Hematopoietic Stem Cell Transplantation
Stem Cell Transplantation
Stem Cell Niche
Hematopoietic Stem Cell Mobilization
Embryonic Stem Cells
Bone Marrow Cells
Colony-Forming Units Assay
Stem Cell Factor
Multipotent Stem Cells
Graft vs Host Disease
Bone Marrow Transplantation
Induced Pluripotent Stem Cells
Mesenchymal Stromal Cells
Neural Stem Cells
Mesenchymal Stem Cell Transplantation
Fetal Stem Cells
Proto-Oncogene Proteins c-kit
Cord Blood Stem Cell Transplantation
Mice, Inbred NOD
Myeloid Progenitor Cells
Granulocyte Colony-Stimulating Factor
Peripheral Blood Stem Cell Transplantation
Neoplastic Stem Cells
Lymphoid Progenitor Cells
Reverse Transcriptase Polymerase Chain Reaction
Green Fluorescent Proteins
Severe Combined Immunodeficiency
Gene Expression Regulation, Developmental
Leukemia, Myeloid, Acute
Gene Expression Regulation
GATA2 Transcription Factor
Core Binding Factor Alpha 2 Subunit
Graft vs Leukemia Effect
Gene Expression Profiling
Hematopoietic Cell Growth Factors
Interleukin Receptor Common gamma Subunit
Blood Cell Count
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Cell- and Tissue-Based Therapy
Gene Transfer Techniques
Totipotent Stem Cells
Erythroid Precursor Cells
Hepatic Veno-Occlusive Disease
Octamer Transcription Factor-3
Platelet Membrane Glycoprotein IIb
Mice, Inbred Strains
Polymerase Chain Reaction
Disease Models, Animal
Combined Modality Therapy
Fetal Tissue Transplantation
Oligonucleotide Array Sequence Analysis
Graft vs Tumor Effect
Basic Helix-Loop-Helix Transcription Factors
Real-Time Polymerase Chain Reaction
Precursor Cell Lymphoblastic Leukemia-Lymphoma
ETO-2, a new member of the ETO-family of nuclear proteins. (1/11748)The t(8;21) is associated with 12-15% of acute myelogenous leukemias of the M2 subtype. The translocation results in the fusion of two genes, AML1 (CBFA2) on chromosome 21 and ETO (MTG8) on chromosome 8. AML1 encodes a DNA binding factor; the ETO protein product is less well characterized, but is thought to be a transcription factor. Here we describe the isolation and characterization of ETO-2, a murine cDNA that encodes a new member of the ETO family of proteins. ETO-2 is 75% identical to murine ETO and shares very high sequence identities over four regions of the protein with ETO (domain I-III and zinc-finger). Northern analysis identifies ETO-2 transcripts in many of the murine tissues analysed and in the developing mouse embryo. ETO-2 is also expressed in myeloid and erythroid cell lines. We confirmed the nuclear localization of ETO-2 and demonstrated that domain III and the zinc-finger region are not required for nuclear localization. We further showed that a region within ETO, containing domain II, mediates dimerization among family members. This region is conserved in the oncoprotein AML-1/ETO. The recent identification of another ETO-like protein, myeloid translocation gene-related protein 1, together with the data presented here, demonstrates that at least three ETO proteins exist with the potential to form dimers in the cell nucleus. (+info)
Establishment of an inducible expression system of chimeric MLL-LTG9 protein and inhibition of Hox a7, Hox b7 and Hox c9 expression by MLL-LTG9 in 32Dcl3 cells. (2/11748)The MLL (HRX/ALL-1 gene is frequently disrupted in infantile leukemias and therapy-related leukemias and fused to various translocation partner genes. We previously showed that chimeric MLL proteins localize in the nuclei in a fashion similar to that of MLL protein even if the partner gene encodes a cytoplasmic protein and indicated the importance of the N-terminal portion of MLL common to various MLL translocations. This time we established an inducible expression system for chimeric MLL-LTG9 and truncated N-terminal MLL proteins (MLL-Zf(-)) in 32Dcl3 cells. By utilizing this system, we were able to show inhibition of Hox a7, Hox b7 and Hox c9 genes' expression by induced MLL-LTG9 and MLL-Zf(-). Up-regulation of Hox a7, Hox b7 and Hox c9 was observed when 32Dcl3 cells were cultured with granulocyte colony stimulating factor (G-CSF) in place of interleukin 3 and induction of MLL-LTG9 and MLL-Zf(-) was shown to suppress this upregulation. At the same time, expression of two mammalian Polycomb group genes, M33 and mel-18, which both reportedly affect Hox genes' expression, was not inhibited by MLL-LTG9 and MLL-Zf(-) induction. These results indicate that MLL has an important effect on the expression of at least some Hox genes in hematopoietic cells and suggest that inhibition of the proper expression of Hox genes by chimeric MLL proteins may dysregulate hematopoietic cell differentiation and proliferation, which then can lead to leukemogenesis. (+info)
Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2 deficient mice results in extended hyperresponsiveness. (3/11748)ICAM-2-deficient mice exhibit prolonged accumulation of eosinophils in lung interstitium concomitant with a delayed increase in eosinophil numbers in the airway lumen during the development of allergic lung inflammation. The ICAM-2-dependent increased and prolonged accumulation of eosinophils in lung interstitium results in prolonged, heightened airway hyperresponsiveness. These findings reveal an essential role for ICAM-2 in the development of the inflammatory and respiratory components of allergic lung disease. This phenotype is caused by the lack of ICAM-2 expression on non-hematopoietic cells. ICAM-2 deficiency on endothelial cells causes reduced eosinophil transmigration in vitro. ICAM-2 is not essential for lymphocyte homing or the development of leukocytes, with the exception of megakaryocyte progenitors, which are significantly reduced. (+info)
Enhanced myeloid progenitor cell cycling and apoptosis in mice lacking the chemokine receptor, CCR2. (4/11748)Chemokines regulate hematopoiesis in part by influencing the proliferative status of myeloid progenitor cells (MPC). Human MCP-1/murine JE, a myelosuppressive chemokine, specifically binds C-C chemokine receptor 2 (CCR2). Transgenic mice containing a targeted disruption in CCR2 that prevents expression of CCR2 mRNA and protein and have MPC that are insensitive to inhibition by MCP-1 and JE in vitro were assessed for potential abnormalities in growth of bone marrow (BM) and spleen MPC. MPC in both unseparated and c-kit+lin- populations of BM from CCR2-deficient (-/-) mice were in a greatly increased proliferation state compared with CCR2 littermate control (+/+) mice, an effect not apparent with progenitors from spleens of CCR2 (-/-) mice. Increased cycling status of CCR2 (-/-) BM MPC did not result in increased numbers of nucleated cells or MPC in BM or spleens of CCR2 (-/-) mice. Possible reasons for this apparent discrepancy were highlighted by flow cytometric analysis of c-kit+lin- BM cells and colony formation by MPC subjected to delayed addition of growth factors. The c-kit+lin- population of BM cells from CCR2 (-/-) mice had a significantly higher percentage of apoptotic cells than those from CCR2 (+/+) BM. However, elevated apoptosis was not associated with decreased numbers of c-kit+lin- cells. The increased percentage of apoptotic c-kit+lin- cells was due to elevated apoptosis within the c-kitdimlin-, but not the c-kitbrightlin-, subpopulations of cells. Consistent with enhanced apoptosis of phenotypically defined cells, MPC from CCR2 (-/-) BM and purified c-kit+lin- cells demonstrated decreased cell survival in vitro upon delayed addition of growth factors. The data suggest that signals received by CCR2 limit proliferation of progenitor cells in the BM, but also enhance survival of these cells. (+info)
Autografting with philadelphia chromosome-negative mobilized hematopoietic progenitor cells in chronic myelogenous leukemia. (5/11748)Intensive chemotherapy given in early chronic phase of chronic myelogenous leukemia (CML) has resulted in high numbers of circulating Philadelphia (Ph) chromosome-negative hematopoietic progenitor cells (HPC). We have autografted 30 consecutive patients with CML in chronic phase with HPC collected in this way to facilitate restoration of Ph-negative hematopoiesis in bone marrow after high-dose therapy. Hematopoietic recovery to greater than 0.5 x10(9)/L neutrophils and to greater than 25 x 10(9)/L platelets occurred in all patients, a median of 13 (range, 9 to 32) days and 16 (range, 6 to 106) days postautograft, respectively. Regenerating marrow cells were Ph-negative in 16 (53%) patients and greater than 66% Ph-negative in 10 (33%) patients. Twenty-eight patients are alive 6 to 76 months (median, 24 months) after autografting. Three patients have developed blast crisis from which 2 have died. Eight patients are in complete cytogenetic remission at a median of 20 (range, 6 to 44) months with a median ratio BCR-ABL/ABL of 0.002 (range, <0.001 to 0.01). Eight patients are in major cytogenetic remission at a median of 22 (range, 6 to 48) months. No patient died as a consequence of the treatment. All patients had some degree of stomatitis that was severe in 15 (50%) patients. Gastrointestinal and hepatic toxicities were observed in about one fourth of patients. Thus, autografting with Ph-negative mobilized HPC can result in prolonged restoration of Ph-negative hematopoiesis for some patients with CML; moreover, most autograft recipients report normal or near normal activity levels, suggesting that this procedure need not to be associated either with prolonged convalescence or with chronic debility. (+info)
H-Ras is involved in the inside-out signaling pathway of interleukin-3-induced integrin activation. (6/11748)The proto-oncogene product, p21(ras), has been implicated in the cellular mechanism of adhesion, although its precise role has been controversial. Numerous cytokines and growth-factors activate Ras, which is an important component of their growth-promoting signaling pathways. On the other hand, the role of Ras in cytokine-induced adhesion has not been elucidated. We therefore investigated the function of H-Ras in the inside-out signaling pathway of interleukin-3 (IL-3)-induced integrin activation in the murine Baf3 cell line after transfection of cells with either constitutively active, dominant-negative, or wild-type H-Ras cDNAs. Adhesion of Baf3 cells to fibronectin was induced by IL-3 in a dose-dependent manner via very late antigen-4 (VLA-4; alpha4beta1 integrins) and VLA-5 (alpha5beta1 integrins) activation. On the other hand, IL-4 did not induce the adhesion of Baf3 cells to fibronectin, although IL-4 did stimulate the cell proliferation of Baf3 cells. Constitutively active H-Ras-transfected Baf3 cells adhered to fibronectin without IL-3 stimulation through VLA-4 and VLA-5, whereas dominant-negative H-Ras-transfected Baf3 cells showed significantly less adhesion induced by IL-3 compared with wild-type and constitutively active H-Ras-transfected Baf3 cells. Anti-beta1 integrin antibody (clone; 9EG7), which is known to change integrin conformation and activate integrins, induced the adhesion of dominant-negative H-Ras-transfected Baf3 cells as much as the other types of H-Ras-transfected Baf3 cells. 8-Br-cAMP, Dibutyryl-cAMP, Ras-Raf-1 pathway inhibitors, and PD98059, a MAPK kinase inhibitor, suppressed proliferation and phosphorylation of MAPK detected by Western blotting with anti-phospho-MAPK antibody, but not adhesion of any type of H-Ras-transfected Baf3 cells, whereas U-73122, a phospholipase C (PLC) inhibitor, suppressed adhesion of these cells completely. These data indicate that H-Ras and PLC, but not Raf-1, MAPK kinase, or the MAPK pathway, are involved in the inside-out signaling pathway of IL-3-induced VLA-4 and VLA-5 activation in Baf3 cells. (+info)
In vitro hematopoietic and endothelial cell development from cells expressing TEK receptor in murine aorta-gonad-mesonephros region. (7/11748)Recent studies have shown that long-term repopulating hematopoietic stem cells (HSCs) first appear in the aorta-gonad-mesonephros (AGM) region. Our immunohistochemistry study showed that TEK+ cells existed in the AGM region. Approximately 5% of AGM cells were TEK+, and most of these were CD34(+) and c-Kit+. We then established a coculture system of AGM cells using a stromal cell line, OP9, which is deficient in macrophage colony-stimulating factor (M-CSF). With this system, we showed that AGM cells at 10.5 days postcoitum (dpc) differentiated and proliferated into both hematopoietic and endothelial cells. Proliferating hematopoietic cells contained a significant number of colony-forming cells in culture (CFU-C) and in spleen (CFU-S). Among primary AGM cells at 10.5 dpc, sorted TEK+ AGM cells generated hematopoietic cells and platelet endothelial cell adhesion molecule (PECAM)-1(+) endothelial cells on the OP9 stromal layer, while TEK- cells did not. When a ligand for TEK, angiopoietin-1, was added to the single-cell culture of AGM, endothelial cell growth was detected in the wells where hematopoietic colonies grew. Although the incidence was still low (1/135), we showed that single TEK+ cells generated hematopoietic cells and endothelial cells simultaneously, using a single-cell deposition system. This in vitro coculture system shows that the TEK+ fraction of primary AGM cells is a candidate for hemangioblasts, which can differentiate into both hematopoietic cells and endothelial cells. (+info)
Organ-selective homing defines engraftment kinetics of murine hematopoietic stem cells and is compromised by Ex vivo expansion. (8/11748)Hematopoietic reconstitution of ablated recipients requires that intravenously (IV) transplanted stem and progenitor cells "home" to organs that support their proliferation and differentiation. To examine the possible relationship between homing properties and subsequent engraftment potential, murine bone marrow (BM) cells were labeled with fluorescent PKH26 dye and injected into lethally irradiated hosts. PKH26(+) cells homing to marrow or spleen were then isolated by fluorescence-activated cell sorting and assayed for in vitro colony-forming cells (CFCs). Progenitors accumulated rapidly in the spleen, but declined to only 6% of input numbers after 24 hours. Although egress from this organ was accompanied by a simultaneous accumulation of CFCs in the BM (plateauing at 6% to 8% of input after 3 hours), spleen cells remained enriched in donor CFCs compared with marrow during this time. To determine whether this differential homing of clonogenic cells to the marrow and spleen influenced their contribution to short-term or long-term hematopoiesis in vivo, PKH26(+) cells were sorted from each organ 3 hours after transplantation and injected into lethally irradiated Ly-5 congenic mice. Cells that had homed initially to the spleen regenerated circulating leukocytes (20% of normal counts) approximately 2 weeks faster than cells that had homed to the marrow, or PKH26-labeled cells that had not been selected by a prior homing step. Both primary (17 weeks) and secondary (10 weeks) recipients of "spleen-homed" cells also contained approximately 50% higher numbers of CFCs per femur than recipients of "BM-homed" cells. To examine whether progenitor homing was altered upon ex vivo expansion, highly enriched Sca-1(+)c-kit+Lin- cells were cultured for 9 days in serum-free medium containing interleukin (IL)-6, IL-11, granulocyte colony-stimulating factor, stem cell factor, flk-2/flt3 ligand, and thrombopoietin. Expanded cells were then stained with PKH26 and assayed as above. Strikingly, CFCs generated in vitro exhibited a 10-fold reduction in homing capacity compared with fresh progenitors. These studies demonstrate that clonogenic cells with differential homing properties contribute variably to early and late hematopoiesis in vivo. The dramatic decline in the homing capacity of progenitors generated in vitro underscores critical qualitative changes that may compromise their biologic function and potential clinical utility, despite their efficient numerical expansion. (+info)
The diagnosis of GVHD is based on a combination of clinical findings, laboratory tests, and biopsies. Treatment options include immunosuppressive drugs, corticosteroids, and in severe cases, stem cell transplantation reversal or donor lymphocyte infusion.
