haemolytic Disease of the Newborn) A clinical term describing an immune response between fetal and ... Fetal Erythroblastosis. This disease is also called Haemolytic Disease of the Newborn, an immune problem from fetus Rh+ / ... A fetal malignancy that leads to an enlarged placenta, with tumor cells in the fetal circulation and rarely in the chorionic ... They can provide immune protection to the embryo, but may also participate in immune disease (fetal erythroblastosis). ...
Fetal characteristics of erythrocytes in sickle cell anemia: an immunofluorescence study of individual cells. Blood. 1979. 54: ... Kobberling J. [Cold agglutinin disease--initial description in erythroblastosis and polycythemia vera]. [German] Klinische ... antigen on the surface of fetal erythrocytes. These interactions occur at sites in which the body temperature is less that 37º ...
If a babys and mothers blood are incompatible, it can lead to fetal anemia, immune hydrops (erythroblastosis fetalis) and ...
Prediction of fetal anemia in rhesus disease by measurement of fetal middle cerebral artery peak systolic velocity. Ultrasound ... Erythroblastosis and reticulocytosis in anemic fetuses. Am J Obstet Gynecol 1988; 159:1063. ... Detection of fetal erythrocytes in maternal blood post partum with the fluorescence-activated cell sorter. Am J Obstet Gynecol ... Detection of fetal erythrocytes in maternal blood post partum with the fluorescence-activated cell sorter. Am J Obstet Gynecol ...
... as erythroblastosis neonatorum) caused by transplacental transmission of maternal antibodies to fetal... read more , and ... severe erythroblastosis fetalis Hemolytic Disease of the Fetus and Neonate Hemolytic disease of the fetus and neonate is ...
... as erythroblastosis neonatorum) caused by transplacental transmission of maternal antibodies to fetal... read more ). ... Fetal compromise (eg, fetal distress, death) or, if placental abruption is chronic, growth restriction or oligohydramnios ... However, the partial or complete separation of the placenta from the uterine wall compromises fetal oxygen exchange. Fetal ... Corticosteroids should be considered (to accelerate fetal lung maturity) if gestational age is < 34 weeks. Corticosteroids may ...
300 mcg (1,500 International Units) IM should be given for every 15 mL of fetal red blood cells (30 mL of fetal whole blood) ... Rh0 [D] immune globulin would not be effective in preventing erythroblastosis fetalis in the Rh0 [D]-negative mother who has ... 300 mcg (1,500 International Units) IM should be given for every 15 mL of fetal red blood cells (30 mL of fetal whole blood) ... Known or suspected massive fetomaternal hemorrhage (more than 15 mL fetal red blood cells or more than 30 mL fetal whole blood ...
Erythroblastosis, Fetal Entry term(s). Erythroblastoses, Fetal Erythroblastosis Fetali Erythroblastosis Fetalis Fetal ... Erythroblastoses, Fetal. Erythroblastosis Fetali. Erythroblastosis Fetalis. Fetal Erythroblastoses. Fetal Erythroblastosis. ... Fetal Erythroblastosis Fetali, Erythroblastosis Fetalis, Erythroblastosis Hemolytic Disease of Newborn Newborn Hemolytic ... Erythroblastosis, Fetal - Preferred Concept UI. M0007688. Scope note. A condition characterized by the abnormal presence of ...
Erythroblastosis, Fetal (MeSH) * Female (MeSH) * Fetomaternal Transfusion (MeSH) * Humans (MeSH) * Isoantibodies (MeSH) ...
fetal erythroblastosis DOID:1098 * peritoneal carcinoma DOID:1791 * biliary atresia DOID:13608 ...
Fetal evaluation of the modified-myocardial performance index in pregnancies complicated by diabetes. Figueroa, H., Silva, M. C ...
Fetal Erythroblastosis 26% * Fc Receptors 21% * Glycosylation 18% * Adaptive Immunity 18% * Therapeutics 17% ...
In 1932, Diamond and colleagues described the relationship among fetal hydrops, jaundice, anemia, and erythroblasts in the ... Hemolytic disease (erythroblastosis fetalis). Creasy RK, Resnik R. Maternal-fetal medicine. 4th edition. Philadelphia: WB ... Fetal anemia due to non-Rhesus-D red-cell alloimmunization. Semin Fetal Neonatal Med. 2008 Aug. 13(4):207-14. [QxMD MEDLINE ... Hydrops fetalis occurs when fetal Hb deficit exceeds 7 g/dL and starts as fetal ascites and evolves into pleural effusions and ...
Keywords: ERYTHROBLASTOSIS, FETAL - blood, immunology, therapy; KELL BLOOD-GROUP SYSTEM - immnunology; ISOANTIBODIES - blood ... Maternal IgG class antibodies cross the placenta into the fetal circulation and attach to the antigenic sites on the surface of ... Hemolytic disease of the newborn (HDN) is a consequence of the mothers alloimmunization towards fetal erythrocyte antigens. ...
... used to be a major cause of fetal loss and death among newborn babies until the 1950s. ... Bowman JM. Hemolytic disease (erythroblastosis fetalis). Creasy RK, Resnik R. Maternal-fetal medicine. 4th edition. ... Semin Fetal Neonatal Med. 2015 Nov 14.. Luchtman-Jones L, Schwartz AL, Wilson DB. The blood and hematopoietic system. Fanaroff ... The number of fetal red cells that enter the maternal circulation can be estimated with the Kleihauer test. ...
Fetal Erythroblastosis Medicine & Life Sciences 100% * Deficiency Diseases Medicine & Life Sciences 95% ...
erythroblastosis fe·ta·lis fi tal əs n a hemolytic disease of the fetus and newborn that is characterized by an increase in ... erythroblastosis fe,tal,is - «fih TAL ihs», erythroblastosis of the fetus: »Erythroblastosis fetalis occurs in about 10 per ... erythroblastosis fetalis - noun Etymology: New Latin, fetal erythroblastosis Date: circa 1934 a hemolytic disease of the fetus ... erythroblastosis neonatorum. Look at other dictionaries:. *. erythroblastosis fetalis - erythroblastosis fetalis. См. ...
... as erythroblastosis neonatorum) caused by transplacental transmission of maternal antibodies to fetal... read more . The ...

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