Erythroid Precursor Cells
Erythropoiesis
Erythroblasts
Erythropoietin
Erythroid Cells
Globins
Erythrocytes
Reticulocytes
Cell Differentiation
Hemoglobins
Cells, Cultured
beta-Thalassemia
Leukemia, Erythroblastic, Acute
Glycophorin
Bone Marrow
GATA1 Transcription Factor
Bone Marrow Cells
Reticulocytosis
Receptors, Erythropoietin
Erythroid-Specific DNA-Binding Factors
Colony-Forming Units Assay
Stem Cells
Hematopoiesis
Polycythemia Vera
Fetal Hemoglobin
Cell Lineage
beta-Globins
K562 Cells
Red-Cell Aplasia, Pure
Thalassemia
alpha-Globins
Cell Division
Molecular Sequence Data
Yolk Sac
Anemia, Sideroblastic
Antigens, CD34
RNA, Messenger
Receptors, Transferrin
Iron Radioisotopes
Base Sequence
Erythrocyte Aging
Friend murine leukemia virus
Transcription Factors
Anemia, Dyserythropoietic, Congenital
Stem Cell Factor
Anemia, Hemolytic
Flow Cytometry
Oligodendroglia
DNA-Binding Proteins
Leukemia, Experimental
Vulva
Gene Expression Regulation, Developmental
Apoptosis
Gene Expression Regulation
Myelodysplastic Syndromes
Mutation
Iron
Gene Expression
Amyloid beta-Protein Precursor
Heme
Fetus
Fetal Blood
Phenotype
Neural Stem Cells
Erythrocyte Membrane
Proto-Oncogene Proteins
Liver
Neurons
Amino Acid Sequence
Tumor Cells, Cultured
Basic Helix-Loop-Helix Transcription Factors
Macrophages
Signal Transduction
Mice, Transgenic
RNA Precursors
Granulocytes
gamma-Globins
Sustained induction of fetal hemoglobin by pulse butyrate therapy in sickle cell disease. (1/1023)
High levels of fetal hemoglobin (Hb F) protect from many of the complications of sickle cell disease and lead to improved survival. Butyrate and other short chain fatty acids were previously shown to increase Hb F production in erythroid cells in vitro and in animal models in vivo. However, butyrates are also known to inhibit the proliferation of many cell types, including erythroid cells. Experience with the use of butyrate in animal models and in early clinical trials demonstrated that the Hb F response may be lost after prolonged administration of high doses of butyrate. We hypothesized that this loss of response may be a result of the antiproliferative effects of butyrate. We designed a regimen consisting of intermittent or pulse therapy in which butyrate was administered for 4 days followed by 10 to 24 days with no drug exposure. This pulse regimen induced fetal globin gene expression in 9 of 11 patients. The mean Hb F in this group increased from 7.2% to 21.0% (P <.002) after intermittent butyrate therapy for a mean duration of 29.9 weeks. This was associated with a parallel increase in the number of F cells and F reticulocytes. The total hemoglobin levels also increased from a mean of 7.8 g/dL to a mean of 8.8 g/dL (P <.006). The increased levels of Hb F were sustained in all responders, including 1 patient who has been on pulse butyrate therapy for more than 28 months. This regimen, which resulted in a marked and sustained increase in Hb F levels in more than two thirds of the adult sickle cell patients enrolled in this study, was well tolerated without adverse side effects. These encouraging results require confirmation along with an appropriate evaluation of clinical outcomes in a larger number of patients with sickle cell disease. (+info)Use of altered specificity mutants to probe a specific protein-protein interaction in differentiation: the GATA-1:FOG complex. (2/1023)
GATA-1 and FOG (Friend of GATA-1) are each essential for erythroid and megakaryocyte development. FOG, a zinc finger protein, interacts with the amino (N) finger of GATA-1 and cooperates with GATA-1 to promote differentiation. To determine whether this interaction is critical for GATA-1 action, we selected GATA-1 mutants in yeast that fail to interact with FOG but retain normal DNA binding, as well a compensatory FOG mutant that restores interaction. These novel GATA-1 mutants do not promote erythroid differentiation of GATA-1- erythroid cells. Differentiation is rescued by the second-site FOG mutant. Thus, interaction of FOG with GATA-1 is essential for the function of GATA-1 in erythroid differentiation. These findings provide a paradigm for dissecting protein-protein associations involved in mammalian development. (+info)Angiogenesis defects and mesenchymal apoptosis in mice lacking SMAD5. (3/1023)
The transforming growth factor-beta (TGF-beta) signals are mediated by a family of at least nine SMAD proteins, of which SMAD5 is thought to relay signals of the bone morphogenetic protein (BMP) pathway. To investigate the role of SMAD5 during vertebrate development and tumorigenesis, we disrupted the Smad5 gene by homologous recombination. We showed that Smad5 was expressed predominantly in mesenchyme and somites during embryogenesis, and in many tissues of the adult. Mice homozygous for the mutation died between days 10.5 and 11.5 of gestation due to defects in angiogenesis. The mutant yolk sacs lacked normal vasculature and had irregularly distributed blood cells, although they contained hematopoietic precursors capable of erythroid differentiation. Smad5 mutant embryos had enlarged blood vessels surrounded by decreased numbers of vascular smooth muscle cells, suffered massive apoptosis of mesenchymal cells, and were unable to direct angiogenesis in vitro. These data suggest that SMAD5 may regulate endothelium-mesenchyme interactions during angiogenesis and that it is essential for mesenchymal survival. (+info)FLI-1 inhibits differentiation and induces proliferation of primary erythroblasts. (4/1023)
Friend virus-induced erythroleukemia involves two members of the ETS family of transcriptional regulators, both activated via proviral insertion in the corresponding loci. Spi-1/PU.1 is expressed in the disease induced by the original Friend virus SFFV(F-MuLV) complex in adult mice. In contrast, FLI-1 is overexpressed in about 75% of the erythroleukemias induced by the F-MuLV helper virus in newborn mice. To analyse the consequences of the enforced expression of FLI-1 on erythroblast differentiation and proliferation and to compare its activity to that of PU.1/Spi-1, we used a heterologous system of avian primary erythroblasts previously described to study the cooperation between Spi-1/PU.1 and the other molecular alterations observed in SFFV-induced disease. FLI-1 was found: (i) to inhibit the apoptotic cell death program normally activated in erythroblasts following Epo deprivation; (ii) to inhibit the terminal differentiation program induced in these cells in response to Epo and; (iii) to induce their proliferation. However, in contrast to Spi-1/PU.1, the effects of FLI-1 on erythroblast, differentiation and proliferation did not require its cooperation with an abnormally activated form of the EpoR. Enhanced survival of FLI-1 expressing erythroblasts correlated with the upregulation of bcl2 expression. FLI-1 also prevented the rapid downregulation of cyclin D2 and D3 expression normally observed during Epo-induced differentiation and delayed the downregulation of several other genes involved in cell cycle or cell proliferation control. Our results show that overexpression of FLI-1 profoundly deregulates the normal balance between differentiation and proliferation in primary erythroblasts. Thus, the activation of FLI-1 expression observed at the onset of F-MuLV-induced erythroleukemia may provide a proliferative advantage to virus infected cells that would otherwise undergo terminal differentiation or cell death. (+info)Correction for erythroid cell contamination in microassay for immunophenotyping of neonatal lymphocytes. (5/1023)
