An acute myeloid leukemia in which 20-30% of the bone marrow or peripheral blood cells are of megakaryocyte lineage. MYELOFIBROSIS or increased bone marrow RETICULIN is common.
Very large BONE MARROW CELLS which release mature BLOOD PLATELETS.
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
The parent cells that give rise to cells in the MEGAKARYOCYTE lineage, and ultimately BLOOD PLATELETS.
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
A chromosome disorder associated either with an extra chromosome 21 or an effective trisomy for chromosome 21. Clinical manifestations include hypotonia, short stature, brachycephaly, upslanting palpebral fissures, epicanthus, Brushfield spots on the iris, protruding tongue, small ears, short, broad hands, fifth finger clinodactyly, Simian crease, and moderate to severe INTELLECTUAL DISABILITY. Cardiac and gastrointestinal malformations, a marked increase in the incidence of LEUKEMIA, and the early onset of ALZHEIMER DISEASE are also associated with this condition. Pathologic features include the development of NEUROFIBRILLARY TANGLES in neurons and the deposition of AMYLOID BETA-PROTEIN, similar to the pathology of ALZHEIMER DISEASE. (Menkes, Textbook of Child Neurology, 5th ed, p213)
A GATA transcription factor that is specifically expressed in hematopoietic lineages and plays an important role in the CELL DIFFERENTIATION of ERYTHROID CELLS and MEGAKARYOCYTES.
A specific pair of GROUP G CHROMOSOMES of the human chromosome classification.
A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.
Leukemia associated with HYPERPLASIA of the lymphoid tissues and increased numbers of circulating malignant LYMPHOCYTES and lymphoblasts.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
Mapping of the KARYOTYPE of a cell.
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.
A de novo myeloproliferation arising from an abnormal stem cell. It is characterized by the replacement of bone marrow by fibrous tissue, a process that is mediated by CYTOKINES arising from the abnormal clone.
The process of generating thrombocytes (BLOOD PLATELETS) from the pluripotent HEMATOPOIETIC STEM CELLS in the BONE MARROW via the MEGAKARYOCYTES. The humoral factor with thrombopoiesis-stimulating activity is designated THROMBOPOIETIN.
An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.
A myeloproliferative disorder characterized by neoplastic proliferation of erythroblastic and myeloblastic elements with atypical erythroblasts and myeloblasts in the peripheral blood.
Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice.
A group of transcription factors that were originally described as being specific to ERYTHROID CELLS.
Cell surface receptors that are specific for THROMBOPOIETIN. They signal through interaction with JANUS KINASES such as JANUS KINASE 2.
A clinical syndrome characterized by repeated spontaneous hemorrhages and a remarkable increase in the number of circulating platelets.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
The GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. The latter may be of viral or cellular origin.
The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.
A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias.
A humoral factor that stimulates the production of thrombocytes (BLOOD PLATELETS). Thrombopoietin stimulates the proliferation of bone marrow MEGAKARYOCYTES and their release of blood platelets. The process is called THROMBOPOIESIS.
Established cell cultures that have the potential to propagate indefinitely.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
A MADS domain-containing transcription factor that binds to the SERUM RESPONSE ELEMENT in the promoter-enhancer region of many genes. It is one of the four founder proteins that structurally define the superfamily of MADS DOMAIN PROTEINS.
A malignant disease of the T-LYMPHOCYTES in the bone marrow, thymus, and/or blood.
An acute myeloid leukemia in which 80% or more of the leukemic cells are of monocytic lineage including monoblasts, promonocytes, and MONOCYTES.
Disease having a short and relatively severe course.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.
Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.
Conditions which cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential. They all involve dysregulation of multipotent MYELOID PROGENITOR CELLS, most often caused by a mutation in the JAK2 PROTEIN TYROSINE KINASE.
A neoplastic disease of the lymphoreticular cells which is considered to be a rare type of chronic leukemia; it is characterized by an insidious onset, splenomegaly, anemia, granulocytopenia, thrombocytopenia, little or no lymphadenopathy, and the presence of "hairy" or "flagellated" cells in the blood and bone marrow.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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.
Leukemia L1210 is a designation for a specific murine (mouse) leukemia cell line that was originally isolated from a female mouse with an induced acute myeloid leukemia, which is widely used as a model in cancer research, particularly for in vivo studies of drug efficacy and resistance.
A malignant disease of the B-LYMPHOCYTES in the bone marrow and/or blood.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.
The type species of DELTARETROVIRUS that causes a form of bovine lymphosarcoma (ENZOOTIC BOVINE LEUKOSIS) or persistent lymphocytosis.
A species of GAMMARETROVIRUS causing leukemia, lymphosarcoma, immune deficiency, or other degenerative diseases in cats. Several cellular oncogenes confer on FeLV the ability to induce sarcomas (see also SARCOMA VIRUSES, FELINE).
Study of intracellular distribution of chemicals, reaction sites, enzymes, etc., by means of staining reactions, radioactive isotope uptake, selective metal distribution in electron microscopy, or other methods.
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.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
Abnormal number or structure of chromosomes. Chromosome aberrations may result in CHROMOSOME DISORDERS.
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 fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in leukemia.
Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.
Leukemia produced by exposure to IONIZING RADIATION or NON-IONIZING RADIATION.
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.
Myeloid-lymphoid leukemia protein is a transcription factor that maintains high levels of HOMEOTIC GENE expression during development. The GENE for myeloid-lymphoid leukemia protein is commonly disrupted in LEUKEMIA and combines with over 40 partner genes to form FUSION ONCOGENE PROTEINS.
Antigens on surfaces of cells, including infectious or foreign cells or viruses. They are usually protein-containing groups on cell membranes or walls and may be isolated.
A cell line derived from cultured tumor cells.
An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
An acute leukemia exhibiting cell features characteristic of both the myeloid and lymphoid lineages and probably arising from MULTIPOTENT STEM CELLS.
Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.

Constitutive activation of the JAK2/STAT5 signal transduction pathway correlates with growth factor independence of megakaryocytic leukemic cell lines. (1/179)

The factor-independent Dami/HEL and Meg-01 and factor-dependent Mo7e leukemic cell lines were used as models to investigate JAK/STAT signal transduction pathways in leukemic cell proliferation. Although Dami/HEL and Meg-01 cell proliferation in vitro was independent of and unresponsive to exogenous cytokines including granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), IL-6, thrombopoietin (TPO), and tumor necrosis factor-alpha (TNF-alpha), the growth of Mo7e cells was dependent on hematopoietic growth factors. When these cell lines were cultured in medium without cytokines, a constitutively activated STAT-like DNA-binding factor was detected in nuclear extracts from both Dami/HEL and Meg-01 cells. However, the STAT-like factor was not detectable in untreated Mo7e cells, but was activated transiently in Mo7e cells in response to cytokine treatments. The constitutively activated and cytokine-induced STAT-like DNA-binding factor in these three cell lines was identified as STAT5 by oligonucleotide competition gel mobility assays and by specific anti-STAT antibody gel supershift assays. Constitutive activation of JAK2 also was detected in the factor-independent cell lines, but not in Mo7e cells without cytokine exposure. Meg-01 cells express a p185 BCR/ABL oncogene, which may be responsible for the constitutive activation of STAT5. Dami/HEL cells do not express the BCR/ABL oncogene, but increased constitutive phosphorylation of Raf-1 oncoprotein was detected. In cytokine bioassays using growth factor-dependent Mo7e and TF-1 cells as targets, conditioned media from Dami/HEL and Meg-01 cells did not show stimulatory effects on cell proliferation. Our results indicate that the constitutive activation of JAK2/STAT5 correlates with the factor-independent growth of Dami/HEL and Meg-01 cells. The constitutive activation of JAK2/STAT5 in Dami/HEL cells is triggered by a mechanism other than autocrine cytokines or the BCR/ABL oncoprotein.  (+info)

Developmental expression of plasminogen activator inhibitor-1 associated with thrombopoietin-dependent megakaryocytic differentiation. (2/179)

Plasminogen activator inhibitor-1 (PAI-1) is present in the platelet alpha-granule and is released on activation. However, there is some debate as to whether the megakaryocyte and platelet synthesize PAI-1, take it up from plasma, or both. We examined the expression of PAI-1 in differentiating megakaryocytic progenitor cells (UT-7) and in CD34(+)/CD41(-) cells from cord blood. UT-7 cells differentiated with thrombopoietin (TPO) resembled megakaryocytes (UT-7/TPO) with respect to morphology, ploidy, and the expression of glycoprotein IIb-IIIa. PAI-1 messenger RNA (mRNA) expression was upregulated and PAI-1 protein synthesized in the UT-7/TPO cells accumulated in the cytoplasm without being released spontaneously. In contrast, erythropoietin (EPO)-stimulated UT-7 cells (UT-7/EPO) did not express PAI-1 mRNA after stimulation with TPO because they do not have endogenous c-Mpl. After cotransfection with human wild-type c-mpl, the cells (UT-7/EPO-MPL) responded to phorbol 12-myristate 13-acetate (PMA), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) with enhanced PAI-1 mRNA expression within 24 to 48 hours. However, induction of PAI-1 mRNA in UT-7/EPO-MPL cells by TPO required at least 14-days stimulation. UT-7/EPO cells expressing c-Mpl changed their morphology and the other characteristics similar to the UT-7/TPO cells. TPO also differentiated human cord blood CD34(+)/CD41(-) cells to CD34(-)/CD41(+) cells, generated morphologically mature megakaryocytes, and induced the expression of PAI-1 mRNA. These results suggest that both PAI-1 mRNA and de novo PAI-1 protein synthesis is induced after differentiation of immature progenitor cells into megakaryocytes by TPO.  (+info)