Prevention of GVHD includes selecting the right donor, using conditioning regimens that minimize damage to the recipient's bone marrow, and providing appropriate immunosuppression after transplantation. Early detection and management of GVHD are critical to prevent long-term complications and improve survival rates.
Hematologic neoplasms refer to abnormal growths or tumors that affect the blood, bone marrow, or lymphatic system. These types of cancer can originate from various cell types, including red blood cells, white blood cells, platelets, and lymphoid cells.
There are several subtypes of hematologic neoplasms, including:
1. Leukemias: Cancers of the blood-forming cells in the bone marrow, which can lead to an overproduction of immature or abnormal white blood cells, red blood cells, or platelets. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
2. Lymphomas: Cancers of the immune system, which can affect the lymph nodes, spleen, liver, or other organs. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
3. Multiple myeloma: A cancer of the plasma cells in the bone marrow that can lead to an overproduction of abnormal plasma cells.
4. Myeloproliferative neoplasms: Cancers that affect the blood-forming cells in the bone marrow, leading to an overproduction of red blood cells, white blood cells, or platelets. Examples include polycythemia vera and essential thrombocythemia.
5. Myelodysplastic syndromes: Cancers that affect the blood-forming cells in the bone marrow, leading to an underproduction of normal blood cells.
The diagnosis of hematologic neoplasms typically involves a combination of physical examination, medical history, laboratory tests (such as complete blood counts and bone marrow biopsies), and imaging studies (such as CT scans or PET scans). Treatment options for hematologic neoplasms depend on the specific type of cancer, the severity of the disease, and the overall health of the patient. These may include chemotherapy, radiation therapy, stem cell transplantation, or targeted therapy with drugs that specifically target cancer cells.
There are several different types of leukemia, including:
1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.
Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.
Examples of hematologic diseases include:
1. Anemia - a condition where there are not enough red blood cells or hemoglobin in the body.
2. Leukemia - a type of cancer that affects the bone marrow and blood, causing an overproduction of immature white blood cells.
3. Lymphoma - a type of cancer that affects the lymphatic system, including the bone marrow, spleen, and lymph nodes.
4. Thalassemia - a genetic disorder that affects the production of hemoglobin, leading to anemia and other complications.
5. Sickle cell disease - a genetic disorder that affects the production of hemoglobin, causing red blood cells to become sickle-shaped and prone to breaking down.
6. Polycythemia vera - a rare disorder where there is an overproduction of red blood cells.
7. Myelodysplastic syndrome - a condition where the bone marrow produces abnormal blood cells that do not mature properly.
8. Myeloproliferative neoplasms - a group of conditions where the bone marrow produces excessive amounts of blood cells, including polycythemia vera, essential thrombocythemia, and primary myelofibrosis.
9. Deep vein thrombosis - a condition where a blood clot forms in a deep vein, often in the leg or arm.
10. Pulmonary embolism - a condition where a blood clot travels to the lungs and blocks a blood vessel, causing shortness of breath, chest pain, and other symptoms.
These are just a few examples of hematologic diseases, but there are many others that can affect the blood and bone marrow. Treatment options for these diseases can range from watchful waiting and medication to surgery, chemotherapy, and stem cell transplantation. It is important to seek medical attention if you experience any symptoms of hematologic disease, as early diagnosis and treatment can improve outcomes.
People with SCID are extremely susceptible to infections, particularly those caused by viruses, and often develop symptoms shortly after birth. These may include diarrhea, vomiting, fever, and failure to gain weight or grow at the expected rate. Without treatment, SCID can lead to life-threatening infections and can be fatal within the first year of life.
Treatment for SCID typically involves bone marrow transplantation or enzyme replacement therapy. Bone marrow transplantation involves replacing the patient's faulty immune system with healthy cells from a donor, while enzyme replacement therapy involves replacing the missing or dysfunctional enzymes that cause the immune deficiency. Both of these treatments can help restore the patient's immune system and improve their quality of life.
In summary, severe combined immunodeficiency (SCID) is a rare genetic disorder that impairs the body's ability to fight infections and can be fatal without treatment. Treatment options include bone marrow transplantation and enzyme replacement therapy.
There are several subtypes of MDS, each with distinct clinical features and prognosis. The most common subtype is refractory anemia with excess blasts (RAEB), followed by chronic myelomonocytic leukemia (CMMoL) and acute myeloid leukemia (AML).
The exact cause of MDS is not fully understood, but it is believed to result from a combination of genetic mutations and environmental factors. Risk factors for developing MDS include exposure to certain chemicals or radiation, age over 60, and a history of previous cancer treatment.
Symptoms of MDS can vary depending on the specific subtype and severity of the disorder, but may include fatigue, weakness, shortness of breath, infection, bleeding, and easy bruising. Diagnosis is typically made through a combination of physical examination, medical history, blood tests, and bone marrow biopsy.
Treatment for MDS depends on the specific subtype and severity of the disorder, as well as the patient's overall health and preferences. Options may include supportive care, such as blood transfusions and antibiotics, or more intensive therapies like chemotherapy, bone marrow transplantation, or gene therapy.
Overall, myelodysplastic syndromes are a complex and heterogeneous group of disorders that can have a significant impact on quality of life and survival. Ongoing research is focused on improving diagnostic accuracy, developing more effective treatments, and exploring novel therapeutic approaches to improve outcomes for patients with MDS.
AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.
There are several subtypes of AML, including:
1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.
The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Confusion or seizures
AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.
Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:
1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.
It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.
The BCR-ABL gene is a fusion gene that is present in the majority of cases of CML. It is created by the translocation of two genes, called BCR and ABL, which leads to the production of a constitutively active tyrosine kinase protein that promotes the growth and proliferation of abnormal white blood cells.
There are three main phases of CML, each with distinct clinical and laboratory features:
1. Chronic phase: This is the earliest phase of CML, where patients may be asymptomatic or have mild symptoms such as fatigue, night sweats, and splenomegaly (enlargement of the spleen). The peripheral blood count typically shows a high number of blasts in the blood, but the bone marrow is still functional.
2. Accelerated phase: In this phase, the disease progresses to a higher number of blasts in the blood and bone marrow, with evidence of more aggressive disease. Patients may experience symptoms such as fever, weight loss, and pain in the joints or abdomen.
3. Blast phase: This is the most advanced phase of CML, where there is a high number of blasts in the blood and bone marrow, with significant loss of function of the bone marrow. Patients are often symptomatic and may have evidence of spread of the disease to other organs, such as the liver or spleen.
Treatment for CML typically involves targeted therapy with drugs that inhibit the activity of the BCR-ABL protein, such as imatinib (Gleevec), dasatinib (Sprycel), or nilotinib (Tasigna). These drugs can slow or stop the progression of the disease, and may also produce a complete cytogenetic response, which is defined as the absence of all Ph+ metaphases in the bone marrow. However, these drugs are not curative and may have significant side effects. Allogenic hematopoietic stem cell transplantation (HSCT) is also a potential treatment option for CML, but it carries significant risks and is usually reserved for patients who are in the blast phase of the disease or have failed other treatments.
In summary, the clinical course of CML can be divided into three phases based on the number of blasts in the blood and bone marrow, and treatment options vary depending on the phase of the disease. It is important for patients with CML to receive regular monitoring and follow-up care to assess their response to treatment and detect any signs of disease progression.
There are several types of MPDs, including:
1. Polycythemia vera (PV): This is a rare disorder characterized by an overproduction of red blood cells, white blood cells, and platelets.
2. Essential thrombocythemia (ET): This is a rare disorder characterized by an overproduction of platelets.
3. Primary myelofibrosis (PMF): This is a rare and severe disorder characterized by the accumulation of scar tissue in the bone marrow, leading to an overproduction of immature white blood cells.
4. Chronic myelogenous leukemia (CML): This is a type of cancer that affects the bone marrow and blood cells, characterized by the overproduction of immature white blood cells.
The symptoms of MPDs can vary depending on the specific disorder, but may include:
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen spleen
* Bone pain
The exact cause of MPDs is not known, but they are thought to be due to genetic mutations that occur in the bone marrow cells. Treatment options for MPDs include:
* Chemotherapy: This is a type of drug that kills cancer cells.
* Radiation therapy: This is a type of treatment that uses high-energy X-rays to kill cancer cells.
* Stem cell transplantation: This is a procedure in which healthy stem cells are transplanted into the body to replace damaged or diseased bone marrow cells.
Overall, MPDs are rare and complex disorders that can have a significant impact on quality of life. While there is no cure for these conditions, treatment options are available to help manage symptoms and improve outcomes.
Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.
In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.
Symptoms of aplastic anemia may include fatigue, weakness, shortness of breath, pale skin, and increased risk of bleeding or infection. Treatment options for aplastic anemia typically involve blood transfusions and immunosuppressive drugs to stimulate the bone marrow to produce new blood cells. In severe cases, a bone marrow transplant may be necessary.
Overall, aplastic anemia is a rare and serious condition that requires careful management by a healthcare provider to prevent complications and improve quality of life.
VOD is most commonly seen in patients who have undergone hematopoietic stem cell transplantation (HSCT) or solid organ transplantation, as well as those with certain inherited genetic disorders. It is caused by a combination of factors, including immune system dysfunction, infection, and exposure to certain drugs or toxins.
Symptoms of VOD can include nausea, vomiting, abdominal pain, fatigue, and jaundice (yellowing of the skin and eyes). In severe cases, VOD can lead to liver failure, sepsis, and death.
Treatment for VOD typically involves supportive care, such as fluids and medications to manage symptoms, as well as therapies aimed at addressing any underlying causes of the condition. In severe cases, a liver transplant may be necessary. Prognosis for VOD varies depending on the severity of the condition and the presence of any underlying medical conditions.
The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.
HP is classified into two types based on the severity of symptoms:
1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.
There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.
Myeloid leukemia can be classified into several subtypes based on the type of cell involved and the degree of maturity of the abnormal cells. The most common types of myeloid leukemia include:
1. Acute Myeloid Leukemia (AML): This is the most aggressive form of myeloid leukemia, characterized by a rapid progression of immature cells that do not mature or differentiate into normal cells. AML can be further divided into several subtypes based on the presence of certain genetic mutations or chromosomal abnormalities.
2. Chronic Myeloid Leukemia (CML): This is a slower-growing form of myeloid leukemia, characterized by the presence of a genetic abnormality known as the Philadelphia chromosome. CML is typically treated with targeted therapies or bone marrow transplantation.
3. Myelodysplastic Syndrome (MDS): This is a group of disorders characterized by the impaired development of immature blood cells in the bone marrow. MDS can progress to AML if left untreated.
4. Chronic Myelomonocytic Leukemia (CMML): This is a rare form of myeloid leukemia that is characterized by the accumulation of immature monocytes in the blood and bone marrow. CMML can be treated with chemotherapy or bone marrow transplantation.
The symptoms of myeloid leukemia can vary depending on the subtype and severity of the disease. Common symptoms include fatigue, weakness, fever, night sweats, and weight loss. Diagnosis is typically made through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment options for myeloid leukemia can include chemotherapy, targeted therapies, bone marrow transplantation, and supportive care to manage symptoms and prevent complications. The prognosis for myeloid leukemia varies depending on the subtype of the disease and the patient's overall health. With current treatments, many patients with myeloid leukemia can achieve long-term remission or even be cured.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are currently no cures for Fanconi anemia, but bone marrow transplantation and other supportive therapies can help manage some of the symptoms and improve quality of life. Research into the genetics and molecular biology of Fanconi anemia is ongoing to better understand the disorder and develop new treatments.
Some of the common symptoms of Fanconi anemia include short stature, limb deformities, hearing loss, vision problems, and an increased risk of infections and cancer. Children with Fanconi anemia may also experience developmental delays, learning disabilities, and social and emotional challenges.
The diagnosis of Fanconi anemia is typically made based on a combination of clinical findings, laboratory tests, and genetic analysis. Treatment options for Fanconi anemia depend on the severity of the disorder and may include bone marrow transplantation, blood transfusions, antibiotics, and other supportive therapies.
Fanconi anemia is a rare disorder that affects approximately 1 in 160,000 births worldwide. It is more common in certain populations, such as Ashkenazi Jews and individuals of Spanish descent. Fanconi anemia can be inherited in an autosomal recessive pattern, meaning that a child must inherit two copies of the mutated gene (one from each parent) to develop the disorder.
Overall, Fanconi anemia is a complex and rare genetic disorder that requires specialized medical care and ongoing research to better understand its causes and develop effective treatments. With appropriate management and supportive therapies, individuals with Fanconi anemia can lead fulfilling lives despite the challenges associated with the disorder.
Multiple myeloma is the second most common type of hematologic cancer after non-Hodgkin's lymphoma, accounting for approximately 1% of all cancer deaths worldwide. It is more common in older adults, with most patients being diagnosed over the age of 65.
The exact cause of multiple myeloma is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. There are several risk factors that have been associated with an increased risk of developing multiple myeloma, including:
1. Family history: Having a family history of multiple myeloma or other plasma cell disorders increases the risk of developing the disease.
2. Age: The risk of developing multiple myeloma increases with age, with most patients being diagnosed over the age of 65.
3. Race: African Americans are at higher risk of developing multiple myeloma than other races.
4. Obesity: Being overweight or obese may increase the risk of developing multiple myeloma.
5. Exposure to certain chemicals: Exposure to certain chemicals such as pesticides, solvents, and heavy metals has been linked to an increased risk of developing multiple myeloma.
The symptoms of multiple myeloma can vary depending on the severity of the disease and the organs affected. Common symptoms include:
1. Bone pain: Pain in the bones, particularly in the spine, ribs, or long bones, is a common symptom of multiple myeloma.
2. Fatigue: Feeling tired or weak is another common symptom of the disease.
3. Infections: Patients with multiple myeloma may be more susceptible to infections due to the impaired functioning of their immune system.
4. Bone fractures: Weakened bones can lead to an increased risk of fractures, particularly in the spine, hips, or ribs.
5. Kidney problems: Multiple myeloma can cause damage to the kidneys, leading to problems such as kidney failure or proteinuria (excess protein in the urine).
6. Anemia: A low red blood cell count can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
7. Increased calcium levels: High levels of calcium in the blood can cause symptoms such as nausea, vomiting, constipation, and confusion.