Immunophenotyping of blood lymphocyte subpopulations in neonates and young infants is hampered by the limited amount of blood that can be collected. Contamination of the flow cytometric "lympho-gate" by normoblasts and analysed erythrocytes, and therefore the underestimation of the relative frequencies of lymphocyte subpopulations, interferes with the precise calculation of absolute counts. A microassay was developed by adapting the lysed whole blood technique. Triple immunostaining in a single antibody staining step was used to reduce washing steps and cell loss. Introduction of a triple staining for CD71 (expressed by erythroid precursors), glycophorin A (GpA, expressed by all erythroid cells), and CD45 (expressed by all leucocytes) permitted the relative frequencies of normoblasts (CD71(+)/GpA+/CD45(-) population) and unlysed erythrocytes (CD71(-)/GpA+/CD45(-) population)to be identified and measured within the "lympho-gate" of neonatal cord blood samples. Particularly high frequencies were found (median: 31%) in cord blood samples from preterm neonates. These erythroid cells disappear rapidly by 1 week of age The relative frequencies of erythroid cells can be used to calculate correct lymphocyte subpopulation values. Using only 0.5-0.8 ml of blood, this micro- assay would also be suitable for rapid prenatal immunodiagnosis of congenital immunodeficiencies. (+info)Insulin-like growth factor I plays a role in regulating erythropoiesis in patients with end-stage renal disease and erythrocytosis. (6/1023)
Erythroid progenitor growth, the serum hormones that regulate erythropoiesis, and the effect of patient's serum on the growth of normal erythroid progenitors were assessed in eight patients with end-stage renal disease (ESRD) and erythrocytosis. All patients were male and had been on maintenance dialysis, they had a hematocrit >50% and/or a red blood cell count >6 x 10(12)/L and an arterial oxygen saturation >95%. Four had acquired cystic disease of the kidney (ACDK), and four other non-ACDK patients did not have known causes of secondary erythrocytosis after appropriate investigations and long-term follow-up. The methylcellulose culture technique was used to assay the erythroid progenitor (BFU-E/CFU-E) growth. Serum erythropoietin (EPO) and insulin-like growth factor I (IGF-I) levels were measured by RIA. Paired experiments were performed to determine the effects of 10% sera from ESRD patients and control subjects on normal marrow CFU-E growth. The numbers of EPO-dependent BFU-E in marrow and/or blood of patients with ESRD and erythrocytosis were higher than those of normal controls. No EPO-independent erythroid colonies were found. Serum EPO levels were constantly normal in one patient and elevated in three patients with ACDK; for non-ACDK patients, EPO levels were normal or low in two patients and persistently increased in one, but fluctuated in the remaining one on serial assays. There was no correlation between serum EPO levels and hematocrit values. The serum IGF-I levels in patients with ESRD and erythrocytosis were significantly increased compared with normal subjects or ESRD patients with anemia. We found an inverse correlation between serum EPO and IGF-I levels. Sera from patients with ESRD and erythrocytosis exhibited a stimulating effect on normal marrow CFU-E growth. The stimulating effect of sera from patients who had a normal serum EPO level and an elevated IGF-I level could be partially blocked by anti-IGF-I. The present study suggests that IGF-I plays an important role in the regulation of erythropoiesis in patients with ESRD and erythrocytosis who did not have an increased EPO production. (+info)c-kitUsing Ly5 congenic mice, we characterized the early differentiation step of pluripotent hemopoietic stem cells. Lineage- (Lin-)/CD71- cells in the bone marrow cells were separated into major histocompatibility complex (MHC) class I(high)/c-kit(low) and MHC class I(high)/c-kit+info)
Apoptosis of erythroid precursors under stimulation with thrombopoietin: contribution to megakaryocytic lineage choice.
(8/1023)
Although the effect of thrombopoietin (TPO) on megakaryocyte production is well established, its role in the commitment of multipotential hematopoietic progenitors to the megakaryocytic lineage remains to be determined. In the present study, we attempted to clarify the determination process of megakaryocytic lineage as a terminal differentiation pathway under stimulation with TPO. Day 7 cultured cells grown by TPO derived from cord blood CD34+ cells were divided into four subpopulations on the basis of CD34 and CD41 expression. The CD34-/CD41- cells showed the labeling pattern of anti-CD42b and anti-CD9 antibodies closer to that of the CD34+/CD41- cells than the CD34+/CD41+ cells. Replating experiments revealed that approximately 40% of the CD34-/CD41- cells proliferated in response to a combination of growth factors, and more than 80% of them were pure erythroid precursors. However, this subpopulation failed to grow/survive and fell into apoptosis in the presence of TPO alone. In contrast, the CD34+/CD41+ cells, which predominantly contained megakaryocytic precursors, exerted a low but significant proliferative potential in the presence of TPO. The insufficient response to TPO of the CD34-/CD41- cells may result from the apparently low expression of c-MpI, as determined by flow cytometric analysis and reverse transcription-polymerase chain reaction analysis. Therefore, these results suggest that the apoptosis of hematopoietic precursors other than megakaryocytic precursors is related to the determination of the terminal differentiation under the influence of TPO. (+info)
Apoptosis of erythroid precursors under stimulation with thrombopoietin: contribution to megakaryocytic lineage choice. (8/1023)
Although the effect of thrombopoietin (TPO) on megakaryocyte production is well established, its role in the commitment of multipotential hematopoietic progenitors to the megakaryocytic lineage remains to be determined. In the present study, we attempted to clarify the determination process of megakaryocytic lineage as a terminal differentiation pathway under stimulation with TPO. Day 7 cultured cells grown by TPO derived from cord blood CD34+ cells were divided into four subpopulations on the basis of CD34 and CD41 expression. The CD34-/CD41- cells showed the labeling pattern of anti-CD42b and anti-CD9 antibodies closer to that of the CD34+/CD41- cells than the CD34+/CD41+ cells. Replating experiments revealed that approximately 40% of the CD34-/CD41- cells proliferated in response to a combination of growth factors, and more than 80% of them were pure erythroid precursors. However, this subpopulation failed to grow/survive and fell into apoptosis in the presence of TPO alone. In contrast, the CD34+/CD41+ cells, which predominantly contained megakaryocytic precursors, exerted a low but significant proliferative potential in the presence of TPO. The insufficient response to TPO of the CD34-/CD41- cells may result from the apparently low expression of c-MpI, as determined by flow cytometric analysis and reverse transcription-polymerase chain reaction analysis. Therefore, these results suggest that the apoptosis of hematopoietic precursors other than megakaryocytic precursors is related to the determination of the terminal differentiation under the influence of TPO. (+info)There are two main types of beta-thalassemia:
1. Beta-thalassemia major (also known as Cooley's anemia): This is the most severe form of the condition, and it can cause serious health problems and a shortened lifespan if left untreated. Children with this condition are typically diagnosed at birth or in early childhood, and they may require regular blood transfusions and other medical interventions to manage their symptoms and prevent complications.
2. Beta-thalassemia minor (also known as thalassemia trait): This is a milder form of the condition, and it may not cause any noticeable symptoms. People with beta-thalassemia minor have one mutated copy of the HBB gene and one healthy copy, which allows them to produce some normal hemoglobin. However, they may still be at risk for complications such as anemia, fatigue, and a higher risk of infections.