Thrombotic microangiopathy associated with reactivation of human herpesvirus-6 following high-dose chemotherapy with autologous bone marrow transplantation in young children. (3/179)

Thrombotic microangiopathy (TMA) is a serious complication of BMT. Several factors are important in the etiology of TMA, such as cyclosporin A, GVHD, irradiation, intensive conditioning chemotherapy and infection, which cause damage to vascular endothelial cells leading to activation of these cells. We describe two young children with TMA following high-dose chemotherapy with autologous BMT. Development of TMA was accompanied by reactivation of HHV-6, which was identified by both an increase in the copy number of HHV-6 DNA in the peripheral blood and a significant increase in antibody titers to HHV-6. Thus, it was suggested that reactivation of HHV-6 together with high-dose chemotherapy played an important role in the pathogenesis of TMA in these patients. Since HHV-6 is known to infect vascular endothelial cells, and CMV which is virologically closely related to HHV-6, has been reported to be a pathogen that causes TMA, infection with HHV-6 of vascular endothelial cells may induce TMA via damage and activation of these cells.  (+info)

Therapy-related megakaryoblastic leukemia with pituitary involvement following treatment for non-Hodgkin's lymphoma. (4/179)

A case of a 66-year-old Japanese man developed therapy-related megakaryoblastic leukemia with pituitary involvement after chemotherapy for non-Hodgkin's lymphoma. Alkylating agents had been administered for the treatment of non-Hodgkin's lymphoma and 6 years later, megakaryoblastic leukemia with myelofibrosis and myelodysplasia developed. The blast cells expressed CD41, and immature antigens also. These findings were compatible with therapy-related megakaryoblastic leukemia. An autopsy revealed blast-cell infiltration into multiple organs including the posterior pituitary lobe. Therapy-related megakaryoblastic leukemia is very rare, and pituitary involvement may be associated with immaturity of blast cells.  (+info)

Allogeneic bone marrow transplantation for therapy-related myelodysplastic syndrome and acute myeloid leukemia: a long-term study of 70 patients-report of the French society of bone marrow transplantation. (5/179)

PURPOSE: To identify predictive factors of survival, relapse, and transplantation-related mortality (TRM) among patients with therapy-related myelodysplastic syndrome (t-MDS) or acute leukemia (t-AML) who underwent allogeneic bone marrow transplantation (BMT). PATIENTS AND METHODS: From 1980 to 1998, 70 patients underwent allogeneic BMT for t-MDS (n = 31) or t-AML (n = 39) after prior cytotoxic exposure. Thirty-three patients had received induction-type chemotherapy before BMT. At the time of transplantation, there were 24 patients in complete remission (CR) and 46 with active disease. RESULTS: With a median follow-up of 7.9 years (range, 1.1 to 18.8 years) after BMT, 16 patients are alive, whereas 19 died of relapse, 34 of TRM, and one of relapse of the primary disease. The estimated 2-year overall survival, event-free survival, relapse, and TRM rates were 30% (95% confidence interval [CI], 19% to 40%), 28% (95% CI, 18% to 39%), 42% (95% CI, 26% to 57%), and 49% (95% CI, 36% to 62%), respectively. In multivariable analysis, age greater than 37 years, male sex, positive recipient cytomegalovirus (CMV) serology, absence of CR at BMT, and intensive schedules used for conditioning were associated with poor outcome. CONCLUSION: BMT is an effective treatment for patients with t-MDS or t-AML who have responsive disease and, in particular, who have no poor-risk cytogenetic features. The poor results of the other patients, especially those with active disease at BMT, emphasize the need to delineate indications and perform prospective protocols.  (+info)

Prenatal HLA-matching to determine suitability for allogeneic bone marrow transplantation. (6/179)

For several haematological malignancies, allogeneic stem cell transplantation is the treatment of choice. In most cases an HLA-identical sibling is required. If the mother of a patient is pregnant, cord blood from a related donor, which can be used for stem cell transplantation, might be obtainable in the near future. For the patient, knowledge of the foetal HLA-type can be important since it might influence choice of treatment and timing of transplantation. If the foetus is HLA compatible, as would be the situation in 25% of cases, the delivery has to be arranged in such a way that cord stem cells can be collected. As a result, in the other 75% of cases (spontaneous) delivery can take place in the home/local setting. Here we report four cases in which amniocentesis was performed and HLA-typing influenced treatment of the patient and delivery of the sibling.  (+info)

Acute megakaryocytic leukemia: the Eastern Cooperative Oncology Group experience. (7/179)

Acute megakaryocytic leukemia (AMegL) is a rare subtype of acute myeloid leukemia (AML) evolving from primitive megakaryoblasts. Because of its rarity and the lack of precise diagnostic criteria in the past, few series of adults treated with contemporary therapy have been reported. Twenty among 1649 (1.2%) patients with newly diagnosed AML entered on Eastern Cooperative Oncology Group (ECOG) trials between 1984 and 1997 were found to have AMegL. The median age was 42.5 years (range 18-70). Marrow fibrosis, usually extensive, was present in the bone marrow. Of the 8 patients who had cytogenetic studies performed, abnormalities of chromosome 3 were the most frequent. The most consistent immunophenotypic finding was absence of myeloperoxidase in blast cells from 5 patients. In the most typical 3 cases, the leukemic cells were positive for one to 2 platelet-specific antigens in addition to lacking myeloperoxidase or an antigen consistent with a lymphoid leukemia. Myeloid antigens other than myeloperoxidase and selected T-cell antigens (CD7 and/or CD2) were frequently expressed. Induction therapy included an anthracycline and cytarabine in all cases. Complete remission (CR) was achieved in 10 of 20 patients (50%). Two patients remain alive, one in CR at 160+ months. Resistant disease was the cause of induction failure in all but 3 patients. The median CR duration was 10.6 months (range 1-160+ months). The median survival for all patients was 10.4 months (range 1-160+ months). Although half of the patients achieved CR, the long-term outcome is extremely poor, primarily attributable to resistant disease. New therapeutic strategies are needed.  (+info)

K562 cells resistant to phorbol 12-myristate 13-acetate-induced growth arrest: dissociation of mitogen-activated protein kinase activation and Egr-1 expression from megakaryocyte differentiation. (8/179)

The K562 cell line undergoes megakaryocytic differentiation in response to phorbol 12-myristate 13-acetate (PMA) stimulation. This event correlates with mitogen-activated protein kinase activation, cell cycle arrest, and expression of the Egr-1 transcription factor. We have isolated K562 cells that are resistant to the growth-inhibitory action of PMA. Molecular characterization demonstrates that PMA resistance is downstream from PMA-induced activation of the mitogen-activated protein kinase pathway. Although the levels of Egr-1 expression and cyclic AMP-responsive element-binding protein phosphorylation are comparable in wild-type and PMA-resistant clones in response to PMA, the expression of megakaryocytic cell surface marker CD41 is detected only in the wild-type cells. The lack of differentiation of the PMA-resistant clones correlates with a failure of the PMA-treated cells to induce dephosphorylation and down-regulation of the retinoblastoma protein. These cells may provide a useful model system to distinguish those events that are connected to cell cycle arrest from those involved in the differentiation program initiated by PMA.  (+info)

Acute Megakaryoblastic Leukemia (AMKL) is a type of cancer that affects the blood and bone marrow. Specifically, it is a subtype of acute myeloid leukemia (AML), which is characterized by the rapid growth of abnormal cells in the bone marrow that interfere with the production of normal blood cells.

In AMKL, the abnormal cells are megakaryoblasts, which are immature cells that should develop into platelet-producing cells called megakaryocytes. However, in AMKL, these cells do not mature properly and instead accumulate in the bone marrow and bloodstream, leading to a shortage of healthy blood cells.

Symptoms of AMKL may include fatigue, weakness, frequent infections, easy bruising or bleeding, and the appearance of small red spots on the skin (petechiae). Diagnosis typically involves a combination of physical exam, medical history, blood tests, bone marrow aspiration and biopsy, and sometimes imaging studies.

Treatment for AMKL usually involves a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the extent of the disease.

Megakaryocytes are large, specialized bone marrow cells that are responsible for the production and release of platelets (also known as thrombocytes) into the bloodstream. Platelets play an essential role in blood clotting and hemostasis, helping to prevent excessive bleeding during injuries or trauma.

Megakaryocytes have a unique structure with multilobed nuclei and abundant cytoplasm rich in organelles called alpha-granules and dense granules, which store various proteins, growth factors, and enzymes necessary for platelet function. As megakaryocytes mature, they extend long cytoplasmic processes called proplatelets into the bone marrow sinuses, where these extensions fragment into individual platelets that are released into circulation.

Abnormalities in megakaryocyte number, size, or function can lead to various hematological disorders, such as thrombocytopenia (low platelet count), thrombocytosis (high platelet count), and certain types of leukemia.