8. Neurological problems: Multiple myeloma can cause neurological problems such as headaches, numbness or tingling in the arms and legs, and difficulty with coordination and balance.
The diagnosis of multiple myeloma typically involves a combination of physical examination, medical history, and laboratory tests. These may include:
1. Complete blood count (CBC): A CBC can help identify abnormalities in the numbers and characteristics of different types of blood cells, including red blood cells, white blood cells, and platelets.
2. Serum protein electrophoresis (SPEP): This test measures the levels of different proteins in the blood, including immunoglobulins (antibodies) and abnormal proteins produced by myeloma cells.
3. Urine protein electrophoresis (UPEP): This test measures the levels of different proteins in the urine.
4. Immunofixation: This test is used to identify the type of antibody produced by myeloma cells and to rule out other conditions that may cause similar symptoms.
5. Bone marrow biopsy: A bone marrow biopsy involves removing a sample of tissue from the bone marrow for examination under a microscope. This can help confirm the diagnosis of multiple myeloma and determine the extent of the disease.
6. Imaging tests: Imaging tests such as X-rays, CT scans, or MRI scans may be used to assess the extent of bone damage or other complications of multiple myeloma.
7. Genetic testing: Genetic testing may be used to identify specific genetic abnormalities that are associated with multiple myeloma and to monitor the response of the disease to treatment.
It's important to note that not all patients with MGUS or smoldering myeloma will develop multiple myeloma, and some patients with multiple myeloma may not have any symptoms at all. However, if you are experiencing any of the symptoms listed above or have a family history of multiple myeloma, it's important to talk to your doctor about your risk and any tests that may be appropriate for you.
CMV infections are more common in people with weakened immune systems, such as those with HIV/AIDS, cancer, or taking immunosuppressive drugs after an organ transplant. In these individuals, CMV can cause severe and life-threatening complications, such as pneumonia, retinitis (inflammation of the retina), and gastrointestinal disease.
In healthy individuals, CMV infections are usually mild and may not cause any symptoms at all. However, in some cases, CMV can cause a mononucleosis-like illness with fever, fatigue, and swollen lymph nodes.
CMV infections are diagnosed through a combination of physical examination, blood tests, and imaging studies such as CT scans or MRI. Treatment is generally not necessary for mild cases, but may include antiviral medications for more severe infections. Prevention strategies include avoiding close contact with individuals who have CMV, practicing good hygiene, and considering immunoprophylaxis (prevention of infection through the use of immune globulin) for high-risk individuals.
Overall, while CMV infections can be serious and life-threatening, they are relatively rare in healthy individuals and can often be treated effectively with supportive care and antiviral medications.
Examples of OIs include:
1. Pneumocystis pneumonia (PCP): A type of pneumonia caused by the fungus Pneumocystis jirovecii, which is commonly found in the lungs of individuals with HIV/AIDS.
2. Cryptococcosis: A fungal infection caused by Cryptococcus neoformans, which can affect various parts of the body, including the lungs, central nervous system, and skin.
3. Aspergillosis: A fungal infection caused by Aspergillus fungi, which can affect various parts of the body, including the lungs, sinuses, and brain.
4. Histoplasmosis: A fungal infection caused by Histoplasma capsulatum, which is commonly found in the soil and can cause respiratory and digestive problems.
5. Candidiasis: A fungal infection caused by Candida albicans, which can affect various parts of the body, including the skin, mouth, throat, and vagina.
6. Toxoplasmosis: A parasitic infection caused by Toxoplasma gondii, which can affect various parts of the body, including the brain, eyes, and lymph nodes.
7. Tuberculosis (TB): A bacterial infection caused by Mycobacterium tuberculosis, which primarily affects the lungs but can also affect other parts of the body.
8. Kaposi's sarcoma-associated herpesvirus (KSHV): A viral infection that can cause various types of cancer, including Kaposi's sarcoma, which is more common in individuals with compromised immunity.
The diagnosis and treatment of OIs depend on the specific type of infection and its severity. Treatment may involve antibiotics, antifungals, or other medications, as well as supportive care to manage symptoms and prevent complications. It is important for individuals with HIV/AIDS to receive prompt and appropriate treatment for OIs to help prevent the progression of their disease and improve their quality of life.
Examples of acute diseases include:
1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.
Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.
PMF is a chronic disease that worsens over time, and it can lead to complications such as bleeding, infection, and bone damage. Treatment options include medications to reduce symptoms and slow the progression of the disease, as well as blood transfusions and splenectomy (removal of the spleen) in severe cases. The median age at diagnosis is around 60 years old, and the disease affects approximately 2-5 cases per million people per year.
* American Cancer Society. (2019). What is primary myelofibrosis? Retrieved from
* Leukemia and Lymphoma Society. (n.d.). Primary Myelofibrosis. Retrieved from
Pre-B ALL is characterized by the abnormal growth of immature white blood cells called B lymphocytes. These cells are produced in the bone marrow and are normally present in the blood. In Pre-B ALL, the abnormal B cells accumulate in the bone marrow, blood, and other organs, crowding out normal cells and causing a variety of symptoms.
The symptoms of Pre-B ALL can vary depending on the individual patient, but may include:
* Easy bruising or bleeding
* Frequent infections
* Swollen lymph nodes
* Enlarged liver or spleen
* Bone pain
* Confusion or seizures (in severe cases)
Pre-B ALL is most commonly diagnosed in children, but it can also occur in adults. Treatment typically involves a combination of chemotherapy and sometimes bone marrow transplantation. The prognosis for Pre-B ALL is generally good, especially in children, with a high survival rate if treated promptly and effectively. However, the cancer can be more difficult to treat in adults, and the prognosis may be less favorable.
Overall, Pre-B ALL is a rare and aggressive form of leukemia that requires prompt and specialized treatment to improve outcomes for patients.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
There are several types of lymphoproliferative disorders, including:
1. Lymphoma: This is a type of cancer that affects the immune system and can arise from either B cells or T cells. There are several subtypes of lymphoma, including Hodgkin lymphoma and non-Hodgkin lymphoma.
2. Leukemia: This is a type of cancer that affects the blood and bone marrow. It occurs when there is an abnormal proliferation of white blood cells, which can lead to an overproduction of immature or malignant cells.
3. Myelodysplastic syndrome (MDS): This is a group of disorders that affect the bone marrow and can lead to an abnormal production of blood cells. MDS can progress to acute myeloid leukemia (AML).
4. Chronic lymphocytic leukemia (CLL): This is a type of cancer that affects the blood and bone marrow, characterized by the accumulation of mature-looking but dysfunctional B cells in the blood.
5. Marginal zone lymphoma: This is a type of cancer that arises from the marginal zone of the spleen, which is the area where the white pulp and red pulp of the spleen meet.
6. Mantle cell lymphoma: This is a type of cancer that affects the lymph nodes and other lymphoid tissues, characterized by the accumulation of malignant B cells in the mantle zone of the lymph node.
7. Primary central nervous system lymphoma (PCNSL): This is a rare type of cancer that affects the brain and spinal cord, characterized by the accumulation of malignant B cells in the central nervous system.
8. Hairy cell leukemia: This is a rare type of cancer that affects the blood and bone marrow, characterized by the accumulation of abnormal B cells with a "hairy" appearance in the blood and bone marrow.
9. Lymphoplasmacytic lymphoma: This is a type of cancer that affects the lymph nodes and other lymphoid tissues, characterized by the accumulation of malignant B cells in the lymph nodes and other lymphoid tissues.
10. AIDS-related lymphoma: This is a type of cancer that affects people with HIV/AIDS, characterized by the accumulation of malignant B cells in the lymph nodes and other lymphoid tissues.
It's important to note that these are just some examples of B-cell non-Hodgkin lymphomas, and there are many other subtypes and variants of this disease. Each type of lymphoma has its own unique characteristics and may require different treatment approaches.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
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Symptoms of pancytopenia may include fatigue, weakness, shortness of breath, and increased risk of bleeding or infection. Treatment depends on the underlying cause, but may include blood transfusions, antibiotics, or immunosuppressive medications. In severe cases, pancytopenia can lead to anemia, infections, or bleeding complications that can be life-threatening.
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There are two main types of beta-thalassemia:
1. Beta-thalassemia major (also known as Cooley's anemia): This is the most severe form of the condition, and it can cause serious health problems and a shortened lifespan if left untreated. Children with this condition are typically diagnosed at birth or in early childhood, and they may require regular blood transfusions and other medical interventions to manage their symptoms and prevent complications.
2. Beta-thalassemia minor (also known as thalassemia trait): This is a milder form of the condition, and it may not cause any noticeable symptoms. People with beta-thalassemia minor have one mutated copy of the HBB gene and one healthy copy, which allows them to produce some normal hemoglobin. However, they may still be at risk for complications such as anemia, fatigue, and a higher risk of infections.
The symptoms of beta-thalassemia can vary depending on the severity of the condition and the age of onset. Common symptoms include:
* Pale skin
* Shortness of breath
* Frequent infections
* Yellowing of the skin and eyes (jaundice)
* Enlarged spleen
Beta-thalassemia is most commonly found in people of Mediterranean, African, and Southeast Asian ancestry. It is caused by mutations in the HBB gene, which is inherited from one's parents. There is no cure for beta-thalassemia, but it can be managed with blood transfusions, chelation therapy, and other medical interventions. Bone marrow transplantation may also be a viable option for some patients.
In conclusion, beta-thalassemia is a genetic disorder that affects the production of hemoglobin, leading to anemia, fatigue, and other complications. While there is no cure for the condition, it can be managed with medical interventions and bone marrow transplantation may be a viable option for some patients. Early diagnosis and management are crucial in preventing or minimizing the complications of beta-thalassemia.
The most common types of mycoses include:
1. Ringworm: This is a common fungal infection that causes a ring-shaped rash on the skin. It can affect any part of the body, including the arms, legs, torso, and face.
2. Athlete's foot: This is a common fungal infection that affects the feet, causing itching, redness, and cracking of the skin.
3. Jock itch: This is a fungal infection that affects the groin area and inner thighs, causing itching, redness, and cracking of the skin.
4. Candidiasis: This is a fungal infection caused by Candida, a type of yeast. It can affect various parts of the body, including the mouth, throat, and vagina.
5. Aspergillosis: This is a serious fungal infection that can affect various parts of the body, including the lungs, sinuses, and brain.
Symptoms of mycoses can vary depending on the type of infection and the severity of the infection. Common symptoms include itching, redness, swelling, and cracking of the skin. Treatment for mycoses usually involves antifungal medications, which can be applied topically or taken orally. In severe cases, hospitalization may be necessary to monitor and treat the infection.
Preventive measures for mycoses include practicing good hygiene, avoiding sharing personal items such as towels and clothing, and using antifungal medications as prescribed by a healthcare professional. Early diagnosis and treatment of mycoses can help prevent complications and reduce the risk of transmission to others.
Examples of Immunologic Deficiency Syndromes include:
1. Primary Immunodeficiency Diseases (PIDDs): These are a group of genetic disorders that affect the immune system's ability to function properly. Examples include X-linked agammaglobulinemia, common variable immunodeficiency, and severe combined immunodeficiency.
2. Acquired Immunodeficiency Syndrome (AIDS): This is a condition that results from the human immunodeficiency virus (HIV) infection, which destroys CD4 cells, a type of immune cell that fights off infections.
3. Immune Thrombocytopenic Purpura (ITP): This is an autoimmune disorder that causes the immune system to attack and destroy platelets, which are blood cells that help the blood to clot.
4. Autoimmune Disorders: These are conditions in which the immune system mistakenly attacks and damages healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, and multiple sclerosis.
5. Immunosuppressive Therapy-induced Immunodeficiency: This is a condition that occurs as a side effect of medications used to prevent rejection in organ transplant patients. These medications can suppress the immune system, increasing the risk of infections.
Symptoms of Immunologic Deficiency Syndromes can vary depending on the specific disorder and the severity of the immune system dysfunction. Common symptoms include recurrent infections, fatigue, fever, and swollen lymph nodes. Treatment options for these syndromes range from medications to suppress the immune system to surgery or bone marrow transplantation.
In summary, Immunologic Deficiency Syndromes are a group of disorders that result from dysfunction of the immune system, leading to recurrent infections and other symptoms. There are many different types of these syndromes, each with its own set of symptoms and treatment options.
Experimental radiation injuries are those that are intentionally caused in animal models or human subjects for research purposes, with the goal of understanding the effects of ionizing radiation on living organisms and developing treatments to mitigate these effects.
The study of experimental radiation injuries involves exposing animals or human subjects to varying levels of ionizing radiation and observing the resulting damage and recovery processes. This research has led to a better understanding of the mechanisms of radiation injury and the development of treatment strategies, such as blood transfusions and antioxidants, to mitigate the effects of radiation exposure.
Experimental radiation injuries are classified into two main types: acute and late-onset injuries. Acute radiation syndrome (ARS), also known as radiation sickness or radiation poisoning, occurs within hours to days after exposure and is characterized by nausea, vomiting, diarrhea, fatigue, and damage to the bone marrow, lungs, and gastrointestinal tract. Late-onset injuries, such as cancer and other chronic effects, can occur months or years after exposure and are caused by DNA damage and epigenetic changes.
Prevention of experimental radiation injuries is essential in reducing the risk of radiation exposure to humans and the environment. This includes using personal protective equipment, minimizing the use of ionizing radiation in medical procedures and research, and developing new technologies that reduce radiation exposure.
In summary, experimental radiation injuries are intentionally caused in animal models or human subjects for research purposes to understand the effects of ionizing radiation on living organisms and develop treatments to mitigate these effects. The study of experimental radiation injuries has led to a better understanding of the mechanisms of radiation injury and the development of treatment strategies, but prevention is essential in reducing the risk of radiation exposure.
XCIDD can present in a variety of ways, including:
1. X-linked severe combined immunodeficiency (XSCID): This is the most common form of XCIDD and is caused by mutations in the IL2RG gene. It is characterized by a complete deficiency of T cells and B cells, which makes individuals with this condition extremely susceptible to infections.
2. X-linked agammaglobulinemia (XLA): This condition is caused by mutations in the Bruton's tyrosine kinase (BTK) gene and results in a deficiency of antibody production.
3. X-linked lymphoproliferative disease (XLP): This condition is caused by mutations in the SH2D1A gene and results in an overactive immune system, which can lead to lymphoma or other cancers.
4. X-linked lymphopenia: This condition is caused by mutations in genes involved in T cell development and results in a deficiency of T cells.
XCIDD are inherited in an X-linked recessive pattern, meaning that the gene mutation is located on the X chromosome and can be passed from mother to son. Female carriers of XCIDD have a 50% chance of passing the mutated gene to their sons, who will inherit the condition. Daughters, however, will not inherit the condition because they do not have an X chromosome.