The symptoms of beta-thalassemia can vary depending on the severity of the condition and the age of onset. Common symptoms include:
* Fatigue
* Weakness
* Pale skin
* Shortness of breath
* Frequent infections
* Yellowing of the skin and eyes (jaundice)
* Enlarged spleen
Beta-thalassemia is most commonly found in people of Mediterranean, African, and Southeast Asian ancestry. It is caused by mutations in the HBB gene, which is inherited from one's parents. There is no cure for beta-thalassemia, but it can be managed with blood transfusions, chelation therapy, and other medical interventions. Bone marrow transplantation may also be a viable option for some patients.
In conclusion, beta-thalassemia is a genetic disorder that affects the production of hemoglobin, leading to anemia, fatigue, and other complications. While there is no cure for the condition, it can be managed with medical interventions and bone marrow transplantation may be a viable option for some patients. Early diagnosis and management are crucial in preventing or minimizing the complications of beta-thalassemia.
Erythroleukemia typically affects adults in their 50s and 60s, although it can occur at any age. Symptoms may include fever, night sweats, weight loss, and fatigue. The cancer cells can spread to other parts of the body, including the spleen, liver, and lymph nodes.
Erythroleukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore normal blood cell production. In some cases, a bone marrow transplant may be necessary. The prognosis for erythroleukemia is generally poor, with a five-year survival rate of about 20%.
Erythroleukemia is classified as an acute leukemia, meaning it progresses rapidly and can lead to life-threatening complications if left untreated. It is important for patients to receive prompt and appropriate treatment to improve their chances of survival and quality of life.
The term "reticulocytosis" is derived from the Latin words "reticulum," meaning net-like, and "cytosis," meaning the condition of cells. This refers to the characteristic net-like appearance of reticulocytes under a microscope.
There are several possible causes of reticulocytosis, including:
1. Inherited disorders such as hereditary elliptocytosis, hereditary spherocytosis, and pyruvate kinase (PK) deficiency.
2. Acquired disorders such as hemolytic anemia, thalassemia, and sickle cell disease.
3. Infections such as malaria, dengue fever, and babesiosis.
4. Medications such as antibiotics, chemotherapy drugs, and anti-inflammatory medications.
5. Other conditions such as chronic kidney disease, liver disease, and autoimmune disorders.
Reticulocytosis can be diagnosed through a blood test called a complete blood count (CBC) or a reticulocyte count. Treatment depends on the underlying cause of the condition. In some cases, no treatment may be necessary, while in other cases, medication or blood transfusions may be required.
There are three main types of polycythemia:
1. Polycythemia vera (PV): This is the most common type and is characterized by an overproduction of red blood cells, white blood cells, and platelets. It is a slowly progressing disease that can lead to complications such as blood clots, bleeding, and an increased risk of cancer.
2. Essential thrombocythemia (ET): This type is characterized by an overproduction of platelets, which can increase the risk of blood clots and other cardiovascular problems.
3. Primary myelofibrosis (PMF): This type is characterized by bone marrow scarring, anemia, fatigue, and an increased risk of blood clots.
Symptoms of polycythemia may include:
* Headache
* Dizziness
* Fatigue
* Shortness of breath
* Pale skin
* Swelling in the spleen or liver
Diagnosis is based on a physical examination, medical history, and laboratory tests such as complete blood counts (CBCs) and bone marrow biopsies. Treatment options for polycythemia include:
1. Phlebotomy (removal of blood): This is the most common treatment for PV and ET, which involves removing excess blood to reduce the number of red blood cells, white blood cells, and platelets.
2. Chemotherapy: This may be used in combination with phlebotomy to treat PV and PMF.
3. Hydroxyurea: This medication is used to reduce the production of blood cells and relieve symptoms such as headache and dizziness.
4. Interferons: These medications are used to treat ET and may be effective in reducing the number of platelets.
5. Stem cell transplantation: In severe cases of PV or PMF, a stem cell transplant may be necessary.
It is important to note that these treatments do not cure polycythemia, but they can help manage symptoms and slow the progression of the disease. Regular monitoring and follow-up with a healthcare provider is essential to ensure the best possible outcomes.
The exact cause of polycythemia vera is not known, but it is believed to be due to a genetic mutation in the JAK2 gene, which is involved in the signaling pathways that regulate blood cell production. The condition typically affects adults over the age of 60 and is more common in men than women.
Symptoms of polycythemia vera can include:
* Fatigue
* Weakness
* Shortness of breath
* Headaches
* Dizziness
* Itching
* Night sweats
* Weight loss
Diagnosis of polycythemia vera is typically made based on a combination of physical examination, medical history, and laboratory tests, including:
* Complete blood count (CBC) to measure the levels of red blood cells, white blood cells, and platelets
* Blood chemistry tests to assess liver function and other body chemicals
* Genetic testing to look for the JAK2 mutation
* Bone marrow biopsy to examine the bone marrow tissue for abnormalities
Treatment for polycythemia vera usually involves phlebotomy (the removal of blood from the body) to reduce the number of red blood cells and relieve symptoms such as itching and night sweats. In some cases, medications may be used to reduce the production of blood cells or to treat specific symptoms. Regular monitoring by a healthcare provider is important to detect any changes in the condition and to prevent complications.
Overall, polycythemia vera is a chronic and progressive disease that can have significant impact on quality of life if left untreated. Early diagnosis and appropriate treatment can help manage symptoms and improve outcomes for patients with this condition.
The symptoms of RCPA can vary depending on the severity of the condition and may include:
* Severe anemia
* Fatigue
* Pale skin
* Shortness of breath
* Increased risk of bleeding
Diagnosis of RCPA typically involves a combination of physical examination, medical history, and laboratory tests, including blood counts, genetic analysis, and bone marrow aspiration. Treatment for RCPA may involve blood transfusions, iron chelation therapy, and in some cases, hematopoietic stem cell transplantation.
The prognosis for RCPA is generally poor, with a high risk of bleeding and death in early childhood if left untreated. However, with timely diagnosis and appropriate treatment, patients with RCPA can have a good quality of life and a normal lifespan.
There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia. Alpha-thalassemia is caused by abnormalities in the production of the alpha-globin chain, which is one of the two chains that make up hemoglobin. Beta-thalassemia is caused by abnormalities in the production of the beta-globin chain.
Thalassemia can cause a range of symptoms, including anemia, fatigue, pale skin, and shortness of breath. In severe cases, it can lead to life-threatening complications such as heart failure, liver failure, and bone deformities. Thalassemia is usually diagnosed through blood tests that measure the levels of hemoglobin and other proteins in the blood.
There is no cure for thalassemia, but treatment can help manage the symptoms and prevent complications. Treatment may include blood transfusions, folic acid supplements, and medications to reduce the severity of anemia. In some cases, bone marrow transplantation may be recommended.
Preventive measures for thalassemia include genetic counseling and testing for individuals who are at risk of inheriting the disorder. Prenatal testing is also available for pregnant women who are carriers of the disorder. In addition, individuals with thalassemia should avoid marriage within their own family or community to reduce the risk of passing on the disorder to their children.
Overall, thalassemia is a serious and inherited blood disorder that can have significant health implications if left untreated. However, with proper treatment and management, individuals with thalassemia can lead fulfilling lives and minimize the risk of complications.