Leukemia is a type of cancer that originates from the bone marrow - the soft, inner part of certain bones where new blood cells are made. It is characterized by an abnormal production of white blood cells, known as leukocytes or blasts. These abnormal cells accumulate in the bone marrow and interfere with the production of normal blood cells, leading to a decrease in red blood cells (anemia), platelets (thrombocytopenia), and healthy white blood cells (leukopenia).

There are several types of leukemia, classified based on the specific type of white blood cell affected and the speed at which the disease progresses:

1. Acute Leukemias - These types of leukemia progress rapidly, with symptoms developing over a few weeks or months. They involve the rapid growth and accumulation of immature, nonfunctional white blood cells (blasts) in the bone marrow and peripheral blood. The two main categories are:
- Acute Lymphoblastic Leukemia (ALL) - Originates from lymphoid progenitor cells, primarily affecting children but can also occur in adults.
- Acute Myeloid Leukemia (AML) - Develops from myeloid progenitor cells and is more common in older adults.

2. Chronic Leukemias - These types of leukemia progress slowly, with symptoms developing over a period of months to years. They involve the production of relatively mature, but still abnormal, white blood cells that can accumulate in large numbers in the bone marrow and peripheral blood. The two main categories are:
- Chronic Lymphocytic Leukemia (CLL) - Affects B-lymphocytes and is more common in older adults.
- Chronic Myeloid Leukemia (CML) - Originates from myeloid progenitor cells, characterized by the presence of a specific genetic abnormality called the Philadelphia chromosome. It can occur at any age but is more common in middle-aged and older adults.

Treatment options for leukemia depend on the type, stage, and individual patient factors. Treatments may include chemotherapy, targeted therapy, immunotherapy, stem cell transplantation, or a combination of these approaches.

Megakaryocyte progenitor cells are a type of hematopoietic (blood-forming) stem or progenitor cell that give rise to megakaryocytes, which are large cells found in the bone marrow. Megakaryocytes are responsible for producing platelets, also known as thrombocytes, which are small cell fragments that play a crucial role in blood clotting and hemostasis.

Megakaryocyte progenitor cells are characterized by their ability to differentiate into megakaryocytes and express specific surface markers, such as CD34, CD41, and CD61. They can be found in the bone marrow and peripheral blood and can be expanded and differentiated in vitro for therapeutic purposes, such as in platelet production for transfusion therapy.

Abnormalities in megakaryocyte progenitor cells can lead to various hematological disorders, including thrombocytopenia (low platelet count) and myeloproliferative neoplasms (abnormal blood cell growth). Therefore, understanding the biology and regulation of megakaryocyte progenitor cells is essential for developing new diagnostic and therapeutic strategies for these conditions.

Acute myeloid leukemia (AML) is a type of cancer that originates in the bone marrow, the soft inner part of certain bones where new blood cells are made. In AML, the immature cells, called blasts, in the bone marrow fail to mature into normal blood cells. Instead, these blasts accumulate and interfere with the production of normal blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia).

AML is called "acute" because it can progress quickly and become severe within days or weeks without treatment. It is a type of myeloid leukemia, which means that it affects the myeloid cells in the bone marrow. Myeloid cells are a type of white blood cell that includes monocytes and granulocytes, which help fight infection and defend the body against foreign invaders.

In AML, the blasts can build up in the bone marrow and spread to other parts of the body, including the blood, lymph nodes, liver, spleen, and brain. This can cause a variety of symptoms, such as fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss.

AML is typically treated with a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the type and stage of the leukemia.

Down syndrome is a genetic disorder caused by the presence of all or part of a third copy of chromosome 21. It is characterized by intellectual and developmental disabilities, distinctive facial features, and sometimes physical growth delays and health problems. The condition affects approximately one in every 700 babies born in the United States.

Individuals with Down syndrome have varying degrees of cognitive impairment, ranging from mild to moderate or severe. They may also have delayed development, including late walking and talking, and may require additional support and education services throughout their lives.

People with Down syndrome are at increased risk for certain health conditions, such as congenital heart defects, respiratory infections, hearing loss, vision problems, gastrointestinal issues, and thyroid disorders. However, many individuals with Down syndrome live healthy and fulfilling lives with appropriate medical care and support.

The condition is named after John Langdon Down, an English physician who first described the syndrome in 1866.

GATA1 (Global Architecture of Tissue/stage-specific Transcription Factors 1) is a transcription factor that belongs to the GATA family, which recognizes and binds to the (A/T)GATA(A/G) motif in the DNA. It plays a crucial role in the development and differentiation of hematopoietic cells, particularly erythroid, megakaryocytic, eosinophilic, and mast cell lineages.

GATA1 regulates gene expression by binding to specific DNA sequences and recruiting other co-factors that modulate chromatin structure and transcriptional activity. Mutations in the GATA1 gene can lead to various blood disorders such as congenital dyserythropoietic anemia type II, Diamond-Blackfan anemia, acute megakaryoblastic leukemia (AMKL), and myelodysplastic syndrome.

In summary, GATA1 Transcription Factor is a protein that binds to specific DNA sequences in the genome and regulates gene expression, playing a critical role in hematopoietic cell development and differentiation.

Human chromosome pair 21 consists of two rod-shaped structures present in the nucleus of each cell in the human body. Each member of the pair is a single chromosome, and they are identical to each other. Chromosomes are made up of DNA, which contains genetic information that determines many of an individual's traits and characteristics.

Chromosome pair 21 is one of the 23 pairs of human autosomal chromosomes, meaning they are not sex chromosomes (X or Y). Chromosome pair 21 is the smallest of the human chromosomes, and it contains approximately 48 million base pairs of DNA. It contains around 200-300 genes that provide instructions for making proteins and regulating various cellular processes.

Down syndrome, a genetic disorder characterized by intellectual disability, developmental delays, distinct facial features, and sometimes heart defects, is caused by an extra copy of chromosome pair 21 or a part of it. This additional genetic material can lead to abnormalities in brain development and function, resulting in the characteristic symptoms of Down syndrome.

Chronic lymphocytic leukemia (CLL) is a type of cancer that starts from cells that become certain white blood cells (called lymphocytes) in the bone marrow. The cancer (leukemia) cells start in the bone marrow but then go into the blood.

In CLL, the leukemia cells often build up slowly. Many people don't have any symptoms for at least a few years. But over time, the cells can spread to other parts of the body, including the lymph nodes, liver, and spleen.

The "B-cell" part of the name refers to the fact that the cancer starts in a type of white blood cell called a B lymphocyte or B cell. The "chronic" part means that this leukemia usually progresses more slowly than other types of leukemia.

It's important to note that chronic lymphocytic leukemia is different from chronic myelogenous leukemia (CML). Although both are cancers of the white blood cells, they start in different types of white blood cells and progress differently.

Leukemia, lymphoid is a type of cancer that affects the lymphoid cells, which are a vital part of the body's immune system. It is characterized by the uncontrolled production of abnormal white blood cells (leukocytes or WBCs) in the bone marrow, specifically the lymphocytes. These abnormal lymphocytes accumulate and interfere with the production of normal blood cells, leading to a decrease in red blood cells (anemia), platelets (thrombocytopenia), and healthy white blood cells (leukopenia).

There are two main types of lymphoid leukemia: acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL). Acute lymphoblastic leukemia progresses rapidly, while chronic lymphocytic leukemia has a slower onset and progression.

Symptoms of lymphoid leukemia may include fatigue, frequent infections, easy bruising or bleeding, weight loss, swollen lymph nodes, and bone pain. Treatment options depend on the type, stage, and individual patient factors but often involve chemotherapy, radiation therapy, targeted therapy, immunotherapy, or 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.

Karyotyping is a medical laboratory test used to study the chromosomes in a cell. It involves obtaining a sample of cells from a patient, usually from blood or bone marrow, and then staining the chromosomes so they can be easily seen under a microscope. The chromosomes are then arranged in pairs based on their size, shape, and other features to create a karyotype. This visual representation allows for the identification and analysis of any chromosomal abnormalities, such as extra or missing chromosomes, or structural changes like translocations or inversions. These abnormalities can provide important information about genetic disorders, diseases, and developmental problems.

Chronic myelogenous leukemia (CML), BCR-ABL positive is a specific subtype of leukemia that originates in the bone marrow and involves the excessive production of mature granulocytes, a type of white blood cell. It is characterized by the presence of the Philadelphia chromosome, which is formed by a genetic translocation between chromosomes 9 and 22, resulting in the formation of the BCR-ABL fusion gene. This gene encodes for an abnormal protein with increased tyrosine kinase activity, leading to uncontrolled cell growth and division. The presence of this genetic abnormality is used to confirm the diagnosis and guide treatment decisions.

Primary myelofibrosis (PMF) is a rare, chronic bone marrow disorder characterized by the replacement of normal bone marrow tissue with fibrous scar tissue, leading to impaired production of blood cells. This results in cytopenias (anemia, leukopenia, thrombocytopenia), which can cause fatigue, infection susceptibility, and bleeding tendencies. Additionally, PMF is often accompanied by the proliferation of abnormal megakaryocytes (large, atypical bone marrow cells that produce platelets) and extramedullary hematopoiesis (blood cell formation outside the bone marrow, typically in the spleen and liver).