There is currently no cure for XCIDD, but bone marrow transplantation and enzyme replacement therapy are being investigated as potential treatments. Management of the condition typically involves antibiotic therapy to prevent infections and immunoglobulin therapy to boost the immune system.
In the medical field, cystitis is also known as urinary tract infection (UTI), which affects not only the bladder but also the kidneys and ureters. The symptoms of cystitis are similar to those of UTI, including fever, chills, nausea, and vomiting. However, cystitis is limited to the bladder only, whereas UTI can affect multiple parts of the urinary tract.
Cystitis is more common in women due to their anatomy, with the shorter urethra providing easier access for bacteria to enter the bladder. Pregnant women and those with diabetes or a weakened immune system are at higher risk of developing cystitis.
While cystitis is not a serious condition in most cases, it can lead to complications such as kidney damage if left untreated. Recurrent cystitis can also cause changes in the bladder muscle and increase the risk of urinary incontinence. Therefore, prompt diagnosis and treatment are essential to manage symptoms and prevent long-term consequences.
In summary, cystitis is a common condition that affects the bladder, characterized by inflammation and symptoms such as painful urination and frequent urination. It can be acute or chronic, and treatment typically involves antibiotics, fluid intake, and pain relief medication. Prompt diagnosis and treatment are essential to manage symptoms and prevent long-term consequences.
There are several types of lymphoma, including:
1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.
The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:
* Swollen lymph nodes
* Weight loss
* Night sweats
Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.
Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.
The symptoms of aspergillosis depend on the location and severity of the infection. In the lungs, it may cause coughing, fever, chest pain, and difficulty breathing. In the sinuses, it can cause headaches, facial pain, and nasal congestion. In the brain, it can cause seizures, confusion, and weakness.
Aspergillosis is typically diagnosed through a combination of imaging tests such as chest X-rays, CT scans, and MRI scans, along with a biopsy to confirm the presence of Aspergillus fungi.
Treatment of aspergillosis depends on the severity and location of the infection. In mild cases, treatment may involve antifungal medications and supportive care such as oxygen therapy and pain management. In severe cases, treatment may require hospitalization and intravenous antifungal medications.
Preventive measures for aspergillosis include avoiding exposure to dusty or damp environments, managing chronic conditions such as asthma and COPD, and taking antifungal medications as prescribed.
Aspergillosis can be a serious condition, especially in people with weakened immune systems, such as those with cancer, HIV/AIDS, or taking immunosuppressive drugs. In severe cases, aspergillosis can lead to life-threatening complications such as respiratory failure, sepsis, and organ damage.
In conclusion, aspergillosis is a common fungal infection that can affect various parts of the body, and it can be serious and potentially life-threatening, especially in people with weakened immune systems. Early diagnosis and appropriate treatment are essential to prevent complications and improve outcomes.
The word "osteopetrosis" comes from the Greek words "osteon," meaning bone, and "petros," meaning rock or stone. This name reflects the dense and hard nature of the bones affected by the disorder.
Osteopetrosis can be caused by mutations in several genes that are involved in bone development and growth. The condition is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the disorder. However, some cases may be caused by spontaneous mutations or other factors.
Symptoms of osteopetrosis can vary depending on the severity of the disorder and the specific affected bones. Common symptoms include bone pain, limited mobility, and an increased risk of fractures. Other symptoms may include fatigue, fever, and difficulty swallowing or breathing.
Treatment for osteopetrosis usually involves a combination of medications and surgery. Medications such as bisphosphonates and denintuzumab mafodotin can help reduce bone pain and the risk of fractures, while surgery may be necessary to correct deformities or repair broken bones. In some cases, bone marrow transplantation may be recommended to replace damaged bone marrow with healthy cells.
Overall, osteopetrosis is a rare and debilitating disorder that can have a significant impact on quality of life. Early diagnosis and appropriate treatment are important for managing symptoms and preventing complications.
Symptoms of neutropenia may include recurring infections, fever, fatigue, weight loss, and swollen lymph nodes. The diagnosis is typically made through a blood test that measures the number of neutrophils in the blood.
Treatment options for neutropenia depend on the underlying cause but may include antibiotics, supportive care to manage symptoms, and in severe cases, bone marrow transplantation or granulocyte-colony stimulating factor (G-CSF) therapy to increase neutrophil production.
It is also known as mouth inflammation.
1. Leukemia: A type of cancer that affects the blood and bone marrow, characterized by an overproduction of immature white blood cells.
2. Lymphoma: A type of cancer that affects the immune system, often involving the lymph nodes and other lymphoid tissues.
3. Multiple myeloma: A type of cancer that affects the plasma cells in the bone marrow, leading to an overproduction of abnormal plasma cells.
4. Myelodysplastic syndrome (MDS): A group of disorders characterized by the impaired development of blood cells in the bone marrow.
5. Osteopetrosis: A rare genetic disorder that causes an overgrowth of bone, leading to a thickened bone marrow.
6. Bone marrow failure: A condition where the bone marrow is unable to produce enough blood cells, leading to anemia, infection, and other complications.
7. Myelofibrosis: A condition characterized by the scarring of the bone marrow, which can lead to an overproduction of blood cells and an increased risk of bleeding and infection.
8. Polycythemia vera: A rare blood disorder that causes an overproduction of red blood cells, leading to an increased risk of blood clots and other complications.
9. Essential thrombocythemia: A rare blood disorder that causes an overproduction of platelets, leading to an increased risk of blood clots and other complications.
10. Myeloproliferative neoplasms (MPNs): A group of rare blood disorders that are characterized by the overproduction of blood cells and an increased risk of bleeding and infection.
These are just a few examples of bone marrow diseases. There are many other conditions that can affect the bone marrow, and each one can have a significant impact on a person's quality of life. If you suspect that you or someone you know may have a bone marrow disease, it is important to seek medical attention as soon as possible. A healthcare professional can perform tests and provide a proper diagnosis and treatment plan.
There are several subtypes of NHL, including:
1. B-cell lymphomas (such as diffuse large B-cell lymphoma and follicular lymphoma)
2. T-cell lymphomas (such as peripheral T-cell lymphoma and mycosis fungoides)
3. Natural killer cell lymphomas (such as nasal NK/T-cell lymphoma)
4. Histiocyte-rich B-cell lymphoma
5. Primary mediastinal B-cell lymphoma
6. Mantle cell lymphoma
7. Waldenström macroglobulinemia
8. Lymphoplasmacytoid lymphoma
9. Myelodysplastic syndrome/myeloproliferative neoplasms (MDS/MPN) related lymphoma
These subtypes can be further divided into other categories based on the specific characteristics of the cancer cells.
Symptoms of NHL can vary depending on the location and size of the tumor, but may include:
* Swollen lymph nodes in the neck, underarm, or groin
* Weight loss
* Night sweats
* Abdominal pain
* Swollen spleen
Treatment for NHL typically involves a combination of chemotherapy, radiation therapy, and in some cases, targeted therapy or immunotherapy. The specific treatment plan will depend on the subtype of NHL, the stage of the cancer, and other individual factors.
Overall, NHL is a complex and diverse group of cancers that require specialized care from a team of medical professionals, including hematologists, oncologists, radiation therapists, and other support staff. With advances in technology and treatment options, many people with NHL can achieve long-term remission or a cure.
There are several types of teratomas, including:
1. Mature teratoma: This type of teratoma is made up of well-differentiated tissues that resemble normal tissues. It can contain structures such as hair follicles, sweat glands, and sebaceous glands.
2. Immature teratoma: This type of teratoma is made up of poorly differentiated cells that do not resemble normal tissues. It can contain structures such as cartilage, bone, and nervous tissue.
3. Teratoid mesodermal tumor: This type of teratoma arises from the mesoderm, which is one of the three primary layers of cells in the embryo. It can contain structures such as muscle, bone, and connective tissue.
4. Teratoid endodermal tumor: This type of teratoma arises from the endoderm, which is another primary layer of cells in the embryo. It can contain structures such as glandular tissue and epithelial tissue.
Teratomas are usually benign, but they can sometimes be malignant. Malignant teratomas can spread to other parts of the body and cause serious complications. The treatment of teratomas depends on their type, size, and location, as well as the patient's overall health. Treatment options can include surgery, chemotherapy, and radiation therapy.
In summary, a teratoma is a type of tumor that contains abnormal cells that grow and multiply in an uncontrolled manner, often forming masses or lumps. There are several types of teratomas, and they can occur in various parts of the body. Treatment options depend on the type, size, location, and patient's overall health.
The primary symptoms of Wiskott-Aldrich syndrome include:
1. Eczema and skin rashes
2. Immune system dysfunction, leading to recurrent infections
3. Bleeding disorders, including easy bruising and nosebleeds
4. Delayed development and growth retardation
5. Short stature
6. Poor muscle tone and coarse facial features
7. Heart defects, such as ventricular septal defects
8. Kidney disease or dysfunction
9. Increased risk of cancer, particularly lymphoma
Wiskott-Aldrich syndrome is diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the condition typically involves managing symptoms and preventing complications through medications, immunoglobulin replacement therapy, and other supportive measures.
The prognosis for individuals with Wiskott-Aldrich syndrome varies depending on the severity of their symptoms and the presence of any comorbidities. With appropriate medical care, many individuals with this condition can lead relatively normal lives, but they may require lifelong monitoring and treatment to manage their symptoms and prevent complications.
The main symptoms of MPS I include:
1. Coarse facial features, such as a large head, prominent forehead, and widely spaced eyes.
2. Short stature and joint deformities, particularly in the hands and feet.
3. Heart valve problems and potential heart failure.
4. Respiratory issues, including sleep apnea and difficulty breathing.
5. Developmental delays and intellectual disability.
6. Vision loss or blindness.
7. Hearing loss or deafness.
8. Increased risk of infections.
MPS I is caused by a deficiency of the enzyme alpha-L-iduronidase, which is needed to break down a specific type of sugar called glycosaminoglycans (GAGs). This accumulation of GAGs in cells and tissues leads to the signs and symptoms of the disorder.
There are several types of MPS I, ranging from mild to severe, and they are classified based on the level of enzyme deficiency and the severity of symptoms. Treatment options for MPS I include enzyme replacement therapy (ERT), which involves replacing the missing enzyme with a synthetic version, as well as other supportive therapies to manage symptoms and prevent complications. Bone marrow transplantation is also being studied as a potential treatment option for MPS I.
In summary, mucopolysaccharidosis type I (MPS I) is a rare genetic disorder that affects the body's ability to break down sugar molecules, leading to progressive damage to various parts of the body and a range of symptoms including joint deformities, heart problems, developmental delays, and vision and hearing loss.
The two main types of TMAs are:
1. Thrombotic thrombocytopenic purpura (TTP): This is a rare autoimmune disorder caused by the formation of antibodies against ADAMTS13, an enzyme involved in platelet function. TTP patients have low levels of ADAMTS13 and abnormal platelets that are prone to clotting.
2. Hemolytic uremic syndrome (HUS): This is a condition that occurs when red blood cells are destroyed and removed from the circulation, leading to anemia, low platelet count, and kidney failure. HUS can be caused by various factors, such as infections, certain medications, or genetic mutations.
Both TTP and HUS can lead to TMAs, which can cause severe morbidity and mortality if left untreated. Treatment options for TMAs include plasmapheresis, corticosteroids, and immunosuppressive drugs, as well as dialysis in cases of acute kidney injury. Early diagnosis and aggressive treatment are essential to prevent long-term complications and improve patient outcomes.
Roseolovirus infections can be diagnosed through physical examination and laboratory tests such as PCR (polymerase chain reaction) or ELISA (enzyme-linked immunosorbent assay). Treatment for roseolovirus infection is generally focused on relieving symptoms such as fever and pain, and may include antiviral medications in severe cases.
There are two main types of roseolovirus:
1. Human roseolovirus A (HRVA): This type is responsible for most cases of roseola infantum.
2. Human roseolovirus B (HRVB): This type is less common and typically affects children under the age of 2.
Roseolovirus infections are highly contagious and can be spread through contact with an infected person's saliva, mucus, or other bodily fluids. The virus can also survive on surfaces for a period of time, allowing it to be transmitted through touching contaminated surfaces and then touching one's face.
Preventive measures such as frequent handwashing, avoiding close contact with people who are sick, and avoiding sharing eating or drinking utensils can help reduce the risk of transmission. Vaccines are not available for roseolovirus infections, but research is ongoing to develop one.
Complications of roseolovirus infections can include:
1. Septicemia: This is a serious condition where the virus spreads through the bloodstream and can cause organ damage.
2. Meningitis: This is an inflammation of the membranes that cover the brain and spinal cord.
3. Encephalitis: This is an inflammation of the brain.
4. Pneumonia: This is an infection of the lungs.
5. Thrombocytopenia: This is a low platelet count, which can increase the risk of bleeding.
Treatment for roseolovirus infections typically involves supportive care, such as hydration, rest, and fever reduction. Antiviral medications may be prescribed in severe cases or for high-risk individuals. Hospitalization may be necessary for more serious complications.
It's important to note that roseolovirus infections can be particularly dangerous for certain populations, such as the elderly, young children, and people with weakened immune systems. If you suspect you or someone else may have a roseolovirus infection, it is important to seek medical attention promptly. Early diagnosis and treatment can help reduce the risk of complications and improve outcomes.
A residual neoplasm is a remaining portion of a tumor that may persist after primary treatment. This can occur when the treatment does not completely remove all of the cancer cells or if some cancer cells are resistant to the treatment. Residual neoplasms can be benign (non-cancerous) or malignant (cancerous).
It is important to note that a residual neoplasm does not necessarily mean that the cancer has come back. In some cases, a residual neoplasm may be present from the start and may not grow or change over time.
Residual neoplasms can be managed with additional treatment, such as surgery, chemotherapy, or radiation therapy. The choice of treatment depends on the type of cancer, the size and location of the residual neoplasm, and other factors.
It is important to follow up with your healthcare provider regularly to monitor the residual neoplasm and ensure that it is not growing or causing any symptoms.
The exact cause of polycythemia vera is not known, but it is believed to be due to a genetic mutation in the JAK2 gene, which is involved in the signaling pathways that regulate blood cell production. The condition typically affects adults over the age of 60 and is more common in men than women.
Symptoms of polycythemia vera can include:
* Shortness of breath
* Night sweats
* Weight loss
Diagnosis of polycythemia vera is typically made based on a combination of physical examination, medical history, and laboratory tests, including:
* Complete blood count (CBC) to measure the levels of red blood cells, white blood cells, and platelets
* Blood chemistry tests to assess liver function and other body chemicals
* Genetic testing to look for the JAK2 mutation
* Bone marrow biopsy to examine the bone marrow tissue for abnormalities
Treatment for polycythemia vera usually involves phlebotomy (the removal of blood from the body) to reduce the number of red blood cells and relieve symptoms such as itching and night sweats. In some cases, medications may be used to reduce the production of blood cells or to treat specific symptoms. Regular monitoring by a healthcare provider is important to detect any changes in the condition and to prevent complications.
