Janus Kinase 2
Janus Kinase 3
Janus Kinases
Janus Kinase 1
Protein-Tyrosine Kinases
Phosphatidylinositol 3-Kinases
MAP Kinase Signaling System
STAT3 Transcription Factor
STAT Transcription Factors
Protein-Serine-Threonine Kinases
Signal Transduction
Protein Kinases
TYK2 Kinase
Phosphorylation
Suppressor of Cytokine Signaling Proteins
STAT1 Transcription Factor
src-Family Kinases
Calcium-Calmodulin-Dependent Protein Kinases
STAT5 Transcription Factor
Proto-Oncogene Proteins
Trans-Activators
p38 Mitogen-Activated Protein Kinases
Tyrphostins
Mitogen-Activated Protein Kinase 1
Protein Kinase C
Milk Proteins
Tyrosine
JNK Mitogen-Activated Protein Kinases
Cyclic AMP-Dependent Protein Kinases
Mitogen-Activated Protein Kinase Kinases
Mitogen-Activated Protein Kinase 3
DNA-Binding Proteins
Enzyme Activation
p21-Activated Kinases
Mitogen-Activated Protein Kinases
Creatine Kinase
Extracellular Signal-Regulated MAP Kinases
CDC2 Protein Kinase
Cyclin-Dependent Kinases
Enzyme Inhibitors
MAP Kinase Kinase Kinases
Transfection
Mutation
eIF-2 Kinase
Casein Kinase II
Casein Kinases
Cells, Cultured
Cytokine Receptor gp130
Pyruvate Kinase
Ribosomal Protein S6 Kinases
Protein Binding
Blotting, Western
Intracellular Signaling Peptides and Proteins
Proto-Oncogene Proteins c-akt
MAP Kinase Kinase 1
Molecular Sequence Data
Receptor Protein-Tyrosine Kinases
Thymidine Kinase
Phosphotyrosine
MAP Kinase Kinase 4
RNA, Messenger
Receptors, Interleukin-9
1-Phosphatidylinositol 4-Kinase
Apoptosis
Phosphotransferases (Alcohol Group Acceptor)
Myeloproliferative Disorders
CDC2-CDC28 Kinases
Receptors, Cytokine
Tumor Cells, Cultured
Gene Expression Regulation
I-kappa B Kinase
Cell Division
Isoenzymes
Glycogen Synthase Kinase 3
Aurora Kinases
rho-Associated Kinases
Interleukin-6
Amino Acid Sequence
Protein Kinase C-delta
Protein Kinase C-alpha
Proteins
Protein Structure, Tertiary
Base Sequence
Recombinant Fusion Proteins
Primary Myelofibrosis
Precipitin Tests
src Homology Domains
Diacylglycerol Kinase
Serine
AMP-Activated Protein Kinases
Dose-Response Relationship, Drug
STAT2 Transcription Factor
Receptors, Erythropoietin
Down-Regulation
Receptors, Oncostatin M
Substrate Specificity
Transcription Factors
Binding Sites
STAT6 Transcription Factor
Focal Adhesion Kinase 1
Polycythemia Vera
Gene Expression Regulation, Enzymologic
Carrier Proteins
Pyrimidines
Myosin-Light-Chain Kinase
Models, Biological
3T3 Cells
Receptors, Interleukin-4
Immunoblotting
Adaptor Proteins, Signal Transducing
Receptors, Leptin
Focal Adhesion Protein-Tyrosine Kinases
RNA, Small Interfering
Receptors, Prolactin
Transcription, Genetic
Sequence Homology, Amino Acid
Mice, Knockout
Ribosomal Protein S6 Kinases, 90-kDa
Cell Survival
Protein Kinase C-epsilon
Up-Regulation
Reverse Transcriptase Polymerase Chain Reaction
Androstadienes
MAP Kinase Kinase Kinase 1
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Pyridines
Cell Nucleus
Thrombocythemia, Essential
Protein Kinase C beta
Repressor Proteins
Tetradecanoylphorbol Acetate
MAP Kinase Kinase 2
Cell Differentiation
Calcium
Cyclin-Dependent Kinase 2
Cyclic GMP-Dependent Protein Kinases
Interferon-Stimulated Gene Factor 3
TOR Serine-Threonine Kinases
NF-kappa B
Cyclin-Dependent Kinase 5
HeLa Cells
Phosphoglycerate Kinase
Oncostatin M
Cell Line, Transformed
Rats, Sprague-Dawley
Receptors, Somatotropin
Phosphorylase Kinase
Cytokines
Fibroblasts
Arginine Kinase
Cell Cycle Proteins
Receptor, Interferon alpha-beta
Nucleoside-Phosphate Kinase
Receptors, Interleukin
MAP Kinase Kinase 6
Gene Expression
Transcriptional Activation
Promoter Regions, Genetic
Interferon-gamma
Casein Kinase I
Receptor, Epidermal Growth Factor
Interleukin-4
MAP Kinase Kinase 3
Mitogen-Activated Protein Kinase 8
Aurora Kinase A
3-Phosphoinositide-Dependent Protein Kinases
Mutagenesis, Site-Directed
Focal Adhesion Kinase 2
Cyclic AMP
DNA Primers
Membrane Proteins
Phosphatidylinositol 3-Kinase
Genistein
Protein Processing, Post-Translational
Adenosine Kinase
Tumor Suppressor Proteins
Nitriles
Cell Cycle
Lim Kinases
Dimerization
Cell Movement
Leukemia Inhibitory Factor
Protein Transport
Cell Membrane
DNA
Prolactin