PMF is a type of myeloproliferative neoplasm (MPN), which is a group of clonal stem cell disorders characterized by excessive proliferation of one or more types of blood cells. PMF can present with various symptoms such as fatigue, weight loss, night sweats, abdominal discomfort due to splenomegaly (enlarged spleen), and bone pain. In some cases, PMF may progress to acute myeloid leukemia (AML).

The exact cause of PMF remains unclear; however, genetic mutations are known to play a significant role in its development. The Janus kinase 2 (JAK2), calreticulin (CALR), and MPL genes have been identified as commonly mutated in PMF patients. These genetic alterations contribute to the dysregulated production of blood cells and the activation of signaling pathways that promote fibrosis.

Diagnosis of PMF typically involves a combination of clinical evaluation, complete blood count (CBC), bone marrow aspiration and biopsy, cytogenetic analysis, and molecular testing to identify genetic mutations. Treatment options depend on the individual patient's symptoms, risk stratification, and disease progression. They may include observation, supportive care, medications to manage symptoms and control the disease (such as JAK inhibitors), and stem cell transplantation for eligible patients.

Thrombopoiesis is the process of formation and development of thrombocytes or platelets, which are small, colorless cell fragments in our blood that play an essential role in clotting. Thrombopoiesis occurs inside the bone marrow, where stem cells differentiate into megakaryoblasts, then progressively develop into promegakaryocytes and megakaryocytes. These megakaryocytes subsequently undergo a process called cytoplasmic fragmentation to produce platelets.

The regulation of thrombopoiesis is primarily controlled by the hormone thrombopoietin (TPO), which is produced mainly in the liver and binds to the thrombopoietin receptor (c-Mpl) on megakaryocytes and their precursors. This binding stimulates the proliferation, differentiation, and maturation of megakaryocytes, leading to an increase in platelet production.

Abnormalities in thrombopoiesis can result in conditions such as thrombocytopenia (low platelet count) or thrombocytosis (high platelet count), which may be associated with bleeding disorders or increased risk of thrombosis, respectively.

K562 cells are a type of human cancer cell that are commonly used in scientific research. They are derived from a patient with chronic myelogenous leukemia (CML), a type of cancer that affects the blood and bone marrow.

K562 cells are often used as a model system to study various biological processes, including cell signaling, gene expression, differentiation, and apoptosis (programmed cell death). They are also commonly used in drug discovery and development, as they can be used to test the effectiveness of potential new therapies against cancer.

K562 cells have several characteristics that make them useful for research purposes. They are easy to grow and maintain in culture, and they can be manipulated genetically to express or knock down specific genes. Additionally, K562 cells are capable of differentiating into various cell types, such as red blood cells and megakaryocytes, which allows researchers to study the mechanisms of cell differentiation.

It's important to note that while K562 cells are a valuable tool for research, they do not fully recapitulate the complexity of human CML or other cancers. Therefore, findings from studies using K562 cells should be validated in more complex model systems or in clinical trials before they can be translated into treatments for patients.

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.

Medical Definition:

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

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

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

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

Erythroid-specific DNA-binding factors are transcription factors that bind to specific sequences of DNA and help regulate the expression of genes that are involved in the development and differentiation of erythroid cells, which are cells that mature to become red blood cells. These transcription factors play a crucial role in the production of hemoglobin, the protein in red blood cells that carries oxygen throughout the body. Examples of erythroid-specific DNA-binding factors include GATA-1 and KLF1.

Thrombopoietin receptors are a type of cell surface receptor found on megakaryocytes and platelets. They are also known as MPL (myeloproliferative leukemia virus) receptors. Thrombopoietin is a hormone that regulates the production of platelets in the body, and it binds to these receptors to stimulate the proliferation and differentiation of megakaryocytes, which are large bone marrow cells that produce platelets.

The thrombopoietin receptor is a type I transmembrane protein with an extracellular domain that contains the thrombopoietin-binding site, a single transmembrane domain, and an intracellular domain that contains several tyrosine residues that become phosphorylated upon thrombopoietin binding. This triggers a signaling cascade that leads to the activation of various downstream pathways involved in cell proliferation, differentiation, and survival.

Mutations in the thrombopoietin receptor gene have been associated with certain myeloproliferative neoplasms, such as essential thrombocythemia and primary myelofibrosis, which are characterized by excessive platelet production and bone marrow fibrosis.

Essential thrombocythemia (ET) is a myeloproliferative neoplasm (MPN), a type of blood cancer characterized by the overproduction of platelets (thrombocytosis) in the bone marrow. In ET, there is an excessive proliferation of megakaryocytes, the precursor cells that produce platelets. This leads to increased platelet counts in the peripheral blood, which can increase the risk of blood clots (thrombosis) and bleeding episodes (hemorrhage).

The term "essential" is used to indicate that the cause of this condition is not known or idiopathic. ET is primarily a disease of older adults, but it can also occur in younger individuals. The diagnosis of essential thrombocythemia requires careful evaluation and exclusion of secondary causes of thrombocytosis, such as reactive conditions, inflammation, or other myeloproliferative neoplasms.

The clinical presentation of ET can vary widely among patients. Some individuals may be asymptomatic and discovered only during routine blood tests, while others may experience symptoms related to thrombosis or bleeding. Common symptoms include headaches, visual disturbances, dizziness, weakness, numbness, or tingling in the extremities, if there are complications due to blood clots in the brain or other parts of the body. Excessive bruising, nosebleeds, or blood in the stool can indicate bleeding complications.

Treatment for essential thrombocythemia is aimed at reducing the risk of thrombosis and managing symptoms. Hydroxyurea is a commonly used medication to lower platelet counts, while aspirin may be prescribed to decrease the risk of blood clots. In some cases, interferon-alpha or ruxolitinib might be considered as treatment options. Regular follow-up with a hematologist and monitoring of blood counts are essential for managing this condition and detecting potential complications early.

'Tumor cells, cultured' refers to the process of removing cancerous cells from a tumor and growing them in controlled laboratory conditions. This is typically done by isolating the tumor cells from a patient's tissue sample, then placing them in a nutrient-rich environment that promotes their growth and multiplication.

The resulting cultured tumor cells can be used for various research purposes, including the study of cancer biology, drug development, and toxicity testing. They provide a valuable tool for researchers to better understand the behavior and characteristics of cancer cells outside of the human body, which can lead to the development of more effective cancer treatments.

It is important to note that cultured tumor cells may not always behave exactly the same way as they do in the human body, so findings from cell culture studies must be validated through further research, such as animal models or clinical trials.

Tetradecanoylphorbol acetate (TPA) is defined as a pharmacological agent that is a derivative of the phorbol ester family. It is a potent tumor promoter and activator of protein kinase C (PKC), a group of enzymes that play a role in various cellular processes such as signal transduction, proliferation, and differentiation. TPA has been widely used in research to study PKC-mediated signaling pathways and its role in cancer development and progression. It is also used in topical treatments for skin conditions such as psoriasis.

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.

An oncogene protein fusion is a result of a genetic alteration in which parts of two different genes combine to create a hybrid gene that can contribute to the development of cancer. This fusion can lead to the production of an abnormal protein that promotes uncontrolled cell growth and division, ultimately resulting in a malignant tumor. Oncogene protein fusions are often caused by chromosomal rearrangements such as translocations, inversions, or deletions and are commonly found in various types of cancer, including leukemia and sarcoma. These genetic alterations can serve as potential targets for cancer diagnosis and therapy.

Bone marrow is the spongy tissue found inside certain bones in the body, such as the hips, thighs, and vertebrae. It is responsible for producing blood-forming cells, including red blood cells, white blood cells, and platelets. There are two types of bone marrow: red marrow, which is involved in blood cell production, and yellow marrow, which contains fatty tissue.

Red bone marrow contains hematopoietic stem cells, which can differentiate into various types of blood cells. These stem cells continuously divide and mature to produce new blood cells that are released into the circulation. Red blood cells carry oxygen throughout the body, white blood cells help fight infections, and platelets play a crucial role in blood clotting.

Bone marrow also serves as a site for immune cell development and maturation. It contains various types of immune cells, such as lymphocytes, macrophages, and dendritic cells, which help protect the body against infections and diseases.

Abnormalities in bone marrow function can lead to several medical conditions, including anemia, leukopenia, thrombocytopenia, and various types of cancer, such as leukemia and multiple myeloma. Bone marrow aspiration and biopsy are common diagnostic procedures used to evaluate bone marrow health and function.

Precursor Cell Lymphoblastic Leukemia-Lymphoma (previously known as Precursor T-lymphoblastic Leukemia/Lymphoma) is a type of cancer that affects the early stages of T-cell development. It is a subtype of acute lymphoblastic leukemia (ALL), which is characterized by the overproduction of immature white blood cells called lymphoblasts in the bone marrow, blood, and other organs.

In Precursor Cell Lymphoblastic Leukemia-Lymphoma, these abnormal lymphoblasts accumulate primarily in the lymphoid tissues such as the thymus and lymph nodes, leading to the enlargement of these organs. This subtype is more aggressive than other forms of ALL and has a higher risk of spreading to the central nervous system (CNS).