Overall, polycythemia vera is a chronic and progressive disease that can have significant impact on quality of life if left untreated. Early diagnosis and appropriate treatment can help manage symptoms and improve outcomes for patients with this condition.
Types of Infection:
1. Bacterial Infections: These are caused by the presence of harmful bacteria in the body. Examples include pneumonia, urinary tract infections, and skin infections.
2. Viral Infections: These are caused by the presence of harmful viruses in the body. Examples include the common cold, flu, and HIV/AIDS.
3. Fungal Infections: These are caused by the presence of fungi in the body. Examples include athlete's foot, ringworm, and candidiasis.
4. Parasitic Infections: These are caused by the presence of parasites in the body. Examples include malaria, giardiasis, and toxoplasmosis.
Symptoms of Infection:
4. Muscle aches
5. Skin rashes or lesions
6. Swollen lymph nodes
7. Sore throat
Treatment of Infection:
1. Antibiotics: These are used to treat bacterial infections and work by killing or stopping the growth of bacteria.
2. Antiviral medications: These are used to treat viral infections and work by interfering with the replication of viruses.
3. Fungicides: These are used to treat fungal infections and work by killing or stopping the growth of fungi.
4. Anti-parasitic medications: These are used to treat parasitic infections and work by killing or stopping the growth of parasites.
5. Supportive care: This includes fluids, nutritional supplements, and pain management to help the body recover from the infection.
Prevention of Infection:
1. Hand washing: Regular hand washing is one of the most effective ways to prevent the spread of infection.
2. Vaccination: Getting vaccinated against specific infections can help prevent them.
3. Safe sex practices: Using condoms and other safe sex practices can help prevent the spread of sexually transmitted infections.
4. Food safety: Properly storing and preparing food can help prevent the spread of foodborne illnesses.
5. Infection control measures: Healthcare providers use infection control measures such as wearing gloves, masks, and gowns to prevent the spread of infections in healthcare settings.
White blood cells are an important part of the immune system and play a crucial role in fighting off infections and diseases. However, when there is an excessive increase in their numbers, it can lead to various complications, including:
1. Increased risk of infection: With too many white blood cells in the bloodstream, there is a higher chance of developing infections.
2. Inflammation: Excessive production of white blood cells can cause inflammation in various parts of the body.
3. Blood clotting disorders: White blood cells can clump together and form clots, which can lead to blockages in blood vessels.
4. Tissue damage: The excessive growth of white blood cells can cause damage to tissues and organs.
5. Bone marrow failure: Prolonged leukocytosis can lead to bone marrow failure, which can result in a decrease in the production of other blood cells, such as red blood cells and platelets.
There are several types of leukocytosis, including:
1. Reactive leukocytosis: This is the most common type and is caused by an infection or inflammation.
2. Chronic leukocytosis: This type is characterized by a persistent increase in white blood cells over a long period of time.
3. Acute leukocytosis: This type is characterized by a sudden and severe increase in white blood cells, often accompanied by other symptoms such as fever and fatigue.
4. Leukemia: This is a type of cancer that affects the bone marrow and blood cells. It can cause an abnormal increase in white blood cells.
Diagnosis of leukocytosis typically involves a physical examination, medical history, and laboratory tests such as complete blood count (CBC) and bone marrow biopsy. Treatment depends on the underlying cause and may include antibiotics for infections, steroids to reduce inflammation, or chemotherapy for leukemia. In some cases, no treatment is necessary if the condition resolves on its own.
Symptoms of EBV infection can vary widely, ranging from asymptomatic to severe, and may include:
* Sore throat
* Swollen lymph nodes in the neck and armpits
* Swollen liver or spleen
* Muscle weakness
In some cases, EBV can lead to more serious complications such as infectious mononucleosis (IM), also known as glandular fever, which can cause:
* Enlarged liver and spleen
* Splenomegaly (enlargement of the spleen)
* Hepatomegaly (enlargement of the liver)
* Thrombocytopenia (low platelet count)
* Anemia (low red blood cell count)
* Leukopenia (low white blood cell count)
EBV is also associated with an increased risk of developing certain types of cancer, including Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma.
There is no specific treatment for EBV infections, and most cases resolve on their own within a few weeks. Antiviral medications may be prescribed in severe cases or to prevent complications. Rest, hydration, and over-the-counter pain relief medication can help alleviate symptoms.
The exact cause of Bronchiolitis Obliterans is not fully understood, but it is believed to be due to a combination of genetic and environmental factors. The condition is often associated with allergies and asthma, and viral infections such as respiratory syncytial virus (RSV) can trigger the onset of symptoms.
Symptoms of Bronchiolitis Obliterans include:
* Persistent coughing, which may be worse at night
* Shortness of breath or wheezing
* Chest tightness or discomfort
* Fatigue and poor appetite
* Recurrent respiratory infections
BO is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or pulmonary function tests. There is no cure for Bronchiolitis Obliterans, but treatment options are available to manage symptoms and slow the progression of the disease. These may include:
* Medications such as bronchodilators and corticosteroids to reduce inflammation and improve lung function
* Pulmonary rehabilitation programs to improve breathing and overall health
* Oxygen therapy to help increase oxygen levels in the blood
* In severe cases, lung transplantation may be considered.
While Bronchiolitis Obliterans can significantly impact quality of life, with proper management and care, many individuals with the condition are able to lead active and productive lives.
Symptoms of macrocytic anemia may include fatigue, weakness, pale skin, and shortness of breath. Diagnosis is typically made through a complete blood count (CBC) test that shows an elevated mean corpuscular volume (MCV) and reticulocyte count. Treatment depends on the underlying cause, but may include vitamin supplements, changes in medication, or addressing any underlying medical conditions.
In summary, macrocytic anemia is a type of anemia characterized by large red blood cells that are prone to breakdown and can be caused by various factors. It can cause symptoms such as fatigue, weakness, and shortness of breath, and diagnosis is made through a CBC test. Treatment depends on the underlying cause.
Blood group incompatibility can occur in various ways, including:
1. ABO incompatibility: This is the most common type of blood group incompatibility and occurs when the patient's blood type (A or B) is different from the donor's blood type.
2. Rh incompatibility: This occurs when the patient's Rh factor is different from the donor's Rh factor.
3. Other antigens: In addition to ABO and Rh, there are other antigens on red blood cells that can cause incompatibility, such as Kell, Duffy, and Xg.
Blood group incompatibility can be diagnosed through blood typing and cross-matching tests. These tests determine the patient's and donor's blood types and identify any incompatible antigens that may cause an immune response.
Treatment of blood group incompatibility usually involves finding a compatible donor or using specialized medications to reduce the risk of a negative reaction. In some cases, plasmapheresis, also known as plasma exchange, may be used to remove the incompatible antibodies from the patient's blood.
Prevention of blood group incompatibility is important, and this can be achieved by ensuring that patients receive only compatible blood products during transfusions. Blood banks maintain a database of donor blood types and perform thorough testing before releasing blood for transfusion to ensure compatibility. Additionally, healthcare providers should carefully review the patient's medical history and current medications to identify any potential allergies or sensitivities that may affect blood compatibility.
Juvenile myelomonocytic leukemia (JMML) typically affects children under the age of six, with most cases occurring before the age of two. The symptoms of JMML can include fever, fatigue, loss of appetite, bleeding, and infection. If left untreated, JMML can progress quickly and lead to life-threatening complications such as anemia, infection, and organ damage.
The exact cause of JMML is not known, but it is believed to be linked to genetic mutations that affect the function of immune cells. Treatment options for JMML include chemotherapy, targeted therapy, and stem cell transplantation. With early diagnosis and appropriate treatment, the prognosis for JMML is generally good, with a five-year survival rate of approximately 70%.
Leukemia, Myelomonocytic, Juvenile
Leukemic infiltration refers to the abnormal growth and spread of cancer cells (leukemia) into normal tissues, organs, or bones. It is a common feature of many types of leukemia, including acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), and acute lymphoblastic leukemia (ALL).
Leukemic infiltration can cause a range of symptoms, including pain, swelling, and difficulty with movement or function. In severe cases, it can also lead to life-threatening complications such as organ failure or sepsis.
The diagnosis of leukemic infiltration typically involves a combination of physical examination, medical history, laboratory tests (such as blood and bone marrow studies), and imaging studies (such as X-rays, CT scans, or PET scans). Treatment options for leukemic infiltration depend on the specific type of leukemia and the severity of the infiltration, but may include chemotherapy, radiation therapy, immunotherapy, or bone marrow transplantation.
Overall, leukemic infiltration is a serious condition that can have significant impacts on quality of life and survival. Early detection and prompt treatment are important for achieving the best possible outcomes.
The symptoms of HLH typically appear in infancy or early childhood and can include fever, skin rash, liver dysfunction, and poor growth. If left untreated, HLH can progress to severe inflammation and organ damage, leading to life-threatening complications such as liver failure, bone marrow failure, and infections.
The exact prevalence of HLH is not known, but it is estimated to affect approximately 1 in 50,000 children worldwide. The condition is caused by mutations in genes that regulate the immune system, such as the UNC93B1 gene, which codes for a protein involved in the regulation of T cells.
There are several treatment options available for HLH, including:
1. Immunosuppressive therapy with drugs such as corticosteroids and cyclosporine to reduce inflammation and suppress the immune system.
2. Chemotherapy to kill cancer cells that may be contributing to the condition.
3. Bone marrow transplantation to replace damaged bone marrow with healthy cells.
4. Gene therapy to correct genetic defects that are causing the condition.
5. Supportive care to manage symptoms and prevent complications.
The prognosis for HLH varies depending on the severity of the condition and the age of onset. With early diagnosis and appropriate treatment, many children with HLH can achieve long-term remission and a normal quality of life. However, if left untreated or if treatment is delayed, the condition can be fatal.
Overall, hemophagocytic lymphohistiocytosis is a rare and complex genetic disorder that affects the immune system and can lead to severe inflammation and multi-organ damage. Early diagnosis and appropriate treatment are critical for improving outcomes and preventing complications.
T-ALL typically occurs in children and young adults, although it can also occur in older adults. The symptoms of T-ALL can include fever, fatigue, loss of appetite, weight loss, swollen lymph nodes, and an enlarged spleen. If left untreated, T-ALL can progress rapidly and lead to life-threatening complications such as infection, bleeding, and organ failure.
The exact cause of T-ALL is not known, but it is believed to be linked to genetic mutations that occur in the T cells. The diagnosis of T-ALL typically involves a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as CT scans or PET scans.
Treatment for T-ALL usually involves a combination of chemotherapy and/or radiation therapy to kill the abnormal T cells. In some cases, bone marrow transplantation may also be recommended. The prognosis for T-ALL depends on several factors, including the age of the patient, the severity of the disease, and the response to treatment. Overall, the survival rate for T-ALL is relatively low, but with intensive treatment, many patients can achieve long-term remission.
1. Autoimmune diseases: These occur when the immune system mistakenly attacks healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, multiple sclerosis, and type 1 diabetes.
2. Allergies: An allergic reaction occurs when the immune system overreacts to a harmless substance, such as pollen, dust mites, or certain foods. Symptoms can range from mild hives to life-threatening anaphylaxis.
3. Immunodeficiency disorders: These are conditions that impair the immune system's ability to fight infections. Examples include HIV/AIDS and primary immunodeficiency diseases.
4. Infectious diseases: Certain infections, such as tuberculosis or bacterial meningitis, can cause immune system dysfunction.
5. Cancer: Some types of cancer, such as lymphoma, affect the immune system's ability to fight disease.
6. Immune thrombocytopenic purpura (ITP): This is a rare autoimmune disorder that causes the immune system to attack and destroy platelets, leading to bleeding and bruising.
7. Guillain-Barré syndrome: This is a rare autoimmune disorder that occurs when the immune system attacks the nerves, leading to muscle weakness and paralysis.
8. Chronic fatigue syndrome (CFS): This is a condition characterized by persistent fatigue, muscle pain, and joint pain, which is thought to be related to an immune system imbalance.
9. Fibromyalgia: This is a chronic condition characterized by widespread muscle pain, fatigue, and sleep disturbances, which may be linked to immune system dysfunction.
10. Autoimmune hepatitis: This is a condition in which the immune system attacks the liver, leading to inflammation and damage to the liver cells.
It's important to note that a weakened immune system can increase the risk of infections and other health problems, so it's important to work with your healthcare provider to identify any underlying causes and develop an appropriate treatment plan.
There are several possible causes of thrombocytopenia, including:
1. Immune-mediated disorders such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus (SLE).
2. Bone marrow disorders such as aplastic anemia or leukemia.
3. Viral infections such as HIV or hepatitis C.
4. Medications such as chemotherapy or non-steroidal anti-inflammatory drugs (NSAIDs).
5. Vitamin deficiencies, especially vitamin B12 and folate.
6. Genetic disorders such as Bernard-Soulier syndrome.
7. Sepsis or other severe infections.
8. Disseminated intravascular coagulation (DIC), a condition where blood clots form throughout the body.
9. Postpartum thrombocytopenia, which can occur in some women after childbirth.
Symptoms of thrombocytopenia may include easy bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding from injuries or surgical sites. Treatment options depend on the underlying cause but may include platelet transfusions, steroids, immunosuppressive drugs, and in severe cases, surgery.
In summary, thrombocytopenia is a condition characterized by low platelet counts that can increase the risk of bleeding and bruising. It can be caused by various factors, and treatment options vary depending on the underlying cause.
The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.
In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.
What is a Chronic Disease?
A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:
2. Heart disease
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
Impact of Chronic Diseases
The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.
Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.
Addressing Chronic Diseases
Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:
1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.
Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.
Types of Adenoviridae Infections:
1. Respiratory adenovirus infection (bronchiolitis, pneumonia)
2. Gastroenteric adenovirus infection (gastroenteritis)
3. Eye adenovirus infection (conjunctivitis)
4. Skin adenovirus infection (keratoconjunctivitis)
5. Intestinal adenovirus infection (diarrhea, vomiting)
6. Adenovirus-associated hemorrhagic cystitis
7. Adenovirus-associated hypertrophic cardiomyopathy
8. Adenovirus-associated myocarditis
Symptoms of Adenoviridae Infections:
1. Respiratory symptoms (cough, fever, difficulty breathing)
2. Gastrointestinal symptoms (diarrhea, vomiting, abdominal pain)
3. Eye symptoms (redness, discharge, sensitivity to light)
4. Skin symptoms (rash, blisters, skin erosion)
5. Intestinal symptoms (abdominal cramps, fever, chills)
6. Cardiovascular symptoms (hypertension, tachycardia, myocarditis)
Diagnosis of Adenoviridae Infections:
1. Physical examination and medical history
2. Laboratory tests (rapid antigen detection, PCR, electron microscopy)
3. Imaging studies (chest X-ray, CT scan, MRI)
4. Biopsy (tissue or organ biopsy)
Treatment of Adenoviridae Infections:
1. Supportive care (fluids, oxygen therapy, pain management)
2. Antiviral medications (ribavirin, cidofovir)
3. Immune modulators (immunoglobulins, corticosteroids)
4. Surgical intervention (in severe cases of adenovirus-associated disease)
Prevention of Adenoviridae Infections:
1. Good hygiene practices (handwashing, surface cleaning)
2. Avoiding close contact with individuals who are infected
3. Properly storing and preparing food
4. Avoiding sharing of personal items (utensils, drinking glasses, towels)
5. Immunization (vaccination against adenovirus)
The incubation period for adenoviruses is typically between 3-7 days, but it can range from 1-2 weeks in some cases.