There are many different types of anemia, each with its own set of causes and symptoms. Some common types of anemia include:
1. Iron-deficiency anemia: This is the most common type of anemia and is caused by a lack of iron in the diet or a problem with the body's ability to absorb iron. Iron is essential for making hemoglobin.
2. Vitamin deficiency anemia: This type of anemia is caused by a lack of vitamins, such as vitamin B12 or folate, that are necessary for red blood cell production.
3. Anemia of chronic disease: This type of anemia is seen in people with chronic diseases, such as kidney disease, rheumatoid arthritis, and cancer.
4. Sickle cell anemia: This is a genetic disorder that affects the structure of hemoglobin and causes red blood cells to be shaped like crescents or sickles.
5. Thalassemia: This is a genetic disorder that affects the production of hemoglobin and can cause anemia, fatigue, and other health problems.
The symptoms of anemia can vary depending on the type and severity of the condition. Common symptoms include fatigue, weakness, pale skin, shortness of breath, and dizziness or lightheadedness. Anemia can be diagnosed with a blood test that measures the number and size of red blood cells, as well as the levels of hemoglobin and other nutrients.
Treatment for anemia depends on the underlying cause of the condition. In some cases, dietary changes or supplements may be sufficient to treat anemia. For example, people with iron-deficiency anemia may need to increase their intake of iron-rich foods or take iron supplements. In other cases, medical treatment may be necessary to address underlying conditions such as kidney disease or cancer.
Preventing anemia is important for maintaining good health and preventing complications. To prevent anemia, it is important to eat a balanced diet that includes plenty of iron-rich foods, vitamin C-rich foods, and other essential nutrients. It is also important to avoid certain substances that can interfere with the absorption of nutrients, such as alcohol and caffeine. Additionally, it is important to manage any underlying medical conditions and seek medical attention if symptoms of anemia persist or worsen over time.
In conclusion, anemia is a common blood disorder that can have significant health implications if left untreated. It is important to be aware of the different types of anemia, their causes, and symptoms in order to seek medical attention if necessary. With proper diagnosis and treatment, many cases of anemia can be successfully managed and prevented.
The symptoms of sideroblastic anemia can vary depending on the severity of the condition, but may include fatigue, weakness, pale skin, shortness of breath, and a rapid heart rate. Treatment options for sideroblastic anemia typically involve addressing the underlying genetic cause of the condition, such as through gene therapy or enzyme replacement therapy, and managing symptoms with medication and lifestyle modifications.
In summary, sideroblastic anemia is a rare inherited disorder characterized by abnormalities in iron metabolism that can lead to impaired red blood cell production and various other symptoms. It is important for individuals with this condition to receive timely and appropriate medical attention to manage their symptoms and prevent complications.
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Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, dizziness, headaches, and pale or yellowish skin. Treatment options depend on the underlying cause but may include blood transfusions, medication to suppress the immune system, antibiotics for infections, and removal of the spleen (splenectomy) in severe cases.
Prevention strategies for hemolytic anemia include avoiding triggers such as certain medications or infections, maintaining good hygiene practices, and seeking early medical attention if symptoms persist or worsen over time.
It is important to note that while hemolytic anemia can be managed with proper treatment, it may not be curable in all cases, and ongoing monitoring and care are necessary to prevent complications and improve quality of life.
Examples of experimental leukemias include:
1. X-linked agammaglobulinemia (XLA): A rare inherited disorder that leads to a lack of antibody production and an increased risk of infections.
2. Diamond-Blackfan anemia (DBA): A rare inherited disorder characterized by a failure of red blood cells to mature in the bone marrow.
3. Fanconi anemia: A rare inherited disorder that leads to a defect in DNA repair and an increased risk of cancer, particularly leukemia.
4. Ataxia-telangiectasia (AT): A rare inherited disorder characterized by progressive loss of coordination, balance, and speech, as well as an increased risk of cancer, particularly lymphoma.
5. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21, which increases the risk of developing leukemia, particularly acute myeloid leukemia (AML).
These experimental leukemias are often used in research studies to better understand the biology of leukemia and to develop new treatments.
There are several subtypes of MDS, each with distinct clinical features and prognosis. The most common subtype is refractory anemia with excess blasts (RAEB), followed by chronic myelomonocytic leukemia (CMMoL) and acute myeloid leukemia (AML).
The exact cause of MDS is not fully understood, but it is believed to result from a combination of genetic mutations and environmental factors. Risk factors for developing MDS include exposure to certain chemicals or radiation, age over 60, and a history of previous cancer treatment.
Symptoms of MDS can vary depending on the specific subtype and severity of the disorder, but may include fatigue, weakness, shortness of breath, infection, bleeding, and easy bruising. Diagnosis is typically made through a combination of physical examination, medical history, blood tests, and bone marrow biopsy.
Treatment for MDS depends on the specific subtype and severity of the disorder, as well as the patient's overall health and preferences. Options may include supportive care, such as blood transfusions and antibiotics, or more intensive therapies like chemotherapy, bone marrow transplantation, or gene therapy.
Overall, myelodysplastic syndromes are a complex and heterogeneous group of disorders that can have a significant impact on quality of life and survival. Ongoing research is focused on improving diagnostic accuracy, developing more effective treatments, and exploring novel therapeutic approaches to improve outcomes for patients with MDS.
Tom Maniatis
Erythropoietin receptor
Erythropoietin
Bcl-xL
TACC3
Peter Klinken
Mir-223
Induced stem cells
VEXAS syndrome
Refractory cytopenia of childhood
Hydroxycarbamide
UBE1C
Diamond-Blackfan anemia
Let-7 microRNA precursor
Chronic neutrophilic leukemia
Anemia of chronic disease
Ghosal hematodiaphyseal dysplasia
Transferrin
List of MeSH codes (A11)
Fanconi anemia
Red blood cell
CFU-E
Transferrin receptor 1
Hematopoietic stem cell niche
Histiocytoma (dog)
Malignant histiocytosis
Granulocyte-macrophage colony-stimulating factor receptor
Acute leukemia
Megaloblastic anemia
Parvovirus B19
MicroRNA 210
David Schlessinger (geneticist)
ALOX15
CASS4
William Vainchenker
FANCA
Tumors of the hematopoietic and lymphoid tissues
Polycythemia vera
Stem cell marker
List of MeSH codes (A15)
HK2
Arsenic biochemistry
Erythropoietin in neuroprotection
Mir-451 microRNA
Acetylcholinesterase
Acute erythroid leukemia
Bone marrow
Biochemical cascade
Dimethyl fumarate
Jane Sowden
Tomas Ganz
ABCB7
Pernicious Anemia: Practice Essentials, Pathophysiology, Etiology
Current Trends
Risks Associated with Human Parvovirus B19 Infection
Publication Detail
Anemia Workup: Approach Considerations, Investigation for Pathogenesis, Evaluation for Blood Loss
PA-13-034: Erythropoiesis: Components and Mechanisms (R01)
Spleen - Extramedullary Hematopoiesis - Nonneoplastic Lesion Atlas
Current Trends Risks Associated with Human Parvovirus B19 Infection
Extramedullary Hematopoiesis (EMH) - The Digitized Atlas of Mouse Liver Lesions
Anemia of Chronic Disease and Kidney Failure: Overview, Mechanism of Anemia of Chronic Disease, Prevalence of Anemia of Chronic...