Granulocyte-macrophage colony-stimulating factor-activated signaling pathways in human neutrophils. Involvement of Jak2 in the stimulation of phosphatidylinositol 3-kinase. (1/1765)
Granulocyte-macrophage colony-stimulating factor (GM-CSF) regulates many of the biological activities of human neutrophils. The signaling pathways via which these effects are mediated are not fully understood. We have shown previously that GM-CSF treatment of human neutrophils activates the Janus kinase/signal transducers and activators of transcription (Jak/STAT) pathway and, more specifically, Jak2, STAT3, and STAT5B in neutrophils. GM-CSF also stimulates the activity of the phosphatidylinositol 3-kinase (PI3-kinase) in a tyrosine kinase-dependent manner. Here we report that pretreating the cells with a Jak2 inhibitor (AG-490) abolishes tyrosine phosphorylation of the p85 subunit of PI3-kinase induced by GM-CSF. Furthermore, p85 was found to associate with Jak2, but not with Lyn, in stimulated cells in situ and with its autophosphorylated form in vitro; however, Jak2 did not bind to either of the two Src homology 2 (SH2) domains of the p85 subunit of PI3-kinase. Although STAT5B bound to the carboxyl-terminal SH2 domain of p85, it was absent from the complex containing PI3-kinase and Jak2. These results suggest that stimulation of the activity of PI3-kinase induced by GM-CSF is mediated by Jak2 and that the association between Jak2 and p85 depends on an adaptor protein yet to be identified. (+info)Constitutive activation of JAK2 confers murine interleukin-3-independent survival and proliferation of BA/F3 cells. (2/1765)
The Janus tyrosine kinase 2 (JAK2) plays an essential role of cytokine receptor signaling, including that of the human granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor. We reported earlier that the activation of JAK2 is essential for all the examined signals induced by human GM-CSF through the box1 region of betac, such as promotion of cell survival and proliferation. To elucidate the role of JAK2 in cell survival and proliferation, we generated an artificial activation system by constructing a chimeric molecule (beta/JAK2) consisting of betac extracellular and transmembrane regions fused with JAK2, and we analyzed various signaling events in interleukin-3-dependent mouse pro-B cell, BA/F3. The beta/JAK2 was constitutively phosphorylated in the absence of human GM-CSF and murine interleukin-3, and this led to proliferation and cell survival. Western blot analysis showed that STAT5, Shc, and SHP-2 were not phosphorylated in the cells, and the consistent activation of beta-casein and c-fos promoters was not enhanced. In contrast, c-myc transcription was constitutively activated. We propose that the activation of beta/JAK2 suffices for survival and proliferation and that the activation of STAT5 and mitogen-activated protein kinase cascade is not required for these activities in BA/F3 cells. (+info)Thrombopoietin-induced conformational change in p53 lies downstream of the p44/p42 mitogen activated protein kinase cascade in the human growth factor-dependent cell line M07e. (3/1765)
Thrombopoietin is a cytokine with potent megakaryocytopoietic and thrombopoietic activities in vivo. Wild-type p53 is a conformationally flexible, anti-oncogenic transcription factor that plays a principal role in mediating growth factor withdrawal-induced apoptosis in factor-dependent hematopoietic cells. We recently reported that Tpo induces a conformational change in and functional inactivation of p53, coincident with its anti-apoptotic effects, in the human factor-dependent cell line M07e. In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner. Furthermore, the expression of constitutively active Raf1 in M07e cells induced conformational change in p53 independent of Tpo stimulation. Inhibition of the JAK/STAT pathway revealed that JAK/STAT signaling plays an insignificant role in conformational modulation of p53 and apoptosis suppression. Inhibition of phosphatidylinositol-3 kinase did not have a significant effect on p53 conformation but did have a weak but significant effect on Tpo-enhanced viability. Cytokine-induced activation of the MAPK pathway and the subsequent functional neutralization of p53, may be an event by which apoptosis is commonly suppressed in hematopoiesis. (+info)The JAK-binding protein JAB inhibits Janus tyrosine kinase activity through binding in the activation loop. (4/1765)