The medical definition of Precursor Cell Lymphoblastic Leukemia-Lymphoma includes:

1. A malignant neoplasm of immature T-cell precursors, also known as lymphoblasts.
2. Characterized by the proliferation and accumulation of these abnormal cells in the bone marrow, blood, and lymphoid tissues such as the thymus and lymph nodes.
3. Often associated with chromosomal abnormalities, genetic mutations, or aberrant gene expression that contribute to its aggressive behavior and poor prognosis.
4. Typically presents with symptoms related to bone marrow failure (anemia, neutropenia, thrombocytopenia), lymphadenopathy (swollen lymph nodes), hepatosplenomegaly (enlarged liver and spleen), and potential CNS involvement.
5. Diagnosed through a combination of clinical evaluation, imaging studies, and laboratory tests, including bone marrow aspiration and biopsy, immunophenotyping, cytogenetic analysis, and molecular genetic testing.
6. Treated with intensive multi-agent chemotherapy regimens, often combined with radiation therapy and/or stem cell transplantation to achieve remission and improve survival outcomes.

Thrombopoietin (TPO) is a glycoprotein hormone that plays a crucial role in the regulation of platelet production, also known as thrombopoiesis. It is primarily produced by the liver and to some extent by megakaryocytes, which are the cells responsible for producing platelets.

TPO binds to its receptor, c-Mpl, on the surface of megakaryocytes and their precursor cells, stimulating their proliferation, differentiation, and maturation into platelets. By regulating the number of platelets in circulation, TPO helps maintain hemostasis, the process that prevents excessive bleeding after injury.

In addition to its role in thrombopoiesis, TPO has been shown to have potential effects on other cell types, including hematopoietic stem cells and certain immune cells. However, its primary function remains the regulation of platelet production.

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.

Blood platelets, also known as thrombocytes, are small, colorless cell fragments in our blood that play an essential role in normal blood clotting. They are formed in the bone marrow from large cells called megakaryocytes and circulate in the blood in an inactive state until they are needed to help stop bleeding. When a blood vessel is damaged, platelets become activated and change shape, releasing chemicals that attract more platelets to the site of injury. These activated platelets then stick together to form a plug, or clot, that seals the wound and prevents further blood loss. In addition to their role in clotting, platelets also help to promote healing by releasing growth factors that stimulate the growth of new tissue.

Serum Response Factor (SRF) is a transcription factor that binds to the serum response element (SRE) in the promoter region of many immediate early genes and some cell type-specific genes. SRF plays a crucial role in regulating various cellular processes, including gene expression related to differentiation, proliferation, and survival of cells. It is activated by various signals such as growth factors, cytokines, and mechanical stress, which leads to changes in the actin cytoskeleton and gene transcription. SRF also interacts with other cofactors to modulate its transcriptional activity, contributing to the specificity of gene regulation in different cell types.

Leukemia, T-cell is a type of cancer that affects the T-cells or T-lymphocytes, which are a type of white blood cells responsible for cell-mediated immunity. It is characterized by an excessive and uncontrolled production of abnormal T-cells in the bone marrow, leading to the displacement of healthy cells and impairing the body's ability to fight infections and regulate immune responses.

T-cell leukemia can be acute or chronic, depending on the rate at which the disease progresses. Acute T-cell leukemia progresses rapidly, while chronic T-cell leukemia has a slower course of progression. Symptoms may include fatigue, fever, frequent infections, weight loss, easy bruising or bleeding, and swollen lymph nodes. Treatment typically involves chemotherapy, radiation therapy, stem cell transplantation, or targeted therapy, depending on the type and stage of the disease.

Acute Monocytic Leukemia (AML-M5) is a subtype of acute myeloid leukemia (AML), which is a type of cancer affecting the blood and bone marrow. In AML-M5, there is an overproduction of abnormal monocytes, a type of white blood cell that normally helps fight infection and is involved in the body's immune response. These abnormal monocytes accumulate in the bone marrow and interfere with the production of normal blood cells, leading to symptoms such as fatigue, frequent infections, and easy bruising or bleeding. The disease progresses rapidly without treatment, making it crucial to begin therapy as soon as possible after diagnosis.

An acute disease is a medical condition that has a rapid onset, develops quickly, and tends to be short in duration. Acute diseases can range from minor illnesses such as a common cold or flu, to more severe conditions such as pneumonia, meningitis, or a heart attack. These types of diseases often have clear symptoms that are easy to identify, and they may require immediate medical attention or treatment.

Acute diseases are typically caused by an external agent or factor, such as a bacterial or viral infection, a toxin, or an injury. They can also be the result of a sudden worsening of an existing chronic condition. In general, acute diseases are distinct from chronic diseases, which are long-term medical conditions that develop slowly over time and may require ongoing management and treatment.

Examples of acute diseases include:

* Acute bronchitis: a sudden inflammation of the airways in the lungs, often caused by a viral infection.
* Appendicitis: an inflammation of the appendix that can cause severe pain and requires surgical removal.
* Gastroenteritis: an inflammation of the stomach and intestines, often caused by a viral or bacterial infection.
* Migraine headaches: intense headaches that can last for hours or days, and are often accompanied by nausea, vomiting, and sensitivity to light and sound.
* Myocardial infarction (heart attack): a sudden blockage of blood flow to the heart muscle, often caused by a buildup of plaque in the coronary arteries.
* Pneumonia: an infection of the lungs that can cause coughing, chest pain, and difficulty breathing.
* Sinusitis: an inflammation of the sinuses, often caused by a viral or bacterial infection.

It's important to note that while some acute diseases may resolve on their own with rest and supportive care, others may require medical intervention or treatment to prevent complications and promote recovery. If you are experiencing symptoms of an acute disease, it is always best to seek medical attention to ensure proper diagnosis and treatment.

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

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

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

Platelet membrane glycoproteins are specialized proteins found on the surface of platelets, which are small blood cells responsible for clotting. These glycoproteins play crucial roles in various processes related to hemostasis and thrombosis, including platelet adhesion, activation, and aggregation.

There are several key platelet membrane glycoproteins, such as:

1. Glycoprotein (GP) Ia/IIa (also known as integrin α2β1): This glycoprotein mediates the binding of platelets to collagen fibers in the extracellular matrix, facilitating platelet adhesion and activation.
2. GP IIb/IIIa (also known as integrin αIIbβ3): This is the most abundant glycoprotein on the platelet surface and functions as a receptor for fibrinogen, von Willebrand factor, and other adhesive proteins. Upon activation, GP IIb/IIIa undergoes conformational changes that enable it to bind these ligands, leading to platelet aggregation and clot formation.
3. GPIb-IX-V: This glycoprotein complex is involved in the initial tethering and adhesion of platelets to von Willebrand factor (vWF) in damaged blood vessels. It consists of four subunits: GPIbα, GPIbβ, GPIX, and GPV.
4. GPVI: This glycoprotein is essential for platelet activation upon contact with collagen. It associates with the Fc receptor γ-chain (FcRγ) to form a signaling complex that triggers intracellular signaling pathways, leading to platelet activation and aggregation.

Abnormalities in these platelet membrane glycoproteins can lead to bleeding disorders or thrombotic conditions. For example, mutations in GPIIb/IIIa can result in Glanzmann's thrombasthenia, a severe bleeding disorder characterized by impaired platelet aggregation. On the other hand, increased expression or activation of these glycoproteins may contribute to the development of arterial thrombosis and cardiovascular diseases.

Myeloproliferative disorders (MPDs) are a group of rare, chronic blood cancers that originate from the abnormal proliferation or growth of one or more types of blood-forming cells in the bone marrow. These disorders result in an overproduction of mature but dysfunctional blood cells, which can lead to serious complications such as blood clots, bleeding, and organ damage.

There are several subtypes of MPDs, including:

1. Chronic Myeloid Leukemia (CML): A disorder characterized by the overproduction of mature granulocytes (a type of white blood cell) in the bone marrow, leading to an increased number of these cells in the blood. CML is caused by a genetic mutation that results in the formation of the BCR-ABL fusion protein, which drives uncontrolled cell growth and division.
2. Polycythemia Vera (PV): A disorder characterized by the overproduction of all three types of blood cells - red blood cells, white blood cells, and platelets - in the bone marrow. This can lead to an increased risk of blood clots, bleeding, and enlargement of the spleen.
3. Essential Thrombocythemia (ET): A disorder characterized by the overproduction of platelets in the bone marrow, leading to an increased risk of blood clots and bleeding.
4. Primary Myelofibrosis (PMF): A disorder characterized by the replacement of normal bone marrow tissue with scar tissue, leading to impaired blood cell production and anemia, enlargement of the spleen, and increased risk of infections and bleeding.
5. Chronic Neutrophilic Leukemia (CNL): A rare disorder characterized by the overproduction of neutrophils (a type of white blood cell) in the bone marrow, leading to an increased number of these cells in the blood. CNL can lead to an increased risk of infections and organ damage.

MPDs are typically treated with a combination of therapies, including chemotherapy, targeted therapy, immunotherapy, and stem cell transplantation. The choice of treatment depends on several factors, including the subtype of MPD, the patient's age and overall health, and the presence of any comorbidities.

Hairy cell leukemia (HCL) is a rare, slow-growing type of cancer in which the bone marrow makes too many B cells (a type of white blood cell). These excess B cells are often referred to as "hairy cells" because they look abnormal under the microscope, with fine projections or "hair-like" cytoplasmic protrusions.