Publications - Tracey Rouault Lab | NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development
Red Blood cell and Bleeding Disorders.pdf
NIH Clinical Center Search the Studies: Study Number, Study Title
Thymic Precursor Cells Generate Acute Myeloid Leukemia in NP23-NHD13 Double Transgenic Mice | NIH Research Festival
mDYRK3 kinase is expressed selectively in late erythroid progenitor cells and attenuates colony-forming unit-erythroid...
BTK (Bruton agammaglobulinemia tyrosine kinase)
DeCS
Ankyrin Mutations in Hereditary Spherocytosis | Acta Haematologica | Karger Publishers
MeSH Browser
JCI -
Bone marrow adipogenic lineage precursors promote osteoclastogenesis in bone remodeling and pathologic bone loss
Pesquisa | Portal Regional da BVS
British Journal of Haematology | Scholars@Duke
Erythropoietin(EPO) - Meaning, Functions, Test, Treatment and FAQs
US Patent for Treatment of sickle cell disease Patent (Patent # 10,085,967 issued October 2, 2018) - Justia Patents Search
GATA1 gene: MedlinePlus Genetics
Fostering Stem Cell Research at NIH | NIH Intramural Research Program
Megaloblasts | Profiles RNS
DeCS 2016 - June 12, 2016 version
DailyMed - REBLOZYL- luspatercept injection, powder, lyophilized, for solution
Succinate Accumulation Links Mitochondrial MnSOD Depletion to Aberrant Nuclear DNA Methylation and Altered Cell Fate
Myeloid and erythroid3
- However, the knockdown embryos had significantly fewer myeloid and erythroid progenitor cells. (zfin.org)
- These results demonstrate that NP23-NHD13 thymic progenitors retain myeloid and erythroid potential and are potently leukemogenic. (nih.gov)
- A, top) represents normal adult bone marrow, showing multinucleated megakaryocytes and myeloid and erythroid precursors distributed in a matrix containing adipocytes. (mhmedical.com)
Progenitor cell2
- B) Representative images of CFU assay plates demonstrating a marked reduction in erythroid colonies in the presence of IFN-γ and restoration of erythroid progenitor cell formation with higher concentrations of EPO in culture. (nih.gov)
- These results indicate that Fgf21 is a newly identified factor essential for the determination of myelo-erythroid progenitor cell fate in vivo. (zfin.org)
Differentiation21
- Components include genes that are expressed (transcriptome) in erythroid cells, either during development or during differentiation, chemical changes to DNA and histone proteins (epigenome) and the proteins (proteome) that are translated in erythroid cells, including post-translational modifications or subcellular localizations that are unique to erythroid cells. (nih.gov)
- Cells were expanded in erythroid differentiation medium (containing SCF, IL-3, and EPO 1, 16 or 64 IU/mL), with or without IFN-γ for 7 days. (nih.gov)
- Following differentiation, cells were collected and the impact of IFN-γ on erythroid progenitors (BFU-E and CFU-E) was assessed by CFU assay. (nih.gov)
- Treatment of the CHRF-288-11 infected cells with phorbol esters, which induces megakaryocytic differentiation, increases expression of the lacZ transgene. (nih.gov)
- Overall, these results demonstrate the feasibility and provide a method for infecting cultured megakaryocytic cell lines with retroviral of vectors such that a molecular analysis of megakaryocyte differentiation can be accomplished. (nih.gov)
- Thus, lack of BTK or expression of dominant-negative BTK splice variants in B cell precursor leukemia cells can inhibit differentiation beyond the pre-B cell stage and protect from radiation-induced apoptosis. (atlasgeneticsoncology.org)
- The kidney can generate and secrete erythropoietin in hypoxic conditions to increase red blood cell development by targeting CFU-E, proerythroblast, and basophilic erythroblast subsets in differentiation. (vedantu.com)
- The colony-forming unit erythroid (CFU-E) stage expresses the highest level of erythropoietin receptor density and is entirely reliant on erythropoietin for differentiation. (vedantu.com)
- By binding to DNA and interacting with other proteins, the GATA1 protein regulates the growth and division (proliferation) of immature red blood cells and platelet-precursor cells (megakaryocytes) to facilitate their specialization (differentiation). (medlineplus.gov)
- This impairment in the GATA1 protein's normal function leads to increased proliferation, decreased differentiation, and premature death of immature blood cells. (medlineplus.gov)
- A lack of differentiation causes a shortage of red blood cells (anemia) and platelets involved in blood clotting (thrombocytopenia), which are characteristic features of dyserythropoietic anemia and thrombocytopenia. (medlineplus.gov)
- Human neural progenitor cells were isolated under selective culture conditions from the developing human brain and directed through lineage differentiation to astrocytes. (nih.gov)
- Microscopic examination over the course of differentiation showed loss of progenitor cells as the cell population increasingly became astrocytes. (nih.gov)
- Stadtman Investigator Ramiro Iglesias-Bartolome (National Cancer Institute, NCI) is elucidating the signaling mechanisms that control and drive tissue-specific stem-cell self-renewal and differentiation and their connections to tumor initiation and growth. (nih.gov)
- He described his team's work exploring the regulation of epithelial stem-cell differentiation and proliferation by heterotrimeric guanine nucleotide-binding (G) proteins. (nih.gov)
- His team is further investigating the role of coupled GPCRs in the regulation of stem-cell differentiation and proliferation in the skin. (nih.gov)
- Since MnSOD has significant effects on SDH activity, and succinate is a key regulator of TET enzymes needed for proper differentiation, we hypothesized that SOD 2 loss would lead to succinate accumulation, inhibition of TET activity, and impaired erythroid precursor differentiation. (scientificarchives.com)
- To test this hypothesis, we genetically disrupted the SOD 2 gene using the CRISPR/Cas9 genetic strategy in a human erythroleukemia cell line (HEL 92.1.7) capable of induced differentiation toward an erythroid phenotype. (scientificarchives.com)
- Differentiation of adult hematopoietic stem cells (HSC) constantly produces the cell types of the blood and immune system. (pluto.bio)
- The dynamics of this process and the hierarchy of downstream oligopotent stem cell differentiation remain controversial. (pluto.bio)
- This suggests a model in which more than one differentiation trajectory can link HSC to several cell types. (pluto.bio)
Megakaryocyte precursor cells2
- There have been no reports, to date, of successful introduction of foreign DNA into committed megakaryocyte precursor cells. (nih.gov)
- TAM is characterized by the accumulation of immature megakaryocyte precursor cells in the blood, liver, and bone marrow. (medlineplus.gov)
Progenitors2
- Erythropoietin's primary effect is to promote the survival of red blood cell progenitors and precursors (which are located in the bone marrow of humans) by shielding them from apoptosis, or cell death. (vedantu.com)
- Erythropoietin is the main erythropoietic factor that works with a variety of other growth factors (such as IL-3, IL-6, glucocorticoids, and SCF) to help multipotent progenitors evolve into erythroid lineages. (vedantu.com)
Lineages3
- A long range goal of this program is to generate a concise description of erythropoiesis that unifies genetics, molecular processes and cytokine determinants in the erythroid lineages so that new therapeutics may be developed to measure and combat anemia. (nih.gov)