The Janus family of protein tyrosine kinases (JAKs) regulate cellular processes involved in cell growth, differentiation and transformation through their association with cytokine receptors. However, compared with other kinases, little is known about cellular regulators of the JAKs. We have recently identified a JAK-binding protein (JAB) that inhibits JAK signaling in cells. In the studies presented here we demonstrate that JAB specifically binds to the tyrosine residue (Y1007) in the activation loop of JAK2, whose phosphorylation is required for activation of kinase activity. Binding to the phosphorylated activation loop requires the JAB SH2 domain and an additional N-terminal 12 amino acids (extended SH2 subdomain) containing two residues (Ile68 and Leu75) that are conserved in JAB-related proteins. An additional N-terminal 12-amino-acid region (kinase inhibitory region) of JAB also contributes to high-affinity binding to the JAK2 tyrosine kinase domain and is required for inhibition of JAK2 signaling and kinase activity. Our studies define a novel type of regulation of tyrosine kinases and might provide a basis for the design of specific tyrosine kinase inhibitors. (+info)TGF-beta does not inhibit IL-12- and IL-2-induced activation of Janus kinases and STATs. (5/1765)
The immune system is an important target for the cytokine TGF-beta1, whose actions on lymphocytes are largely inhibitory. TGF-beta has been reported to inhibit IL-12- and IL-2-induced cell proliferation and IFN-gamma production by T cells and NK cells; however, the mechanisms of inhibition have not been clearly defined. It has been suggested by some studies that TGF-beta blocks cytokine-induced Janus kinase (JAK) and STAT activation, as in the case of IL-2. In contrast, other studies with cytokines like IFN-gamma have not found such an inhibition. The effect of TGF-beta on the IL-12-signaling pathway has not been addressed. We examined this and found that TGF-beta1 did not have any effect on IL-12-induced phosphorylation of JAK2, TYK2, and STAT4 although TGF-beta1 inhibited IL-2- and IL-12-induced IFN-gamma production. Similarly, but in contrast to previous reports, we found that TGF-beta1 did not inhibit IL-2-induced phosphorylation of JAK1, JAK3, and STAT5A. Furthermore, gel shift analysis showed that TGF-beta1 did not prevent activated STAT4 and STAT5A from binding to DNA. Our results demonstrate that the inhibitory effects of TGF-beta on IL-2- and IL-12-induced biological activities are not attributable to inhibition of activation of JAKs and STATs. Rather, our data suggest the existence of alternative mechanisms of inhibition by TGF-beta. (+info)Lineage-specific activation of STAT3 by interferon-gamma in human neutrophils. (6/1765)
Binding of interferon-gamma (IFN-gamma) to its heterodimeric receptor induces activation of the tyrosine kinases JAK1 and JAK2 followed by tyrosine phosphorylation of STAT1alpha. Selective activation of STAT1alpha at the IFN-gamma receptor is achieved by specific interaction between a cytosolic tyrosine motif including Y440 in the IFN-gamma receptor alpha-chain and the SH2 domain of STAT1alpha. We demonstrate that, in addition to STAT1alpha, STAT3 is also activated by IFN-gamma in human neutrophils. The activation of STAT3 was not found in human eosinophils, monocytes, and HL-60 cells, although the STAT3 protein was expressed in these cells. The cell type-specific activation of STAT3 by IFN-gamma was also observed in neutrophils that are differentiated in vitro from human CD34+ hematopoietic stem cells. These results indicate that a single cytokine receptor can activate different STAT family members in a cell-specific manner, which might result in cell-specific gene transcription. (+info)Growth hormone-dependent differentiation of 3T3-F442A preadipocytes requires Janus kinase/signal transducer and activator of transcription but not mitogen-activated protein kinase or p70 S6 kinase signaling. (7/1765)