Adenoviruses are highly contagious and can be transmitted before symptoms appear and during the entire course of illness. The virus can be shed for several weeks after infection.
Individuals with weakened immune systems (children, elderly, those with chronic illnesses) are at a higher risk of developing severe adenovirus infections. Additionally, those who live in crowded or unsanitary conditions and those who engage in behaviors that compromise their immune system (smoking, excessive alcohol consumption) are also at a higher risk.
Adenovirus infections can lead to a variety of complications, including pneumonia, meningitis, encephalitis, and other respiratory, gastrointestinal, and eye infections. In severe cases, adenovirus infections can be fatal.
The recovery time for adenovirus infections varies depending on the severity of the infection and the individual's overall health. Mild cases of adenovirus may resolve within a few days to a week, while more severe cases may take several weeks to recover from. In some cases, hospitalization may be necessary for individuals with severe infections or those who experience complications.
There is no specific contraceptive measure that can prevent adenovirus infections. However, practicing good hygiene, such as frequent handwashing and avoiding close contact with people who are sick, can help reduce the risk of transmission.
Adenovirus infections during pregnancy are rare but can be severe. Pregnant women who develop adenovirus infections may experience complications such as preterm labor and low birth weight. It is essential for pregnant women to seek medical attention immediately if they suspect they have an adenovirus infection.
Adenovirus infections can be diagnosed through a variety of tests, including polymerase chain reaction (PCR), electron microscopy, and culture. A healthcare provider will typically perform a physical examination and take a medical history to determine the likelihood of an adenovirus infection.
There is no specific treatment for adenovirus infections, but symptoms can be managed with supportive care such as hydration, rest, and over-the-counter pain relievers. Antiviral medications may be prescribed in severe cases or for individuals with compromised immune systems.
Preventing the spread of adenovirus is essential, especially in high-risk populations such as young children and those with weakened immune systems. Practicing good hygiene, such as frequent handwashing and avoiding close contact with people who are sick, can help reduce the risk of transmission. Vaccines are also available for some types of adenovirus.
The prognosis for adenovirus infections is generally good, especially for mild cases. However, severe cases can lead to complications such as pneumonia, meningitis, and encephalitis, which can be life-threatening. In some cases, long-term health problems may persist after recovery from an adenovirus infection.
Adenovirus infections can lead to various complications, including:
1. Pneumonia: Adenovirus can cause pneumonia, which is an inflammation of the lungs that can lead to fever, chest pain, and difficulty breathing.
2. Meningitis: Adenovirus can cause meningitis, which is an inflammation of the membranes surrounding the brain and spinal cord. Symptoms include headache, stiff neck, and sensitivity to light.
3. Encephalitis: Adenovirus can cause encephalitis, which is an inflammation of the brain that can lead to confusion, seizures, and coma.
4. Gastrointestinal symptoms: Adenovirus can cause gastrointestinal symptoms such as diarrhea, vomiting, and abdominal pain.
5. Long-term health problems: In some cases, adenovirus infections can lead to long-term health problems such as asthma, allergies, and autoimmune disorders.
There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia. Alpha-thalassemia is caused by abnormalities in the production of the alpha-globin chain, which is one of the two chains that make up hemoglobin. Beta-thalassemia is caused by abnormalities in the production of the beta-globin chain.
Thalassemia can cause a range of symptoms, including anemia, fatigue, pale skin, and shortness of breath. In severe cases, it can lead to life-threatening complications such as heart failure, liver failure, and bone deformities. Thalassemia is usually diagnosed through blood tests that measure the levels of hemoglobin and other proteins in the blood.
There is no cure for thalassemia, but treatment can help manage the symptoms and prevent complications. Treatment may include blood transfusions, folic acid supplements, and medications to reduce the severity of anemia. In some cases, bone marrow transplantation may be recommended.
Preventive measures for thalassemia include genetic counseling and testing for individuals who are at risk of inheriting the disorder. Prenatal testing is also available for pregnant women who are carriers of the disorder. In addition, individuals with thalassemia should avoid marriage within their own family or community to reduce the risk of passing on the disorder to their children.
Overall, thalassemia is a serious and inherited blood disorder that can have significant health implications if left untreated. However, with proper treatment and management, individuals with thalassemia can lead fulfilling lives and minimize the risk of complications.
The most common types of hemoglobinopathies include:
1. Sickle cell disease: This is caused by a point mutation in the HBB gene that codes for the beta-globin subunit of hemoglobin. It results in the production of sickle-shaped red blood cells, which can cause anemia, infections, and other complications.
2. Thalassemia: This is a group of genetic disorders that affect the production of hemoglobin and can result in anemia, fatigue, and other complications.
3. Hemophilia A: This is caused by a defect in the F8 gene that codes for coagulation factor VIII, which is essential for blood clotting. It can cause bleeding episodes, especially in males.
4. Glucose-6-phosphate dehydrogenase (G6PD) deficiency: This is caused by a point mutation in the G6PD gene that codes for an enzyme involved in red blood cell production. It can cause hemolytic anemia, especially in individuals who consume certain foods or medications.
5. Hereditary spherocytosis: This is caused by point mutations in the ANK1 or SPTA1 genes that code for proteins involved in red blood cell membrane structure. It can cause hemolytic anemia and other complications.
Hemoglobinopathies can be diagnosed through genetic testing, such as DNA sequencing or molecular genetic analysis. Treatment options vary depending on the specific disorder but may include blood transfusions, medications, and in some cases, bone marrow transplantation.
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
There are several different types of preleukemia, including:
1. Myelodysplastic syndrome (MDS): A condition where there is a defect in the development of immature blood cells in the bone marrow, leading to an overproduction of blasts and a decrease in the number of healthy red blood cells, white blood cells, and platelets.
2. Myeloproliferative neoplasms (MPNs): A group of conditions characterized by an overproduction of one or more types of blood cells, including red blood cells, white blood cells, and platelets. MPNs can progress to leukemia over time.
3. Chronic myelogenous leukemia (CML): A type of leukemia that develops from a preleukemic condition called chronic myeloid leukemia. CML is characterized by the presence of a genetic abnormality known as the Philadelphia chromosome, which leads to an overproduction of white blood cells.
4. Acute myeloid leukemia (AML): A type of leukemia that can develop from preleukemic conditions such as MDS and MPNs. AML is characterized by the rapid growth of immature white blood cells in the bone marrow, which can crowd out healthy cells and lead to a decrease in the number of normal red blood cells, white blood cells, and platelets.
Preleukemia can be difficult to diagnose, as it often does not have clear symptoms in its early stages. However, doctors may use a variety of tests, including blood tests and bone marrow biopsies, to detect abnormalities in the blood or bone marrow that could indicate preleukemia.
Treatment for preleukemia depends on the specific type of condition and its severity. Some common treatments include:
1. Chemotherapy: A type of cancer treatment that uses drugs to kill cancer cells. Chemotherapy may be used to treat preleukemia, particularly in cases where there are abnormalities in the blood or bone marrow.
2. Blood transfusions: Transfusions of healthy red blood cells, platelets, or plasma may be given to patients with preleukemia who have low levels of these cells.
3. Supportive care: Patients with preleukemia may require supportive care, such as antibiotics or other medications, to manage symptoms and prevent complications.
4. Stem cell transplantation: In some cases, stem cell transplantation may be recommended for patients with preleukemia who have a high risk of developing acute leukemia. This involves replacing the patient's defective bone marrow stem cells with healthy ones from a donor.
Overall, early detection and treatment of preleukemia can improve outcomes and reduce the risk of developing acute leukemia. If you have been diagnosed with preleukemia or are experiencing symptoms that may indicate preleukemia, it is important to discuss your treatment options with your healthcare provider.
Symptoms of ARS can include:
* Nausea and vomiting
* Damage to the bone marrow, leading to a decrease in white blood cells, red blood cells, and platelets
* Damage to the gastrointestinal system, including inflammation and ulcers
* Damage to the lung tissue, leading to pneumonia or respiratory failure
* Damage to the central nervous system, including confusion, seizures, and coma
* Skin burns and ulcers
Treatment for ARS typically involves supportive care, such as fluids, nutrition, and pain management, as well as medications to help manage specific symptoms. In severe cases, hospitalization may be necessary, and patients may receive blood transfusions or other treatments to help their body recover from the effects of radiation exposure.
Prevention is key in avoiding ARS, and this includes using protective gear, such as gloves and masks, when working with radioactive materials, as well as following proper safety protocols and guidelines. Additionally, individuals who work with or around radiation sources should be trained on the risks of radiation exposure and how to minimize their risk of injury.
Overall, ARS is a serious condition that can have severe consequences if left untreated. Prompt medical attention is essential for those who suspect they may have been exposed to high levels of ionizing radiation.
Hodgkin Disease can spread to other parts of the body through the lymphatic system, and it can affect people of all ages, although it is most common in young adults and teenagers. The symptoms of Hodgkin Disease can vary depending on the stage of the disease, but they may include swollen lymph nodes, fever, night sweats, fatigue, weight loss, and itching.
There are several types of Hodgkin Disease, including:
* Classical Hodgkin Disease: This is the most common type of Hodgkin Disease and is characterized by the presence of Reed-Sternberg cells.
* Nodular Lymphocytic predominant Hodgkin Disease: This type of Hodgkin Disease is characterized by the presence of nodules in the lymph nodes.
* Mixed Cellularity Hodgkin Disease: This type of Hodgkin Disease is characterized by a mixture of Reed-Sternberg cells and other immune cells.
Hodgkin Disease is usually diagnosed with a biopsy, which involves removing a sample of tissue from the affected lymph node or other area and examining it under a microscope for cancer cells. Treatment for Hodgkin Disease typically involves chemotherapy, radiation therapy, or a combination of both. In some cases, bone marrow or stem cell transplantation may be necessary.
The prognosis for Hodgkin Disease is generally good, especially if the disease is detected and treated early. According to the American Cancer Society, the 5-year survival rate for people with Hodgkin Disease is about 85%. However, the disease can sometimes recur after treatment, and the long-term effects of radiation therapy and chemotherapy can include infertility, heart problems, and an increased risk of secondary cancers.
Hodgkin Disease is a rare form of cancer that affects the immune system. It is most commonly diagnosed in young adults and is usually treatable with chemotherapy or radiation therapy. However, the disease can sometimes recur after treatment, and the long-term effects of treatment can include infertility, heart problems, and an increased risk of secondary cancers.
Examples of autoimmune diseases include:
1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.
The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.
The term "blast crisis" was first used in the medical literature in 1998 to describe this phenomenon, which was previously known as "accelerated phase." The blast crisis is the most advanced stage of CML and is associated with a poor prognosis if left untreated.
The exact cause of blast crisis is not fully understood, but it is believed to be related to the development of resistance to TKIs, which can lead to an increase in the number of abnormal cells in the bone marrow and blood. The condition typically occurs after several years of TKI therapy, although it can sometimes occur within the first few months of treatment.
The symptoms of blast crisis are non-specific and can include fatigue, fever, night sweats, and weight loss. Laboratory tests will show an elevated white blood cell count, anemia, and thrombocytopenia. The diagnosis of blast crisis is based on the presence of blasts in the blood and bone marrow, as well as other laboratory and radiological findings.
Treatment of blast crisis typically involves the use of more intensive chemotherapy or hematopoietic stem cell transplantation (HSCT). In some cases, the TKI therapy may be discontinued and replaced with a different medication or combination of medications. The prognosis for patients with blast crisis is generally poor, with a five-year survival rate of around 50%. However, with appropriate treatment, some patients can achieve long-term remission or even a cure.
Also known as: chronic granulomatous disease, CGD.
COP typically affects middle-aged adults and is more common in women than men. Symptoms include cough, shortness of breath, fever, and fatigue. The condition can be acute or chronic, and it can lead to respiratory failure if left untreated.
The exact cause of COP is not known, but it is believed to be related to an abnormal immune response to environmental triggers, such as cigarette smoke or other inhaled substances. The disease is often associated with other autoimmune disorders, such as rheumatoid arthritis or lupus.
Diagnosis of COP is based on a combination of clinical findings, radiologic imaging (such as chest x-rays and CT scans), and lung biopsy. Treatment typically involves corticosteroids to reduce inflammation and improve lung function. In severe cases, respiratory support may be necessary.
The prognosis for COP varies depending on the severity of the disease and the response to treatment. In general, the condition can be managed with appropriate therapy, but it can be challenging to diagnose and treat effectively.
1. Types of Polyomaviruses: There are several types of polyomaviruses that can infect humans, including the common cold virus (Rhinovirus), respiratory syncytial virus (RSV), human metapneumovirus (HMPV), and the newly identified Parechovirus.
2. Infection: Polyomaviruses can be transmitted through contact with an infected person's respiratory secretions, such as mucus and saliva, or through contaminated surfaces. Inhaling the virus can lead to an infection in the respiratory tract.
3. Symptoms: The symptoms of polyomavirus infections can vary depending on the type of virus and the individual's age and overall health. Common symptoms include runny nose, cough, fever, sore throat, headache, and fatigue. In severe cases, polyomaviruses can cause pneumonia, bronchiolitis, and other respiratory disorders.
4. Diagnosis: A diagnosis of a polyomavirus infection is typically made based on the symptoms and medical history of the individual, as well as through laboratory tests such as PCR (polymerase chain reaction) or viral culture.
5. Treatment: There is no specific treatment for polyomavirus infections, but antiviral medications may be prescribed to help manage symptoms and prevent complications. Supportive care, such as rest, hydration, and over-the-counter pain relievers, may also be recommended.
6. Prevention: Preventing the spread of polyomaviruses can be challenging, but good hygiene practices such as frequent handwashing, avoiding close contact with people who are sick, and disinfecting surfaces can help reduce the risk of transmission. Vaccines are also being developed to protect against certain types of polyomaviruses.
7. Prognosis: In most cases, polyomavirus infections are mild and self-limiting, with symptoms resolving on their own within a few days to a week. However, severe infections can be life-threatening, particularly in individuals with weakened immune systems or underlying medical conditions.