- BTK is expressed in all cell lineages of the hematopoietic system, except for T cells. (atlasgeneticsoncology.org)
- Analysis of initial HSC commitment defines marked bifurcation of erythroid/megakaryocytic cells from myeloid/lymphoid lineages. (pluto.bio)
Erythroblasts2
- Proerythroblasts and basophilic erythroblasts, which are precursors to red cells, express the erythropoietin receptor and are thus impaired by it. (vedantu.com)
- Red blood cell precursors, corresponding to ERYTHROBLASTS, that are larger than normal, usually resulting from a FOLIC ACID DEFICIENCY or VITAMIN B 12 DEFICIENCY. (uams.edu)
Megakaryocytes1
- In human hematopoiesis, the bone-marrow cells-megakaryocytes and erythroid cells-differentiate from a shared precursor, the megakaryocyte-erythroid progenitor (MEP). (nih.gov)
Hemolysis2
- The excess unpaired alpha-globin chains aggregate to form precipitates that damage red cell membranes, resulting in intravascular hemolysis. (medscape.com)
- This impairment leads to ineffective RBC production and intramedullary hemolysis that is characterized by large cells with arrested nuclear maturation. (lecturio.com)
Platelets4
- She was transfused with two units packed red cells and one adult dose of platelets. (wikidoc.org)
- Therefore BTK expression is found in B lymphocytes, platelets, erythroid and myeloid cells (monocytes, macrophages, granulocytes and dendritic cells). (atlasgeneticsoncology.org)
- The Sickled-shaped erythrocytes together with endothelial cells, activated leukocytes, platelets and plasma proteins participate in the multistep vaso-occlusion process (Frenette 2002). (justia.com)
- Red blood cells help carry oxygen to various tissues throughout the body and platelets aid in blood clotting. (medlineplus.gov)
Differentiate4
- DN thymocytes from non-leukemic mice were cultured on an OP9 stromal layer and showed markedly enhanced ability to differentiate into myeloid lineage cells compared to WT. (nih.gov)
- To function properly, these immature cells must differentiate into specific types of mature blood cells. (medlineplus.gov)
- David Bodine (National Human Genome Research Institute) focuses on hematopoiesis (formation of blood cells) and erythropoiesis (the regenerative process in which undifferentiated hematopoietic cells differentiate into red blood cells). (nih.gov)
- Finally, when stimulated with δ-aminolevulonic acid (δ-ALA), SOD 2 -/- - HEL cells failed to properly differentiate toward an erythroid phenotype, likely due to failure to complete the necessary global DNA demethylation program required for erythroid maturation. (scientificarchives.com)
Maturation3
- Anemia: Overview and Types is a subset of macrocytic anemias characterized by increased RBC size and an arrest in nuclear maturation arising from abnormal cell division Cell Division A type of cell nucleus division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. (lecturio.com)
- maturation and cell death. (scirp.org)
- The GATA1 protein is also important for the maturation of several types of white blood cells that help fight infection, including eosinophils, mast cells, and dendritic cells. (medlineplus.gov)
Proliferation5
- CD71 plays a role in the control of cellular proliferation by facilitating the uptake of iron via ferrotransferrin binding and the recycling of apotransferrin to the cell surface. (biolegend.com)
- however, severe myeloid cell proliferation may resemble granulocytic leukemia histologically. (nih.gov)
- Previous terms include "hematopoietic cell proliferation," "myeloid hyperplasia," and "erythroid hyperplasia. (nih.gov)
- In contrast, Fgf21 had no significant effect on cell proliferation and apoptosis in the intermediate cell mass. (zfin.org)
- Acute lymphoblastic leukaemia in childhood: cell proliferation without rest. (duke.edu)
Erythropoietin8
- Co-operative signalling mechanisms required for erythroid precursor expansion in response to erythropoietin and stem cell factor. (duke.edu)
- Erythropoietin, also known as erythropoietin, hematopoietin, or hemopoietin, is a glycoprotein cytokine that stimulates red blood cell formation (erythropoiesis) in the bone marrow in response to cellular hypoxia. (vedantu.com)
- EPO erythropoietin is secreted at low levels (around 10 mU/mL) in order to compensate for normal red blood cell turnover. (vedantu.com)
- EPO Erythropoietin is a hormone that is needed for the development of red blood cells. (vedantu.com)
- The burst-forming unit-erythroid (BFU-E) cells begin to express erythropoietin receptors and are erythropoietin responsive. (vedantu.com)
- Beyond erythropoiesis stimulation, erythropoietin has been shown to have a variety of actions, including vasoconstriction-dependent hypertension, angiogenesis stimulation, and cell survival through activation of EPO receptors, resulting in anti-apoptotic effects on ischemic tissues. (vedantu.com)
- Epogen/Procrit (epoetin alfa) and Aranesp are erythropoietin that are available for use as therapeutic agents and are developed using recombinant DNA technology in cell culture. (vedantu.com)
- Erythropoietin replacement therapy can help increase red cell production in the bone marrow if the erythropoietin level is poor. (vedantu.com)
Anemia11
- Impaired IF production in pernicious anemia occurs as a result of autoimmune destruction of parietal cells, which secrete IF, or the development of auto-antibodies targeted against IF itself. (medscape.com)
- The profound anemia typically is associated with erythroid hyperplasia and extramedullary hematopoiesis. (medscape.com)
- Conditions with an increase in plasma volume, such as during the last trimester of pregnancy, are associated with lower values without an existent anemia, because the red cell mass is normal. (medscape.com)
- Often, the etiology of a patient's anemia can be determined if the red blood cells (RBCs) are altered in either size or shape or if they contain certain inclusion bodies. (medscape.com)
- B19 is the primary etiologic agent causing TAC in patients with chronic hemolytic anemias (e.g., sickle cell disease, hemoglobin SC disease, hereditary spherocytosis, alpha-thalassemia, and autoimmune hemolytic anemia) (22,23). (cdc.gov)
- It can also cause TAC in other conditions in which increased red cell production is necessary to maintain stable red cell indices, as may occur in anemia due to blood loss. (cdc.gov)
- In the acute phase of the illness, patients usually have a moderate to severe anemia with absence f reticulocytes, and bone marrow examination shows a hypoplastic or an aplastic erythroid series with a normal myeloid series. (cdc.gov)
- Erythroid precursor cells may predominate secondary to hemorrhage or erythrocyte destruction (i.e., hemolytic anemia or autoimmune-mediated anemia), whereas myeloid precursor cells may predominate secondary to inflammatory, neoplastic, or immune-mediated conditions. (nih.gov)
- Clinical presentation is variable, ranging from asymptomatic to severe form of anemia, and can be exacerbated by pregnancy, sudden blood loss, or superimposed infection, i.e., parvovirus that targets the erythroid precursors. (karger.com)
- The most common type of SCD is sickle cell anemia (SCA) (also referred to as HbSS or SS disease or hemoglobin S) in which there is homozygosity for the mutation that causes HbS. (justia.com)
- In another project, Bodine's lab is comparing the epigenetic profiles of normal and Diamond-Blackfan anemia (DBA) patient cells to determine whether specific genes and pathways are altered. (nih.gov)
Bone8
- Uncovering the emergence of HSCs in the human fetal bone marrow by single-cell RNA-seq analysis. (nih.gov)