In HCL, these abnormal B cells can build up in the bone marrow and spleen, causing both of them to enlarge. The accumulation of hairy cells in the bone marrow can crowd out healthy blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia). This can result in fatigue, increased risk of infection, and easy bruising or bleeding.

HCL is typically an indolent disease, meaning that it progresses slowly over time. However, some cases may require treatment to manage symptoms and prevent complications. Treatment options for HCL include chemotherapy, immunotherapy, targeted therapy, and stem cell transplantation. Regular follow-up with a healthcare provider is essential to monitor the disease's progression and adjust treatment plans as needed.

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.

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.

Leukemia L1210 is not a medical definition itself, but it refers to a specific mouse leukemia cell line that was established in 1948. These cells are a type of acute myeloid leukemia (AML) and have been widely used in cancer research as a model for studying the disease, testing new therapies, and understanding the biology of leukemia. The L1210 cell line has contributed significantly to the development of various chemotherapeutic agents and treatment strategies for leukemia and other cancers.

Leukemia, B-cell is a type of cancer that affects the blood and bone marrow, characterized by an overproduction of abnormal B-lymphocytes, a type of white blood cell. These abnormal cells accumulate in the bone marrow and interfere with the production of normal blood cells, leading to anemia, infection, and bleeding.

B-cells are a type of lymphocyte that plays a crucial role in the immune system by producing antibodies to help fight off infections. In B-cell leukemia, the cancerous B-cells do not mature properly and accumulate in the bone marrow, leading to a decrease in the number of healthy white blood cells, red blood cells, and platelets.

There are several types of B-cell leukemia, including acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL). ALL is more common in children and young adults, while CLL is more common in older adults. Treatment options for B-cell leukemia depend on the type and stage of the disease and may include chemotherapy, radiation therapy, stem cell transplantation, or targeted therapies.

Transcription factors are proteins that play a crucial role in regulating gene expression by controlling the transcription of DNA to messenger RNA (mRNA). They function by binding to specific DNA sequences, known as response elements, located in the promoter region or enhancer regions of target genes. This binding can either activate or repress the initiation of transcription, depending on the properties and interactions of the particular transcription factor. Transcription factors often act as part of a complex network of regulatory proteins that determine the precise spatiotemporal patterns of gene expression during development, differentiation, and homeostasis in an organism.

A fatal outcome is a term used in medical context to describe a situation where a disease, injury, or illness results in the death of an individual. It is the most severe and unfortunate possible outcome of any medical condition, and is often used as a measure of the severity and prognosis of various diseases and injuries. In clinical trials and research, fatal outcome may be used as an endpoint to evaluate the effectiveness and safety of different treatments or interventions.

Bovine Leukemia Virus (BLV) is a retrovirus that infects cattle and causes enzootic bovine leukosis, a neoplastic disease characterized by the proliferation of malignant B-lymphocytes. The virus primarily targets the animal's immune system, leading to a decrease in the number of white blood cells (leukopenia) and an increased susceptibility to other infections.

The virus is transmitted horizontally through close contact with infected animals or vertically from mother to offspring via infected milk or colostrum. The majority of BLV-infected cattle remain asymptomatic carriers, but a small percentage develop clinical signs such as lymphoma, weight loss, and decreased milk production.

BLV is closely related to human T-cell leukemia virus (HTLV), and both viruses belong to the Retroviridae family, genus Deltaretrovirus. However, it's important to note that BLV does not cause leukemia or any other neoplastic diseases in humans.

Feline Leukemia Virus (FeLV) is a retrovirus that primarily infects cats, causing a variety of diseases and disorders. It is the causative agent of feline leukemia, a name given to a syndrome characterized by a variety of symptoms such as lymphoma (cancer of the lymphatic system), anemia, immunosuppression, and reproductive disorders. FeLV is typically transmitted through close contact with infected cats, such as through saliva, nasal secretions, urine, and milk. It can also be spread through shared litter boxes and feeding dishes.

FeLV infects cells of the immune system, leading to a weakened immune response and making the cat more susceptible to other infections. The virus can also integrate its genetic material into the host's DNA, potentially causing cancerous changes in infected cells. FeLV is a significant health concern for cats, particularly those that are exposed to outdoor environments or come into contact with other cats. Vaccination and regular veterinary care can help protect cats from this virus.

Histochemistry is the branch of pathology that deals with the microscopic localization of cellular or tissue components using specific chemical reactions. It involves the application of chemical techniques to identify and locate specific biomolecules within tissues, cells, and subcellular structures. This is achieved through the use of various staining methods that react with specific antigens or enzymes in the sample, allowing for their visualization under a microscope. Histochemistry is widely used in diagnostic pathology to identify different types of tissues, cells, and structures, as well as in research to study cellular and molecular processes in health and disease.

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.

DNA-binding proteins are a type of protein that have the ability to bind to DNA (deoxyribonucleic acid), the genetic material of organisms. These proteins play crucial roles in various biological processes, such as regulation of gene expression, DNA replication, repair and recombination.

The binding of DNA-binding proteins to specific DNA sequences is mediated by non-covalent interactions, including electrostatic, hydrogen bonding, and van der Waals forces. The specificity of binding is determined by the recognition of particular nucleotide sequences or structural features of the DNA molecule.

DNA-binding proteins can be classified into several categories based on their structure and function, such as transcription factors, histones, and restriction enzymes. Transcription factors are a major class of DNA-binding proteins that regulate gene expression by binding to specific DNA sequences in the promoter region of genes and recruiting other proteins to modulate transcription. Histones are DNA-binding proteins that package DNA into nucleosomes, the basic unit of chromatin structure. Restriction enzymes are DNA-binding proteins that recognize and cleave specific DNA sequences, and are widely used in molecular biology research and biotechnology applications.

Chromosome aberrations refer to structural and numerical changes in the chromosomes that can occur spontaneously or as a result of exposure to mutagenic agents. These changes can affect the genetic material encoded in the chromosomes, leading to various consequences such as developmental abnormalities, cancer, or infertility.

Structural aberrations include deletions, duplications, inversions, translocations, and rings, which result from breaks and rearrangements of chromosome segments. Numerical aberrations involve changes in the number of chromosomes, such as aneuploidy (extra or missing chromosomes) or polyploidy (multiples of a complete set of chromosomes).

Chromosome aberrations can be detected and analyzed using various cytogenetic techniques, including karyotyping, fluorescence in situ hybridization (FISH), and comparative genomic hybridization (CGH). These methods allow for the identification and characterization of chromosomal changes at the molecular level, providing valuable information for genetic counseling, diagnosis, and research.

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.

Cell division is the process by which a single eukaryotic cell (a cell with a true nucleus) divides into two identical daughter cells. This complex process involves several stages, including replication of DNA, separation of chromosomes, and division of the cytoplasm. There are two main types of cell division: mitosis and meiosis.

Mitosis is the type of cell division that results in two genetically identical daughter cells. It is a fundamental process for growth, development, and tissue repair in multicellular organisms. The stages of mitosis include prophase, prometaphase, metaphase, anaphase, and telophase, followed by cytokinesis, which divides the cytoplasm.

Meiosis, on the other hand, is a type of cell division that occurs in the gonads (ovaries and testes) during the production of gametes (sex cells). Meiosis results in four genetically unique daughter cells, each with half the number of chromosomes as the parent cell. This process is essential for sexual reproduction and genetic diversity. The stages of meiosis include meiosis I and meiosis II, which are further divided into prophase, prometaphase, metaphase, anaphase, and telophase.

In summary, cell division is the process by which a single cell divides into two daughter cells, either through mitosis or meiosis. This process is critical for growth, development, tissue repair, and sexual reproduction in multicellular organisms.

Gene expression regulation in leukemia refers to the processes that control the production or activation of specific proteins encoded by genes in leukemic cells. These regulatory mechanisms include various molecular interactions that can either promote or inhibit gene transcription and translation. In leukemia, abnormal gene expression regulation can lead to uncontrolled proliferation, differentiation arrest, and accumulation of malignant white blood cells (leukemia cells) in the bone marrow and peripheral blood.

Dysregulated gene expression in leukemia may involve genetic alterations such as mutations, chromosomal translocations, or epigenetic changes that affect DNA methylation patterns and histone modifications. These changes can result in the overexpression of oncogenes (genes with cancer-promoting functions) or underexpression of tumor suppressor genes (genes that prevent uncontrolled cell growth).

Understanding gene expression regulation in leukemia is crucial for developing targeted therapies and improving diagnostic, prognostic, and treatment strategies.

Leukemia, myeloid is a type of cancer that originates in the bone marrow, where blood cells are produced. Myeloid leukemia affects the myeloid cells, which include red blood cells, platelets, and most types of white blood cells. In this condition, the bone marrow produces abnormal myeloid cells that do not mature properly and accumulate in the bone marrow and blood. These abnormal cells hinder the production of normal blood cells, leading to various symptoms such as anemia, fatigue, increased risk of infections, and easy bruising or bleeding.