8. Epidemiology: Polyomaviruses are common and widespread, with the majority of individuals worldwide being infected at some point in their lives. Outbreaks of polyomavirus infections can occur in settings such as hospitals, long-term care facilities, and daycare centers, where individuals with weakened immune systems are more susceptible to infection.
9. Research: Research on polyomaviruses is ongoing to better understand the viruses, their transmission, and their clinical impact. This includes development of vaccines and antiviral medications, as well as studies to identify risk factors for severe infections and to improve diagnostic tests.
10. Public health: Polyomaviruses are a public health concern, particularly in settings where individuals with weakened immune systems are more susceptible to infection. Prevention strategies include practicing good hygiene, such as frequent handwashing, and avoiding close contact with individuals who are sick.
Overall, polyomaviruses are a diverse group of viruses that can cause a range of diseases, from mild and self-limiting to severe and life-threatening. Understanding the clinical features, diagnosis, treatment, prognosis, epidemiology, research, and public health implications of polyomavirus infections is essential for providing appropriate care and preventing outbreaks.
Hematopoietic stem cell
Hematopoietic stem cell niche
Hematopoietic stem cell transplantation
List of conditions treated with hematopoietic stem cell transplantation
Techniques to isolate haematopoietic stem cells
Chronic myelomonocytic leukemia
National Kidney Registry
Stem cell factor
Stem cell transplantation for articular cartilage repair
Endothelial stem cell
Adult stem cell
Malignant infantile osteopetrosis
Narinder Kumar Mehra
Total body irradiation
Human betaherpesvirus 5
Stem cell marker
Follicular dendritic cells
Maria Grazia Roncarolo
Mitochondrial ribosomal protein L18
C. Glenn Begley
Stem cell laws
Pattern recognition receptor
Mitochondrial ribosomal protein L1
DNA damage theory of aging
Hal E. Broxmeyer
Hematopoiesis & Hematopoietic Stem Cell Biology - NIDDK
DailyMed - Search Results for Hematopoietic Stem Cell Mobilizer
NIH Guide: LINEAGE-SPECIFIC DIFFERENTIATION OF HEMATOPOIETIC STEM CELLS
Hierarchically related lineage-restricted fates of multipotent haematopoietic stem cells | Nature
Hematopoietic Stem Cell Transplantation (HSCT): Practice Essentials, Historical Background, Indications for HSCT
New Process of Developing Patient-Specific Hematopoietic Stem Cells Identified
Hematopoietic stem cells - PubMed
NIH VideoCast - Regulation of Hematopoietic Stem Cells
Vaccines | Free Full-Text | Protective Cancer Vaccine Using Genetically Modified Hematopoietic Stem Cells
Hematopoietic Stem Cells - MeSH - NCBI
Lkb1 regulates cell cycle and energy metabolism in haematopoietic stem cells
Autologous hematopoietic stem cell transplantation in multiple sclerosis | Neurology
Protein tyrosine phosphatase - sigma inhibitors for hematopoietic regeneration | California's Stem Cell Agency
Safety Study of Zinc Finger Nuclease CCR5-modified Hematopoietic Stem/Progenitor Cells in HIV-1 Infected Patients - Full Text...
Venetoclax in Combination With Non-myeloablative Conditioning Allogeneic Haematopoietic Stem Cell Transplantation - No Study...
Dry eye after haematopoietic stem cell transplantation | British Journal of Ophthalmology
Hematopoietic stem cell transplantation alters susceptibility to pulmonary hypertension in Bmpr2-deficient mice.
Allogeneic hematopoietic stem cell transplantation for paroxysmal nocturnal hemoglobinuria - multicenter analysis by Polish...
Development of a coordinated allo T cell and auto B cell response against autosomal PTK2B after allogeneic hematopoietic stem...
1 Introduction | Cord Blood: Establishing a National Hematopoietic Stem Cell Bank Program |The National Academies Press
Cxcr4 haploinsufficiency enhances hematopoietic stem cell engraftment | NIH Research Festival
High-level Gpr56 expression is dispensable for the maintenance and function of hematopoietic stem and progenitor cells in mice<...
Conditional Cre/LoxP strategies for the study of hematopoietic stem cell formation - Fingerprint - Northwestern Scholars
Hematopoietic stem progenitor cells (HSPCs) are present in very little numbers - THE PRESENT STUDY AIMED TO ELUCIDATE THE...
hematopoietic stem cells
JMML tumor cells disrupt normal hematopoietic stem cells by imposing inflammatory stress through overproduction of IL-1β.
"A Randomized Study of Virtual Survivorship Support for Allogeneic Hematopoietic Stem Cell Transplant Survivors (Be The Match...
Regulation of hematopoietic stem cells by the niche<...
- and hematopoietic stem cell transplantation and the development of techniques for establishing stable hematopoietic chimeras in order to treat heritable blood diseases. (nih.gov)
- An increased understanding of the molecular mechanisms controlling these events would increase our ability to combat selective cytopenias, and could facilitate hematopoietic reconstitution following radiation, chemotherapy, and marrow transplantation. (nih.gov)
- Hematopoietic stem cell transplantation (HSCT) involves the intravenous infusion of hematopoietic stem cells in order to reestablish blood cell production in patients whose bone marrow or immune system is damaged or defective. (medscape.com)
- To summarize the evidence on immunoablative therapy followed by autologous hematopoietic stem cell transplantation (aHSCT) to manage severe and treatment-refractory multiple sclerosis (MS). (neurology.org)
- Hematopoietic stem cell transplantation alters susceptibility to pulmonary hypertension in Bmpr2-deficient mice. (cam.ac.uk)
- The results raise the possibility that hematopoietic stem cell transplantation might be a potential treatment strategy in genetic forms of PAH. (cam.ac.uk)
- Allogeneic hematopoietic stem cell transplantation for paroxysmal nocturnal hemoglobinuria - multicenter analysis by Polish Adult Leukemia Group. (stembook.org)
- It is well known that allo-reactive T cells play a crucial role in graft- versus -leukemia and graft- versus -host disease after allogeneic hematopoietic stem cell transplantation (alloSCT). (haematologica.org)
- Allogeneic hematopoietic stem cell transplantation (alloSCT) is often the only therapeutic option for patients with hematologic malignancies. (haematologica.org)
- Early research specifically into cord blood transplantation was based on the hypothesis that the immune cells in cord blood may be less mature than those in adult bone marrow or peripheral blood. (nationalacademies.org)
- Factors already shown to influence the outcome of cord blood transplantation include the numbers of cells in the cord blood, the size of the recipient, and the degree of human leukocyte antigen (HLA) match 4 between the donor and the recipient. (nationalacademies.org)
- Hematopoietic stem cell transplantation (HSCT) is used to treat SCD. (nih.gov)
- In latest years, BMT offers been changed by transplantation of mobilized peripheral bloodstream (PB) come cells (PBSCs), which is definitely safer and much less unpleasant for the donor. (woofahs.com)
- This study evaluated the relative impact of the intensity of the conditioning regimen and the alloreactivity in the endothelial dysfunction occurring after allogeneic hematopoietic stem cell transplantation (allo-HSCT). (redheracles.net)
- The release of stem cells from the bone marrow into the peripheral blood circulation for the purpose of leukapheresis, prior to stem cell transplantation. (wakehealth.edu)
- This working group reviews matters associated with hematopoietic stem cell transplantation. (nih.gov)
- This study aimed to know the perceptions and experiences of family companions facing illness and transplantation of hematopoietic stem cells (HSCT) in light of the theory of anticipatory grief. (bvsalud.org)
- This led to experiments in mice where the inventors clearly demonstrated in a bone marrow transplantation model, that donor cells with a single copy of the Cxcr4 gene repopulate recipient mice much faster and last much longer than donor cells having two copies of the Cxcr4 gene. (nih.gov)
- Aim of Study: Cardiac complications may be observed after hematopoietic stem cell transplantation (HSCT). (who.int)
- Here we use highly sensitive tracking of progenitors and mature cells of the megakaryocyte/platelet, erythroid, myeloid and B and T cell lineages, produced from singly transplanted HSCs, to reveal a highly organized, predictable and stable framework for lineage-restricted fates of long-term self-renewing HSCs. (nature.com)
- Most notably, a distinct class of HSCs adopts a fate towards effective and stable replenishment of a megakaryocyte/platelet-lineage tree but not of other blood cell lineages, despite sustained multipotency. (nature.com)
- No HSCs contribute exclusively to any other single blood-cell lineage. (nature.com)
- Hematopoietic stem cells (HSCs) yield both the myeloid and lymphoid lineages of blood cells and can be reprogrammed into tumor antigen (Ag)-specific CD8 + cytotoxic T lymphocytes (CTLs) to prevent tumor growth. (mdpi.com)
- In the current study, we showed that a combination of genetic modification of HSCs and in vivo T cell development facilitates the generation of Ag-specific CTLs that suppressed tumor growth. (mdpi.com)
- HSCs depended more acutely on Lkb1 for cell-cycle regulation and survival than many other haematopoietic cells. (nih.gov)
- Lkb1 is therefore required for HSC maintenance through AMPK-dependent and AMPK-independent mechanisms, revealing differences in metabolic and cell-cycle regulation between HSCs and some other haematopoietic progenitors. (nih.gov)
- The chemokine receptor CXCR4 plays an important role in homing, retention, and quiescence of hematopoietic stem cells (HSCs) in the bone marrow (BM). (nih.gov)
- Blood formation by hematopoietic stem cells (HSCs) is regulated by a still incompletely defined network of general and HSC-specific regulators. (ed.ac.uk)
- Gpr56-deficient HSCs also responded normally to physiological and pharmacological mobilization signals, despite the reported role of this GPCR as a regulator of cell adhesion and migration in neuronal cells. (ed.ac.uk)
- To address this question, we induced the most common mutation identified in JMML (Ptpn11E76K) specifically in the myeloid lineage with hematopoietic stem cells (HSCs) spared. (escholarship.org)
- A similar result was observed in wild-type (WT) donor HSCs when co-transplanted with Ptpn11E76K/+ BM cells into WT mice. (escholarship.org)
- The quiescent state in the cell cycle is thought to be indispensable for the maintenance of hematopoietic stem cells (HSCs). (elsevier.com)
- Interaction of HSCs with their particular microenvironments, known as niches, is critical for maintaining the stem cell properties of HSCs, including cell adhesion, survival, and cell division. (elsevier.com)
- Tie2/Ang-1 signaling occurs in interactions between HSCs and niche cells. (elsevier.com)
- The interaction of Tie2 with Ang-1 in vitro induces tight adhesion of HSCs to stromal cells and is sufficient to maintain the long-term blood-repopulating (LTR) activity of HSCs in vivo by preventing cell division. (elsevier.com)
- Aged hematopoietic stem cells (HSCs) exhibit compromised reconstitution capacity and differentiation- bias towards myeloid lineage. (bvsalud.org)
- In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in aged hematopoietic stem and progenitor cells (HSPCs) and enforced PUS10 recapitulates the phenotype of aged HSCs, which is not achieved by its Ψ synthase activity. (bvsalud.org)
- Hematopoietic stem cells (HSCs) are ultimately responsible for the lifelong renewal of all blood cell lineages. (nih.gov)
- The application of mice models with endogenous ablation of specific cell types, advanced imaging technologies, high-throughput single-cell RNA sequencing, and single-cell mass cytometry methods have provided deep insights into communications between HSCs and niche cells. (nih.gov)
- and (3) co-culturing the sorted cells with purified HSCs for further functional assays of HSCs. (nih.gov)
- The goal of our team is to understand the biology of hematopoietic stem cells (HSCs). (nicheworks.eu)
- Methods of enhancing engraftment of donor hematopoietic stem cells (HSCs) by reducing expression or activity of CXCR4 in HSCs is described. (nih.gov)
- This technology which shows that HSCs with one copy of the CXCR4 gene have a durable selective advantage in bone marrow repopulation can solve the problem frequently encountered in gene therapy, i.e., the short-lived nature of gene-corrected cells, by utilizing recently discovered gene editing methods that can be used to delete one copy of CXCR4 gene in gene-corrected cells. (nih.gov)
- Self-renewal ensures that a pool of HSCs persists throughout life, whereas differentiation leads to the continuous generation of all circulating blood cells including lymphocytes, myeloid cells, erythrocytes and platelets. (nih.gov)
- Cells for HSCT may be obtained from the patient himself or herself (autologous transplant) or from another person, such as a sibling or unrelated donor (allogeneic transplant) or an identical twin (syngeneic transplant). (medscape.com)
- These results offer immediate proof showing a potential part for UDP-glucose in HSPC mobilization and may offer an Phenytoin sodium (Dilantin) supplier appealing technique to improve the produce of come cells in poor-mobilizing allogeneic or autologous contributor. (woofahs.com)
- Appropriately, mobilized cells possess become a main resource of HSPCs for autologous and allogeneic transplantations. (woofahs.com)
- To cure disease in the long-term, we need to be able to transplant something that can keep producing new blood cells and won't be rejected by the patient's body," said the senior author of the study, Kateri Moore, DVM, Associate Professor of Developmental and Regenerative Biology at the Icahn School of Medicine at Mount Sinai. (medindia.net)
- The researchers analyzed information obtained within 3 months before transplant and at 12 months after transplant on 35 patients who received successful HSCT, including their number of hospital admissions for pain per year, whether they used short-acting and/or long-acting opioids, and their level of hemoglobin (a protein in red blood cells). (nih.gov)
- Under immunosuppression conditions, all infectious foci can be activated and, for this reason, all active infections in hematopoietic stem cell pre-transplant patients must be eradicated prior to transplant so as to prevent or reduce the risk of systemic complications in these patients. (bvsalud.org)
- Aim: Present a case report of dental care provided to a non-Hodgkin lymphoma patient with an urgent need for hematopoietic stem cell transplant. (bvsalud.org)
- This report focuses on the development of an integrated system for the use of one specific type of stem cell, the hematopoietic progenitor cell (HPC), which is a multipotent stem cell responsible for the continual production of the diverse array of normal blood cells. (nationalacademies.org)
- Throughout this report the committee uses the term hematopoietic progenitor cell and the abbreviation HPC to avoid confusion with other forms or sources of stem cells. (nationalacademies.org)
- Atf7ip and Setdb1 interaction orchestrates the hematopoietic stem and progenitor cell state with diverse lineage differentiation. (bvsalud.org)
- The Hematopoiesis and Hematopoietic Stem Cell Biology program focuses on understanding the basic cellular and molecular mechanisms underlying the production and function of blood cells in health and disease. (nih.gov)
- 3) Developmentally-related changes in stem cell biology and differentiation. (nih.gov)
- Topics of interest include fundamental stem cell biology, ontogeny, gerontology, and the therapeutic potential of stem cells. (nih.gov)
- Other members of the research team included Ihor R. Lemischka, Professor of Developmental and Regenerative Biology, Pharmacology and Systems Therapeutics and member of The Black Family Stem Cell Institute and first author Carlos-Filipe Pereira, former Postdoctoral Fellow of Developmental and Regenerative Biology at the Icahn School of Medicine at Mount Sinai, currently an Assistant Professor at the University of Coimbra, Portugal, Cell Institute. (medindia.net)