- 6. Expression of CD10, CD19 and CD34 markers in bone marrow samples of children with precursor B-cell acute lymphoblastic leukemia in clinical and hematological remission. (nih.gov)
- 16. Expression of CD58 in normal, regenerating and leukemic bone marrow B cells: implications for the detection of minimal residual disease in acute lymphocytic leukemia. (nih.gov)
- Immune bone marrow failure is a condition that occurs when a person s immune system attacks the cells of the bone marrow. (nih.gov)
- A micrograph shows dense presence of mutinuecleared cells in the bone marrow. (mhmedical.com)
- Effect of myeloablative bone marrow transplantation on growth in children with sickle cell anaemia: results of the multicenter study of haematopoietic cell transplantation for sickle cell anaemia. (duke.edu)
- Expression of multidrug resistance gene mdr1 mRNA in a subset of normal bone marrow cells. (duke.edu)
- Here we dissect hematopoietic progenitor populations in a minimally biased fashion using extensive single cell sampling from murine bone marrow. (pluto.bio)
Basophilic1
- Typical morphological features consist of small aggregates of cells with intensely basophilic nuclei (erythroid) or small collections of immature and mature myelocytic cells (myelopoiesis) located in the sinusoids and, in severe cases, in portal areas. (nih.gov)
Hyperplasia1
- Plasma cell hyperplasia may accompany EMH within the red pulp. (nih.gov)
Erythropoiesis4
- In erythroid precursor cells, we hypothesize that FPN1B expression enhances real-time sensing of systemic iron status and facilitates restriction of erythropoiesis in response to low systemic iron. (nih.gov)
- Robust cell purification methods are available for highly enriching particular stages of erythropoiesis in several mammalian species, including, human, rabbit, goat, and mouse. (nih.gov)
- Given the fact that there are relatively few genes expressed during the latter stages of erythropoiesis, these cells provide a model system with which to characterize exactly how the genetic program specifies the formation of a particular cell type. (nih.gov)
- Premature destruction of erythroid precursors results in intramedullary death and ineffective erythropoiesis. (medscape.com)
Ferroportin1
- The FPN1B transcript encodes ferroportin with an identical open reading frame and contributes significantly to ferroportin protein expression in erythroid precursors and likely also in the duodenum of iron-starved animals. (nih.gov)
Blood cells4
- 96 fL) or if certain abnormal RBCs or white blood cells (WBCs) are observed in the blood smear, the investigative approach can be limited. (medscape.com)
- decreased red blood cells and deficiency in oxygen and body tissues hypoxia. (slideshare.net)
- The cells in the erythroid series derived from MYELOID PROGENITOR CELLS or from the bi-potential MEGAKARYOCYTE-ERYTHROID PROGENITOR CELLS which eventually give rise to mature RED BLOOD CELLS . (nih.gov)
- Immature blood cells cannot perform the functions of specialized, mature blood cells. (medlineplus.gov)
Megaloblasts1
- abnormally large RBCs and erythroid precursors (megaloblasts). (slideshare.net)
Extramedullary2
- Extramedullary hematopoiesis in this case includes increased numbers of erythroid (arrow) and myeloid (arrowhead) precursor cells. (nih.gov)
- B-cell lymphoma, leukemia and extramedullary plasmacytomas can also produce a monoclonal gammopathy.2 The addition of anti-immunoglobulin antibodies to the analysis (immunoelectrophoresis) can aid in identifying the immunoglobulin class and heavy chain isotype (IgA, IgG, IgM) as well as the light chain class (kappa or lambda). (dvm360.com)
Epithelial1
- However, here we demonstrate that duodenal epithelial and erythroid precursor cells utilize an alternative upstream promoter to express a FPN1 transcript, FPN1B, which lacks the IRE and is not repressed in iron-deficient conditions. (nih.gov)
Lymphocytes1
- In this example of CLL, the leukemic cells resemble small lymphocytes. (mhmedical.com)
Dendritic2
Hematopoiesis1
- At the symposium, he described his lab's work on single-cell analysis of hematopoiesis. (nih.gov)
Inhibition2
- Inhibition of BTK activity specifically induces apoptosis in BCR-ABL1+ leukemia cells to a similar extent as inhibition of BCR-ABL1 kinase activity itself. (atlasgeneticsoncology.org)
- Cells obtained in this manner displayed significant inhibition of SDH activity and ~10-fold increases in cellular succinate levels compared to their parent cell controls. (scientificarchives.com)
Megakaryocytic3
- Retroviral mediated gene transfer in megakaryocytic cell lines. (nih.gov)
- We have successfully infected two megakaryocytic cell lines, one a committed cell line (CHRF-288-11) and the other a bipotential cell line (K562), with a retroviral vector containing the bacterial lacZ gene and a neomycin resistance marker. (nih.gov)
- If one cell type predominates (i.e., myeloid, erythroid, megakaryocytic), this can be discussed in the pathology narrative. (nih.gov)
Hematopoietic3
- Treatment for patients with thalassemia major includes long-term transfusion therapy, iron chelation, splenectomy, allogeneic hematopoietic stem cell transplantation, gene therapy, and supportive measures. (medscape.com)
- The red pulp is markedly expanded by numerous hematopoietic cells (arrow). (nih.gov)
- In leukemia (B, bottom), the marrow fat and normal hematopoietic cells have been replaced by leukemic cells. (mhmedical.com)
Genes1
- In infant pre-B MLL-AF4+ leukemia cells full-length BTK was detectable in only half of the cases, whereas in ALL cells harboring other fusion genes (including BCR-ABL1, E2A - PBX1 and TEL - AML1 ) full-length BTK was typically co-expressed with kinase-deficient variants. (atlasgeneticsoncology.org)
Plasma2
- Within the B cell lineage, BTK is already expressed in the earliest detectable B cell precursors, and expression is downregulated in plasma cells. (atlasgeneticsoncology.org)
- The monoclonal peak is so named because it is composed of a large quantity of immunoglobulin proteins being produced by a single clone of neoplastic plasma cells.1 Multiple myeloma is the most common cause of a monoclonal gammopathy, and the source of the increased immunoglobulin (known as a paraprotein-typically IgA or IgG) is a single clone of neoplastic plasma cells. (dvm360.com)
Protein6
- is caused by cytoskeletal or red cell membrane protein defects. (slideshare.net)
- The translocation to the membrane brings the BTK protein in close proximity to the Lyn en Syk kinases that transphosphorylate BTK at tyrosine Y551. (atlasgeneticsoncology.org)
- In an analysis of BTK protein and mRNA expression in infant B-lineage leukemia cells variable but often reduced levels of BTK expression was found. (atlasgeneticsoncology.org)
- G-protein-coupled receptors (GPCRs) make up the largest family of cell-surface molecules involved in cell signal transduction, physiological processes, and pathological conditions. (nih.gov)
- Recently his team demonstrated in mice that conditional epidermal deletion of the gene coding for the stimulatory G-protein alpha heteromeric subunit (Gnas) or the inactivation of protein kinase A are sufficient to cause an aberrant expansion of basal progenitor keratinocytes in the skin, resulting in basal-cell carcinoma. (nih.gov)
- Probe Set ID Ref Seq Protein ID Signal Strength Name Gene Symbol Species Function Swiss-Prot ID Amino Acid Sequence 1367452_at NP_598278 16.8 small ubiquitin-related modifier 2 precursor Sumo2 Rattus norvegicus " Ubiquitin-like protein that can be covalently attached to proteins as a monomer or as a lysine-linked polymer. (nih.gov)
Lymphoid cells3