The signals mediating growth hormone (GH)-dependent differentiation of 3T3-F442A preadipocytes under serum-free conditions have been studied. GH priming of cells was required before the induction of terminal differentiation by a combination of epidermal growth factor, tri-iodothyronine, and insulin. Cellular depletion of Janus kinase-2 (JAK-2) using antisense oligodeoxynucleotides (ODNs) prevented GH-stimulated JAK-2 and signal transducer and activator of transcription (STAT)-5 tyrosine phosphorylation and severely attenuated the ability of GH to promote differentiation. Although p42(MAPK)/p44(MAPK) mitogen-activated protein kinases were activated during GH priming, treatment of cells with PD 098059, which prevented activation of these kinases, did not block GH priming. However, antisense ODN-mediated depletion of mitogen-activated protein kinases from the cells showed that their expression was necessary for terminal differentiation. Similarly, although p70(s6k) was activated during GH priming, pretreatment of cells with rapamycin, which prevented the activation of p70(s6k), had no effect on GH priming. However, rapamycin did partially block epidermal growth factor, tri-iodothyronine, and insulin-stimulated terminal differentiation. By contrast, cellular depletion of STAT-5 with antisense ODNs completely abolished the ability of GH to promote differentiation. These results indicate that JAK-2, acting specifically via STAT-5, is necessary for GH-dependent differentiation of 3T3-F442A preadipocytes. Activation of p42(MAPK)/p44(MAPK) and p70(s6k) is not essential for the promotion of differentiation by GH, although these signals are required for GH-independent terminal differentiation. (+info)Constitutive activation of the JAK2/STAT5 signal transduction pathway correlates with growth factor independence of megakaryocytic leukemic cell lines. (8/1765)
The factor-independent Dami/HEL and Meg-01 and factor-dependent Mo7e leukemic cell lines were used as models to investigate JAK/STAT signal transduction pathways in leukemic cell proliferation. Although Dami/HEL and Meg-01 cell proliferation in vitro was independent of and unresponsive to exogenous cytokines including granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), IL-6, thrombopoietin (TPO), and tumor necrosis factor-alpha (TNF-alpha), the growth of Mo7e cells was dependent on hematopoietic growth factors. When these cell lines were cultured in medium without cytokines, a constitutively activated STAT-like DNA-binding factor was detected in nuclear extracts from both Dami/HEL and Meg-01 cells. However, the STAT-like factor was not detectable in untreated Mo7e cells, but was activated transiently in Mo7e cells in response to cytokine treatments. The constitutively activated and cytokine-induced STAT-like DNA-binding factor in these three cell lines was identified as STAT5 by oligonucleotide competition gel mobility assays and by specific anti-STAT antibody gel supershift assays. Constitutive activation of JAK2 also was detected in the factor-independent cell lines, but not in Mo7e cells without cytokine exposure. Meg-01 cells express a p185 BCR/ABL oncogene, which may be responsible for the constitutive activation of STAT5. Dami/HEL cells do not express the BCR/ABL oncogene, but increased constitutive phosphorylation of Raf-1 oncoprotein was detected. In cytokine bioassays using growth factor-dependent Mo7e and TF-1 cells as targets, conditioned media from Dami/HEL and Meg-01 cells did not show stimulatory effects on cell proliferation. Our results indicate that the constitutive activation of JAK2/STAT5 correlates with the factor-independent growth of Dami/HEL and Meg-01 cells. The constitutive activation of JAK2/STAT5 in Dami/HEL cells is triggered by a mechanism other than autocrine cytokines or the BCR/ABL oncoprotein. (+info)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:
* Fatigue
* Weakness
* Shortness of breath
* Headaches
* Dizziness
* 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.