- Our team has made great attempts to unlock this puzzle, working together for over 20 years in the fields of hematopoiesis and stem cell biology," said Dr. Moore, senior author of the study. (medindia.net)
- First, this research provides fundamental new knowledge regarding hematopoietic stem cell biology to the field. (ca.gov)
- Dr. Passagué's research investigates the biology of blood-forming hematopoietic stem cells in normal and deregulated contexts such as development of hematological malignancies and physiological aging. (nih.gov)
- Shanghai Key Laboratory of Regulatory Biology, Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Institute of Molecular Medicine, East China Normal University School of Life Sciences, Shanghai 200241, China. (bvsalud.org)
- Applications are solicited that are centered around investigations into the mechanisms of gene regulation during hematopoietic cell maturation and differentiation. (nih.gov)
- Little is known about metabolic regulation in stem cells and how this modulates tissue regeneration or tumour suppression. (nih.gov)
- In series with this, latest advances possess highlighted the physical significance of extracellular nucleotides in HSPCs: uridine-5-triphosphate (UTP) can be capable to chemoattract human being Compact disc34+ cells, and ex girlfriend or boyfriend vivo treatment of human being Compact disc34+ cells with UTP enhances the engraftment of HSPCs (19, 20). (woofahs.com)
- The National Marrow Donor Program (NMDP), founded in 1986, and the World Marrow Donor Association (WMDA), founded in 1988, were established to (1) locate and secure appropriate unrelated-donor HSCT sources for patients by promoting volunteer donation of bone marrow and peripheral blood stem cells in the community and (2) promote ethical practices of sharing stem cell sources by need, rather than by geographic location of the donor. (medscape.com)
- In HSCT, stem cells are taken from the bone marrow or blood of someone (often a matched sibling) who does not have SCD and are transplanted into the patient. (nih.gov)
- It involved a comparative analysis of the effect of incubating human umbilical vein endothelial cells (ECs) with serum samples from patients receiving autologous HSCT (auto-HSCT) or unrelated donor allo-HSCT. (redheracles.net)
- The purpose is to deliver chemotherapy, immunotherapy, and/or radiation to eliminate malignancy, prevent rejection of new stem cells, and create space for the new cells. (medscape.com)
- nbsp;By inhibiting this protein on blood stem cells, this therapeutic causes human blood stem cells to regenerate following exposure to chemotherapy or radiation, treatments commonly administered to patients being treated for cancer. (ca.gov)
- During this treatment, patient hematopoiesis is eradicated by high-dose radio-/chemotherapy and the patient is rescued by infusion of hematopoietic stem cells of an (HLA-matched) donor. (haematologica.org)
- 1 While in the early days of alloSCT, infusion of donor hematopoiesis was solely meant to rescue the patient from the otherwise lethal radio-/chemotherapy, it is now known that its beneficial effect is actually mediated by an immune response of donor cells against residual malignant cells of the patient: the so-called graft- versus -leukemia (GvL) effect. (haematologica.org)
- Malignancy individuals whose personal hematopoietic systems possess been broken by chemotherapy or rays also need BMT. (woofahs.com)
- 4 , 5 CD4 T cells help by inducing maturation of dendritic cells and stimulation of CD8 T cells, 6 and they are also known to deliver essential signals for B cells to produce IgG antibodies. (haematologica.org)
- The objective of the study is to evaluate the safety and feasibility of giving autologous SB-728mR-HSPC to HIV-1 (R5) infected patients who are being treated with cART and have undetectable virus but suboptimal CD4+ cell levels. (clinicaltrials.gov)
- Many opportunities for basic research exist in the control of the genes expressed in various hematopoietic lineages. (nih.gov)
- The processes of lineage-specific differentiation of the hematopoietic stem cells are central to the maintenance of normal hematopoiesis. (nih.gov)
- Also, leukemias and lymphomas usually are regarded as hematopoietic cells frozen at various stages of differentiation. (nih.gov)
- S tem cells are a primitive cell type found in all animals and are capable of both self-renewal and differentiation. (nationalacademies.org)
- It is this capacity for self-renewal and for differentiation into repair cells that offers great potential for regenerative medicine. (nationalacademies.org)
- Co-culture testing demonstrated that JMML/MPN cells robustly accelerated differentiation in mouse and human normal hematopoietic stem/progenitor cells. (escholarship.org)
- Hematopoietic stem and progenitor cells (HSPCs) are a heterogeneous group of cells with expansion, differentiation, and repopulation capacities. (bvsalud.org)
- Here, we show that zebrafish mutants that are deficient in an epigenetic regulator Atf7ip or Setdb1 methyltransferase undergo excessive myeloid differentiation with impaired HSPC expansion, manifesting a decline in T cells and erythroid lineage. (bvsalud.org)
- During hematopoiesis , the interaction of Atf7ip and Setdb1 triggers H3K9me3 depositions in hematopoietic regulatory genes including cebpß and cdkn1a, preventing HSPCs from loss of expansion and premature differentiation into myeloid lineage. (bvsalud.org)
- The hematopoietic system is composed of a functionally diverse group of cells that originate from a common hematopoietic stem cell (HSC) capable of long-term self-renewal and multi-lineage differentiation. (nih.gov)
- Figure 1: Stable long-term lineage-restricted reconstitution patterns by single Vwf -tdTomato + LSK CD34 − CD150 + CD48 − cells. (nature.com)
- Researchers at the Icahn School of Medicine at Mount Sinai identified cells in the embryos of mice that are precursors to blood stem cells or hematopoietic stem/progenitor cells (HSPCs). (medindia.net)
- In previous studies, they reprogrammed mouse skin cells in the lab to become HSPCs. (medindia.net)
- Now, they have identified a precursor cell in the placenta and embryo of mice that can be matured in the lab to make HSPCs. (medindia.net)
- Their results, published online in the journal Developmental Cell , could eventually lead to a process of developing patient-specific HSPCs and more differentiated blood products for cell-replacement therapy. (medindia.net)
- The reprogramming process developed by researchers at Icahn School of Medicine at Mount Sinai appears to mimic normal blood cell creation or developmental hematopoiesis -- going from precursor cells to cells that eventually become HSPCs. (medindia.net)
- The team analyzed mouse placentas and embryos for the presence of cells with the same phenotype as the precursor cells, and confirmed that they could be matured to HSPCs in the lab. (medindia.net)
- The precursor cells can be matured in the lab to transplantable HSPCs. (medindia.net)
- To strengthen the possibility that CCR5-disrupted HSPCs engraft, patients will receive either a two- or three-day (Cohort 1 or Cohort 2) course of busulfan (dose targeting AUC of 4000 µM/day) before being infused with the genetically modified cells. (clinicaltrials.gov)
- Hematopoietic stem progenitor cells (HSPCs) are present in very little numbers in the going around blood in steady-state conditions. (woofahs.com)
- Likened with G-CSFCmobilized cells, UDP-glucoseCmobilized cells backed long lasting repopulation and displayed lymphoid-biased difference preferentially, recommending that UDP-glucose activates the mobilization of distinctive subsets of HSPCs functionally. (woofahs.com)
- Functionally, PBSCs engraft better than bone tissue marrowCderived hematopoietic come progenitor cells (HSPCs) and enable quicker recovery of the white bloodstream cell count number, therefore reducing the risk of illness in individuals during the early posttransplant period (1C3). (woofahs.com)
- Early hematopoietic cell precursors]. (nih.gov)
- Their study, titled, "Hematopoietic Reprograming In Vitro Informs in Vivo Identification of Hemogenic Precursors to Definitive Hematopoietic Stem Cells," establishes that the reprogramming process can work back and forth in blood cell development. (medindia.net)
- Major areas of interest include the basic mechanisms involved in regulating the production and terminal development of blood cells, referred to as hematopoiesis. (nih.gov)
- Hematopoietic stem cells balance quiescence and cell division in the stem cell niche and also maintain the potential for long-term hematopoiesis. (elsevier.com)
- 1 One example of a pluripotent stem cell is the embryonic stem cell, found in the blastocyst stage of the developing embryo. (nationalacademies.org)
- Human mesenchymal stem cells (MSCs) for treatment towards immune- and inflammation-mediated diseases: review of current clinical trials. (nih.gov)
- In this chapter, we have focused on three important cell types in the BM niche: mesenchymal stem cells (MSCs), osteoblasts (OBs), and endothelial cells (ECs). (nih.gov)
- In addition, we are using microarray and subtractive cloning to identify genes involved in T cell signaling and T cell development. (nih.gov)
- JMML tumor cells disrupt normal hematopoietic stem cells by imposing inflammatory stress through overproduction of IL-1β. (escholarship.org)
- During this funding period, we have successfully developed a lead candidate therapeutic that inhibits a protein that is expressed on blood stem cells. (ca.gov)
- Development of normal blood cells is often suppressed in juvenile myelomonocytic leukemia (JMML), a myeloproliferative neoplasm (MPN) of childhood, causing complications and impacting therapeutic outcomes. (escholarship.org)
- These findings suggest IL-1β signaling as a potential therapeutic target for preserving normal hematopoietic development in JMML. (escholarship.org)
- At 9-12 months after SB-728mR-HSPC infusion, subjects who are aviremic with CD4 cell counts ≥600 cells/µL and have ≥1% CCR5-modified CD4 cells within the peripheral blood detected by pentamer PCR will undergo an ATI. (clinicaltrials.gov)
- We previously identified 5 HLA class II restricted polymorphic antigens as targets for allo-reactive CD4 T cells in a patient with relapsed chronic myeloid leukemia who responded to donor lymphocyte infusion (DLI) after HLA-matched alloSCT. (haematologica.org)
- Publication: Interactions of Hematopoietic Stem Cells with Bone Marrow Niche. (nih.gov)
- Zhao X, Zhang C, Cui X, Liang Y. Interactions of Hematopoietic Stem Cells with Bone Marrow Niche. (nih.gov)
- We are studying the interactions between the hematopoietic stem cells and their niche in the bone marrow. (nicheworks.eu)
- Immune complexes may subsequently be processed and presented by professional antigen presenting cells and stimulate induction of specific CD8 + T cells. (haematologica.org)
- To our knowledge, this is the first description of a coordinated allo-reactive CD4 + T-cell and auto-reactive antibody response against an autosomal antigen. (haematologica.org)
- 7 Although the capacity of CD4 T cells to stimulate production of antibodies is well-known, and induction of auto- and allo-reactive antibodies after HLA-matched alloSCT has been demonstrated by various studies, 8 - 15 the link between CD4 T- and B-cell immunity after alloSCT has only been demonstrated for DDX3Y, a male specific antigen encoded on the Y-chromosome. (haematologica.org)
- Stem cell infusion is a relatively simple process that is performed at the bedside. (medscape.com)
- Our goal is to identify the molecular mechanisms, which drive the premature senescence of endothelial cells and to determine the intracellular molecule switching between the senescent and apoptotic fate. (nicheworks.eu)
- The inventors have identified a patient in which one copy of CXCR4 had been deleted in a somatic mutation of an HSC and this cell had clonally repopulated the bone marrow. (nih.gov)
- Figure 2: Single reconstituting LSK CD34 − CD150 + CD48 − cells establish lineage-restricted haematopoietic hierarchies but remain multipotent. (nature.com)
- Both treatments induced a proinflammatory state (ie, expression of adhesion receptors, leukocyte adhesion, and p38 MAPK activation) and cell proliferation (ie, morphology and activation of ErK42/44). (redheracles.net)
- The basic cellular and molecular mechanisms underlying the production and function of blood cells. (nih.gov)
- Of particular interest is the elucidation of specific DNA sequences, DNA binding proteins, signal transduction mechanisms, extracellular matrix proteins, and cell-surface proteins that influence gene expression. (nih.gov)
- Deletion of the Lkb1 (also called Stk11) gene in mice caused increased haematopoietic stem cell (HSC) division, rapid HSC depletion and pancytopenia. (nih.gov)
- No significant alteration of hematopoietic homeostasis and HSC function is observed in young Pus10-/- mice , while aged Pus10-/- mice exhibit mild alteration of hematopoietic homeostasis and HSC function. (bvsalud.org)
- These studies should provide insight into the fundamental processes involved in the maintenance of the stem cell compartment and its production of committed progenitor cells through the lifespan of the organism. (nih.gov)
- These findings demonstrate that the hematopoietic stem cell compartment is involved in the susceptibility to PAH in the Mut mouse. (cam.ac.uk)
- Hematopoietic Stem Cell Mobilization" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (wakehealth.edu)
- 2 The same immune reaction, however, can also be directed against healthy non-hematopoietic tissues of the patient causing detrimental graft- versus -host disease (GvHD). (haematologica.org)
- Identification of hematopoietic stem/progenitor cells: strength and drawbacks of functional assays. (nih.gov)
Sickle Cell Di3
- A collaborative intramural study cofunded by the National Center for Complementary and Integrative Health and three other agencies at the National Institutes of Health offers new information on pain in sickle cell disease, the use of opioids for this pain, and psychological and quality-of-life challenges faced by people with this disease. (nih.gov)
- Sickle cell disease (SCD) is an inherited disease in which a person's red blood cells have an abnormal crescent shape, block small blood vessels, and do not live as long as normal red blood cells. (nih.gov)
- The 2021 NHLBI Annual Sickle Cell Disease Research Meeting is a 3-day meeting that provides a forum for investigators, practitioners, and interested health care providers to discuss the progress of ongoing clinical trials, hear presentations about new developments in scientific and clinical aspects of sickle cell disease, and interact with other investigators and NHLBI program staff. (nih.gov)
- TCR signal amplification was found to be critical for thymocyte selection, the process by which potentially useful immature T cells are instructed to survive and differentiate further-(positive selection), and potentially auto-reactive cells that may cause auto-immune disease are deleted in the thymus (negative selection). (nih.gov)
- It is believed that stem cells form reservoirs of repair cells to replace cells and tissues that degenerate over the life span of the organism. (nationalacademies.org)
- For instance, recently it has become evident that beta-2 integrins are not simply adhesion sites on the cell surface of hematopoietic cells but may modulate a number of cellular processes including signal transduction pathways and gene expression. (nih.gov)
- HSC niche consists of complex components including heterogeneous cell populations, growth factors, and extracellular matrix molecules. (nih.gov)
- We investigate pancreatic cancer as a complex tissue that consists of cancer cells, tumor-associated activated pancreatic stellate cells and tumor stroma, focusing on calcium signaling. (nicheworks.eu)
- Generate and functionally evaluate candidate PTP - sigma inhibitors that antagonize PTP - sigma mediated signaling in hematopoietic stem cells for the purpose of hematopoietic regeneration. (ca.gov)