- Fgf21-knockdown zebrafish embryos lacked erythroid and myeloid cells but not blood vessels and lymphoid cells. (zfin.org)
- A monoclonal gammopathy is the result of a single clone of neoplastic lymphoid cells producing a single type of immunoglobulin.Chronic infectious and inflammatory diseases can also cause increases in immunoglobulin concentrations, although we expect these conditions to produce a polyclonal gammopathy, which is differentiated from monoclonal gammopathy by a wide-based peak in the β2 to γ region ( Figure 3 ). (dvm360.com)
- The shorter, wider base indicates that the peak is composed of multiple immunoglobulin types being produced by different populations of inflammatory lymphoid cells. (dvm360.com)
Biol3
- Rev. Cell Biol. (biolegend.com)
- J Cell Biol (2005) 170 (3): 477-485. (rupress.org)
- Semin Cell Dev Biol. (medlineplus.gov)
Biology2
- Cell and Molecular Biology of the Liver. (nih.gov)
- The field of the present invention includes at least biology, cell biology, and medicine. (justia.com)
Leukemia8
- 4. Minimal residual disease values discriminate between low and high relapse risk in children with B-cell precursor acute lymphoblastic leukemia and an intrachromosomal amplification of chromosome 21: the Austrian and German acute lymphoblastic leukemia Berlin-Frankfurt-Munster (ALL-BFM) trials. (nih.gov)
- 7. Pure erythroid leukemia following precursor B-cell lymphoblastic leukemia. (nih.gov)
- 10. ABL deletion without associated BCR-ABL in precursor B-cell acute lymphoblastic leukemia. (nih.gov)
- 11. 12p chromosomal aberrations in precursor B childhood acute lymphoblastic leukemia predict an increased risk of relapse in the central nervous system and are associated with typical blast cell morphology. (nih.gov)
- 12. Parvovirus B19 infection presenting as pre-B-cell acute lymphoblastic leukemia: a transient and progressive course in two children. (nih.gov)
- Spontaneous pre-B cell leukemia development in Slp65-deficient mice demonstrate that Slp65 acts as a tumor suppressor. (atlasgeneticsoncology.org)
- Surprisingly, 100% of the NP23-NHD13 mice developed acute myeloid leukemia (AML) within 3 months and were characterized by extraordinarily high WBC and replacement of the thymus with Mac1+/Gr1+ myeloid cells. (nih.gov)
- It is estimated that 20 to 30 percent of children with TAM will later develop a cancer of the blood-forming cells called acute megakaryoblastic leukemia (AMKL). (medlineplus.gov)
Mobilization1
- Human CD34+ cells were collected by apheresis of normal volunteers after G-CSF mobilization. (nih.gov)
Gene3
- Peripheral smear in beta-zero thalassemia minor showing microcytes (M), target cells (T), and poikilocytes.The genetic defect usually is a missense or nonsense mutation in the beta-globin gene, although occasional defects due to gene deletions of the beta-globin gene and surrounding regions also have been reported. (medscape.com)
- Some gene mutations can be acquired during a person's lifetime and are present only in certain cells. (medlineplus.gov)
- Somatic mutations in the GATA1 gene increase the risk of developing a disease of blood-forming cells called transient abnormal myelopoiesis (TAM). (medlineplus.gov)
Mechanisms1
- The staining pattern of the lacZ reaction product was perinuclear and punctate in the CHRF-288-11 cells, whereas it was uniform throughout the cytoplasm of the K562 cells, suggesting different sorting mechanisms for bacterial beta-galactosidase in these two cell types. (nih.gov)
Stem Cells5
- In recent years, paramount investigations in research of stem cells and growth factors became the leitmotiv of all international Hematology conferences. (ispub.com)
- The knockdown embryos had haemangioblasts and haematopoietic stem cells. (zfin.org)
- To achieve precision use of desired human pluripotent stem cells (hPSCs) for medical and pharmaceutical applications, it is essential to have a thorough understanding of all fundamental properties of these starting cell sources. (nih.gov)
- One of the most important properties is related to the naive pluripotent state that is primarily established in mouse embryonic stem cells. (nih.gov)
- Staff Scientist Kevin Chen (National Institute of Neurological Disorders and Stroke) talked about how his current research on characterizing pluripotent stem cells (PSCs) and adult stem cells aims to identify optimal signaling cascades that precisely control diverse pluripotent and differentiated states in vivo and in vitro. (nih.gov)
Haematopoietic1
- Absence of phosphatidylinositol (PI)-linked proteins in a very early human multipotential haematopoietic marrow cell. (duke.edu)
Significantly1
- Furthermore, SOD 2 -/- cells exhibited significantly reduced TET enzyme activity concomitant with decreases in genomic 5-hmC and corresponding increases in 5-mC. (scientificarchives.com)
Sickle6
- Matched-related donor transplantation for sickle cell disease: report from the Center for International Blood and Transplant Research. (duke.edu)
- Genetic polymorphisms associated with priapism in sickle cell disease. (duke.edu)
- The present invention includes embodiments for treatment and/or prevention of sickle cell disease that employ Hydroxyfasudil or Isocoronarin D alone or either in conjunction with each other or an inducer of HbF production. (justia.com)
- In particular aspects, the field of the present invention includes treatment and/or prevention of a blood disorder, such as sickle cell disease. (justia.com)
- Sickle cell disease (SCD) is the most common life-threatening monogenic disorder in the world with statistics indicating that approximately 80% (230,000) of children affected globally are born in sub-Saharan Africa (Modell and Darlison 2008). (justia.com)
- Sickle cell disease (SCD) can arise from a single point mutation that causes erythrocyte deformation or sickle-shaped erythrocytes (Ingram 1957). (justia.com)
Chromosome 211
- These mutations usually occur during fetal development, and the increased risk only applies to people who are born with an extra copy of chromosome 21 in each of their cells, a condition known as trisomy 21 or Down syndrome . (medlineplus.gov)
Membrane2
- The E41K gain-of-function BTK mutant, in which the E41 residue is mutated in to a lysine residue, manifests increased membrane localization in quiescent cells, independent of PI3K activity, probably resulting from increased affinity for PIP2. (atlasgeneticsoncology.org)
- Hereditary spherocytosis (HS) is the most common cause of inherited red cell membrane disorders and affects approximately 1 out of every 2,000-5,000 people. (karger.com)
Receptor3
- BTK is a signaling mediator downstream of a variety of receptors in several different cell types (listed in Table 1), including the B cell receptor (BCR). (atlasgeneticsoncology.org)
- Thus, truncated BTK enables BCR-ABL1-dependent activation of full-length BTK, which initiates downstream survival signals and mimics pre-B cell receptor signaling. (atlasgeneticsoncology.org)
- Expression of the pre-B cell receptor (pre-BCR) leads to activation of the adaptor molecule Slp65 (also termed Bash or Blnk) and Btk. (atlasgeneticsoncology.org)
Synthesis1
- This leads to megaloblastic changes in all rapidly dividing cells because DNA synthesis is diminished. (medscape.com)
Acute2
- 2. Prognostic relevance of dic(9;20)(p11;q13) in childhood B-cell precursor acute lymphoblastic leukaemia treated with Berlin-Frankfurt-Münster (BFM) protocols containing an intensive induction and post-induction consolidation therapy. (nih.gov)
- acute (viral etiology) or chronic (setting of B-cell neoplasms). (slideshare.net)
Types1
- or various combinations of all three cell types. (nih.gov)