There are several types of myeloid leukemias, including acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). AML progresses rapidly and requires immediate treatment, while CML tends to progress more slowly. The exact causes of myeloid leukemia are not fully understood, but risk factors include exposure to radiation or certain chemicals, smoking, genetic disorders, and a history of chemotherapy or other cancer treatments.

Radiation-induced leukemia is a type of cancer that affects the blood-forming tissues of the body, such as the bone marrow. It is caused by exposure to high levels of radiation, which can damage the DNA of cells and lead to their uncontrolled growth and division.

There are several types of radiation-induced leukemia, depending on the specific type of blood cell that becomes cancerous. The most common types are acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). These forms of leukemia tend to progress quickly and require prompt treatment.

Radiation-induced leukemia is a rare complication of radiation therapy, which is used to treat many types of cancer. The risk of developing this type of leukemia increases with the dose and duration of radiation exposure. It is important to note that the benefits of radiation therapy in treating cancer generally outweigh the small increased risk of developing radiation-induced leukemia.

Symptoms of radiation-induced leukemia may include fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss. If you have been exposed to high levels of radiation and are experiencing these symptoms, it is important to seek medical attention promptly. A diagnosis of radiation-induced leukemia is typically made through a combination of physical exam, medical history, and laboratory tests, such as blood counts and bone marrow biopsy. Treatment may include chemotherapy, radiation therapy, and/or stem cell transplantation.

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.

The Myeloid-Lymphoid Leukemia (MLL) protein, also known as MLL1 or HRX, is a histone methyltransferase that plays a crucial role in the regulation of gene expression. It is involved in various cellular processes, including embryonic development and hematopoiesis (the formation of blood cells).

The MLL protein is encoded by the MLL gene, which is located on chromosome 11q23. This gene is frequently rearranged or mutated in certain types of leukemia, leading to the production of abnormal fusion proteins that contribute to tumor development and progression. These MLL-rearranged leukemias are aggressive and have a poor prognosis, making them an important area of research in the field of oncology.

Surface antigens are molecules found on the surface of cells that can be recognized by the immune system as being foreign or different from the host's own cells. Antigens are typically proteins or polysaccharides that are capable of stimulating an immune response, leading to the production of antibodies and activation of immune cells such as T-cells.

Surface antigens are important in the context of infectious diseases because they allow the immune system to identify and target infected cells for destruction. For example, viruses and bacteria often display surface antigens that are distinct from those found on host cells, allowing the immune system to recognize and attack them. In some cases, these surface antigens can also be used as targets for vaccines or other immunotherapies.

In addition to their role in infectious diseases, surface antigens are also important in the context of cancer. Tumor cells often display abnormal surface antigens that differ from those found on normal cells, allowing the immune system to potentially recognize and attack them. However, tumors can also develop mechanisms to evade the immune system, making it difficult to mount an effective response.

Overall, understanding the properties and behavior of surface antigens is crucial for developing effective immunotherapies and vaccines against infectious diseases and cancer.

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

I'm sorry for any confusion, but "Leukemia P388" is not a widely recognized medical term or a specific type of leukemia. The term "P388" is often used to refer to a particular type of mouse leukemia that is commonly used in laboratory research for testing potential anti-cancer drugs.

Leukemia, in general, is a type of cancer that originates in the bone marrow and results in an overproduction of abnormal white blood cells (leukocytes). These abnormal cells crowd out the healthy cells in the bone marrow, leading to a weakened immune system and various complications.

There are many different types of leukemia, classified based on the type of white blood cell affected (myeloid or lymphocytic) and the speed of progression (acute or chronic). If you're looking for information about a specific type of leukemia, I would be happy to help if you could provide more details.

Flow cytometry is a medical and research technique used to measure physical and chemical characteristics of cells or particles, one cell at a time, as they flow in a fluid stream through a beam of light. The properties measured include:

* Cell size (light scatter)
* Cell internal complexity (granularity, also light scatter)
* Presence or absence of specific proteins or other molecules on the cell surface or inside the cell (using fluorescent antibodies or other fluorescent probes)

The technique is widely used in cell counting, cell sorting, protein engineering, biomarker discovery and monitoring disease progression, particularly in hematology, immunology, and cancer research.

Biphenotypic acute leukemia (BAL) is a rare subtype of acute leukemia that possesses the features of both myeloid and lymphoid lineages. It is characterized by the presence of blasts that express antigens associated with both cell lines, which can make it challenging to diagnose and treat. BAL is considered an aggressive form of leukemia and requires prompt medical attention and treatment. The exact cause of BAL is not well understood, but like other forms of leukemia, it is thought to result from genetic mutations that lead to uncontrolled cell growth and division.

Bone marrow cells are the types of cells found within the bone marrow, which is the spongy tissue inside certain bones in the body. The main function of bone marrow is to produce blood cells. There are two types of bone marrow: red and yellow. Red bone marrow is where most blood cell production takes place, while yellow bone marrow serves as a fat storage site.

The three main types of bone marrow cells are:

1. Hematopoietic stem cells (HSCs): These are immature cells that can differentiate into any type of blood cell, including red blood cells, white blood cells, and platelets. They have the ability to self-renew, meaning they can divide and create more hematopoietic stem cells.
2. Red blood cell progenitors: These are immature cells that will develop into mature red blood cells, also known as erythrocytes. Red blood cells carry oxygen from the lungs to the body's tissues and carbon dioxide back to the lungs.
3. Myeloid and lymphoid white blood cell progenitors: These are immature cells that will develop into various types of white blood cells, which play a crucial role in the body's immune system by fighting infections and diseases. Myeloid progenitors give rise to granulocytes (neutrophils, eosinophils, and basophils), monocytes, and megakaryocytes (which eventually become platelets). Lymphoid progenitors differentiate into B cells, T cells, and natural killer (NK) cells.

Bone marrow cells are essential for maintaining a healthy blood cell count and immune system function. Abnormalities in bone marrow cells can lead to various medical conditions, such as anemia, leukopenia, leukocytosis, thrombocytopenia, or thrombocytosis, depending on the specific type of blood cell affected. Additionally, bone marrow cells are often used in transplantation procedures to treat patients with certain types of cancer, such as leukemia and lymphoma, or other hematologic disorders.

... (AMKL) is life-threatening leukemia in which malignant megakaryoblasts proliferate abnormally ... Wang SA, Hasserjian RP (July 2015). "Acute Erythroleukemias, Acute Megakaryoblastic Leukemias, and Reactive Mimics: A Guide to ... Gassmann W, Löffler H (1995). "Acute megakaryoblastic leukemia". Leukemia & Lymphoma. 18 Suppl 1: 69-73. doi:10.3109/ ... "GATA1 mutations in transient leukemia and acute megakaryoblastic leukemia of Down syndrome". Blood. 101 (11): 4301-4. doi: ...
Gassmann W, Winfried; Löffler H. (1995). "Acute megakaryoblastic leukemia". Leuk. Lymphoma. 18 Suppl 1: Leukemia and Lymphoma. ... Löwenberg B, Downing JR, Burnett A (Sep 30, 1999). "Acute myeloid leukemia". N Engl J Med (Review). 341 (14): 1051-62. doi: ... Leukemia is a malignancy producing of white blood cells in bone marrow. It can be a serious disease if not treated early. ... These cancers include leukemias, lymphomas, and myelomas. These particular types of cancers can arise as defected mature cell ...
TMD may be followed within weeks to ~5 years by a subtype of myeloid leukemia, acute megakaryoblastic leukemia. AMKL is ... Gassmann W, Löffler H (1995). "Acute megakaryoblastic leukemia". Leukemia & Lymphoma. 18 Suppl 1: 69-73. doi:10.3109/ ... It is not known if these regimens have an impact on the development of acute megakaryoblastic leukemia. Currently, it is ... Moreover, ~10% of individuals diagnosed with TMD develop acute megakaryoblastic leukemia at some time during the 5 years ...
Acute megakaryoblastic leukemia is a subtype of acute myeloid leukemia that is extremely rare in adults and, although still ... It resolves totally within ~3 months but in the following 1-3 years progresses to acute megakaryoblastic leukemia in 20% to 30 ... These same individuals can develop secondary mutations in other genes that results in acute megakaryoblastic leukemia. GATA1 ... Gruber TA, Downing JR (August 2015). "The biology of pediatric acute megakaryoblastic leukemia". Blood. 126 (8): 943-9. doi: ...
Bloomfield CD, Brunning RD (September 1985). "FAB M7: acute megakaryoblastic leukemia--beyond morphology". Annals of Internal ... "Acute Myeloid Leukemia Staging". Retrieved 26 August 2011. Mihova D. "Leukemia acute - Acute myeloid leukemia with minimal ... Acute leukemias of ambiguous lineage (also known as mixed phenotype or biphenotypic acute leukemia) occur when the leukemic ... "acute leukemia" in 1889 to differentiate rapidly progressive and fatal leukemias from the more indolent chronic leukemias. The ...
May 2005). "Acute panmyelosis with myelofibrosis: an entity distinct from acute megakaryoblastic leukemia". Mod. Pathol. 18 (5 ... Acute myeloid leukemia Panmyelosis Myelofibrosis (Articles with short description, Short description is different from Wikidata ... Controversy remains today whether this disorder is a subtype of acute myeloid leukemia or myelodysplastic syndromes; however, ... All articles with unsourced statements, Articles with unsourced statements from December 2008, Acute myeloid leukemia). ...
2007). "A novel fusion of RBM6 to CSF1R in acute megakaryoblastic leukemia". Blood. 110 (1): 323-33. doi:10.1182/blood-2006-10- ...
Rare cases of adult onset acute megakaryoblastic leukemia are associated with malignant mediastinal germ cell tumor. In these ... the mediastinal germ cell tumor develops before or concomitantly with but not after acute megakaryoblastic leukemia. The three ...
Chronic myelogenous leukemia: A cancer of the white blood cells. Acute megakaryoblastic leukemia: A life-threatening leukemia ... Myeloid leukemia is a type of leukemia affecting myeloid tissue. Types include: Acute myeloid leukemia: A cancer of the myeloid ...
For instance, in cases of acute megakaryoblastic leukemia, TMEM241 was found to be one of the most upregulated genes. In ... "Integrated differential transcriptome maps of Acute Megakaryoblastic Leukemia (AMKL) in children with or without Down Syndrome ...
July 2001). "Fusion of two novel genes, RBM15 and MKL1, in the t(1;22)(p13;q13) of acute megakaryoblastic leukemia". Nature ... MKL/megakaryoblastic leukemia 1 (also termed MRTFA/myocardin related transcription factor A) is a protein that in humans is ... "Entrez Gene: MKL1 megakaryoblastic leukemia (translocation) 1". Vartiainen MK, Guettler S, Larijani B, Treisman R (June 2007 ... Cen B, Selvaraj A, Burgess RC, Hitzler JK, Ma Z, Morris SW, Prywes R (September 2003). "Megakaryoblastic leukemia 1, a potent ...
... of acute megakaryoblastic leukemia". Nat Genet. 28 (3): 220-1. doi:10.1038/90054. PMID 11431691. S2CID 36236342. Mercher T, ... 2005). "RBM15-MKL1 (OTT-MAL) fusion transcript in an adult acute myeloid leukemia patient". Am. J. Hematol. 79 (1): 43-5. doi: ... translocation of acute megakaryocytic leukemia". Proc Natl Acad Sci U S A. 98 (10): 5776-9. Bibcode:2001PNAS...98.5776M. doi: ...
Upregulation of miR-125b occurs in patients with B-cell acute lymphoblastic leukemia, megakaryoblastic leukemia, myelodysplasia ... and acute myeloid leukemia. While miR-125a acts as an oncogenic miRNA in non-blood cancers, its oncogenic functions have been ... Leukemia. 26 (9): 2011-2018. doi:10.1038/leu.2012.90. ISSN 0887-6924. PMID 22456625. S2CID 30128839. Emmrich, Stephan; Rasche, ...
"High incidence of CALM-AF10 fusion and the identification of a novel fusion transcript in acute megakaryoblastic leukemia in ... 2007). "Acute myeloid leukemia is propagated by a leukemic stem cell with lymphoid characteristics in a mouse model of CALM/ ... 2003). "A novel chromosomal inversion at 11q23 in infant acute myeloid leukemia fuses MLL to CALM, a gene that encodes a ... "Expression of a CALM-AF10 fusion gene leads to Hoxa cluster overexpression and acute leukemia in transgenic mice". Cancer Res. ...
In addition, oncogenic JAK3 mutations have been identified in acute megakaryoblastic leukemia, T-cell prolymphocytic leukemia, ... JAK3 activating mutations are found in 16% of T-cell acute lymphoblastic leukemia (T-ALL) patients. ... causing T-cell acute lymphoblastic leukemia in a mouse model". Blood. 124 (20): 3092-100. doi:10.1182/blood-2014-04-566687. ... sequencing identifies associations between IL7R-JAK mutations and epigenetic modulators in T-cell acute lymphoblastic leukemia ...
"Acute megakaryoblastic leukemia: establishment of a new cell line (MKPL-1) in vitro and in vivo". Leukemia. 6 (6): 588-94. PMID ... Asou, H; Tashiro, S; Hamamoto, K; Otsuji, A; Kita, K; Kamada, N (1 May 1991). "Establishment of a human acute myeloid leukemia ... Findley HW, Jr; Cooper, MD; Kim, TH; Alvarado, C; Ragab, AH (December 1982). "Two new acute lymphoblastic leukemia cell lines ... Kishi, K (1985). "A new leukemia cell line with Philadelphia chromosome characterized as basophil precursors". Leukemia ...
... acute megakaryoblastic leukemia), is 500 times more common. Acute megakaryoblastic leukemia (AMKL) is a leukemia of ... In particular, acute lymphoblastic leukemia is 20 times more common and the megakaryoblastic form of acute myeloid leukemia ( ... including acute lymphoblastic leukemia (ALL) and acute megakaryoblastic leukemia (AMKL) is increased while the risk of other ... pathogenesis and clinical aspects of acute lymphoblastic leukemia in children with Down syndrome". Leukemia. 30 (9): 1816-23. ...
... aniridia Acute lymphocytic leukemia Acute megakaryoblastic leukemia Acute monoblastic leukemia Acute monocytic leukemia Acute ... leukemia without maturation Acute myelocytic leukemia Acute myelogenous leukemia Acute myeloid leukemia Acute myeloid leukemia ... leukemia type 1 Acute myeloblastic leukemia type 2 Acute myeloblastic leukemia type 3 Acute myeloblastic leukemia type 4 Acute ... myeloblastic leukemia type 5 Acute myeloblastic leukemia type 6 Acute myeloblastic leukemia type 7 Acute myeloblastic leukemia ...
... progresses to acute megakaryoblastic leukemia. The elimination of other causes of cytopenias, along with a dysplastic bone ... September 2007). "Phase I study of decitabine alone or in combination with valproic acid in acute myeloid leukemia". Journal of ... Seewald L, Taub JW, Maloney KW, McCabe ER (September 2012). "Acute leukemias in children with Down syndrome". Molecular ... Block M, Jacobson LO, Bethard WF (July 1953). "Preleukemic acute human leukemia". Journal of the American Medical Association. ...
Acute myelogenous leukemia (AML) Acute megakaryoblastic leukemia (AMKL), a sub-type of acute myelogenous leukemia Chronic ... T-cell prolymphocytic leukemia (T-PLL) B-cell prolymphocytic leukemia (B-PLL) Chronic neutrophilic leukemia (CNL) Hairy cell ... Myelomas Multiple myeloma Waldenström macroglobulinemia Plasmacytoma Leukemias increased WBC Acute lymphocytic leukemia (ALL) ... leukemia (HCL) T-cell large granular lymphocyte leukemia (T-LGL) Aggressive NK-cell leukemia Hemochromatosis Asplenia ...
... acute myeloid; 601626; FLT3 Leukemia, acute myeloid; 601626; KIT Leukemia, acute myeloid; 601626; LPP Leukemia, acute myeloid; ... PTPN11 Leukemia, megakaryoblastic, of Down syndrome; 190685; GATA1 Leukemia, megakaryoblastic, with or without Down syndrome; ... acute myelogenous; 601626; JAK2 Leukemia, acute myeloid; 601626; MLF1 Leukemia, acute myeloid; 601626; NSD1 Leukemia, acute ... acute myeloid; 601626; NUP214 Leukemia, acute myeloid; 601626; PICALM Leukemia, acute myeloid; 601626; RUNX1 Leukemia, acute ...
Lymphomas, lymphocytic leukemias, and myeloma are from the lymphoid line, while acute and chronic myelogenous leukemia, ... leukaemia Acute monoblastic and monocytic leukaemia Pure erythroid leukaemia Acute megakaryoblastic leukaemia Acute basophilic ... NOS Mixed-phenotype acute leukaemia, T/myeloid, NOS Mixed-phenotype acute leukaemia, NOS, rare types Acute leukaemias of ... dendritic cell neoplasm Acute leukaemias of ambiguous lineage Acute undifferentiated leukaemia Mixed-phenotype acute leukaemia ...
Kitamura N, Koshiba M, Horie O, Ryo R (2002). "Expression of granulysin mRNA in the human megakaryoblastic leukemia cell line ... June 2004). "Enhanced granulysin mRNA expression in urinary sediment in early and delayed acute renal allograft rejection". ...
Subtypes of AML include acute promyelocytic leukemia, acute myeloblastic leukemia, and acute megakaryoblastic leukemia. Chronic ... Nearly all leukemias appearing in pregnant women are acute leukemias. Acute leukemias normally require prompt, aggressive ... There are four main types of leukemia-acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic ... Subtypes include precursor B acute lymphoblastic leukemia, precursor T acute lymphoblastic leukemia, Burkitt's leukemia, and ...
MLL M9910/3 Acute megakaryoblastic leukemia, NOS Megakaryocytic leukemia (FAB-M7) M9920/3 Acute myeloid leukemia and ... Acute myelogenous leukemia Acute non-lymphocytic leukemia Acute granulocytic leukemia Acute myelogenous leukemia Acute ... NOS Acute lymphocytic leukemia Acute lymphoid leukemia Acute lymphatic leukemia Acute lymphoblastic leukemia, L2 type, NOS FAB ... Stem cell leukemia M9805/3 Acute biphenotypic leukemia Acute leukemia of ambiguous lineage Acute mixed lineage leukemia Acute ...

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