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.
Sources:
* American Cancer Society. (2019). What is primary myelofibrosis? Retrieved from
* Leukemia and Lymphoma Society. (n.d.). Primary Myelofibrosis. Retrieved from
The exact cause of polycythemia vera is not known, but it is believed to be due to a genetic mutation in the JAK2 gene, which is involved in the signaling pathways that regulate blood cell production. The condition typically affects adults over the age of 60 and is more common in men than women.
Symptoms of polycythemia vera can include:
* Fatigue
* Weakness
* Shortness of breath
* Headaches
* Dizziness
* Itching
* Night sweats
* Weight loss
Diagnosis of polycythemia vera is typically made based on a combination of physical examination, medical history, and laboratory tests, including:
* Complete blood count (CBC) to measure the levels of red blood cells, white blood cells, and platelets
* Blood chemistry tests to assess liver function and other body chemicals
* Genetic testing to look for the JAK2 mutation
* Bone marrow biopsy to examine the bone marrow tissue for abnormalities
Treatment for polycythemia vera usually involves phlebotomy (the removal of blood from the body) to reduce the number of red blood cells and relieve symptoms such as itching and night sweats. In some cases, medications may be used to reduce the production of blood cells or to treat specific symptoms. Regular monitoring by a healthcare provider is important to detect any changes in the condition and to prevent complications.
Overall, polycythemia vera is a chronic and progressive disease that can have significant impact on quality of life if left untreated. Early diagnosis and appropriate treatment can help manage symptoms and improve outcomes for patients with this condition.
1. Primary essential thrombocythemia (PET): This is the more common form, usually occurring spontaneously without any identifiable cause. Symptoms may include headache, migraine, seizures, and stroke-like episodes.
2. Secondary essential thrombocythemia: This form is caused by another medical condition or medication that stimulates the production of platelets. Symptoms are similar to those of PET, but there may be an underlying cause such as a tumor or an adverse reaction to medication.
Treatment for essential thrombocythemia includes medications to reduce platelet count and prevent blood clots, as well as close monitoring and management of any underlying causes. In some cases, surgery may be necessary to remove a tumor or other contributing factor.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
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.
The term splenomegaly is used to describe any condition that results in an increase in the size of the spleen, regardless of the underlying cause. This can be caused by a variety of factors, such as infection, inflammation, cancer, or genetic disorders.
Splenomegaly can be diagnosed through a physical examination, where the doctor may feel the enlarged spleen during an abdominal palpation. Imaging tests, such as ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI), may also be used to confirm the diagnosis and evaluate the extent of the splenomegaly.
Treatment for splenomegaly depends on the underlying cause. For example, infections such as malaria or mononucleosis are treated with antibiotics, while cancerous conditions may require surgical intervention or chemotherapy. In some cases, the spleen may need to be removed, a procedure known as splenectomy.
In conclusion, splenomegaly is an abnormal enlargement of the spleen that can be caused by various factors and requires prompt medical attention for proper diagnosis and treatment.
There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
Janus kinase 2
Janus kinase 3
JAKMIP2
Thrombocythemia
Ion transporter
Fedratinib
Janus kinase inhibitor
Polycythemia vera
Ruxolitinib
PTPN11
PPP2R4
Janus kinase 1
Interleukin 23
YES1
Signal transducing adaptor molecule
Janus kinase 3 inhibitor
SH2B1
Pacritinib
Interleukin 12 receptor, beta 2 subunit
USP18
Deucravacitinib
Deuterated drug
STAT5B
Prolactin
SH2B2
INSL3
Erythropoietin receptor
Growth hormone receptor
Interleukin-23 receptor
Surveyor nuclease assay
Interferon
TIAF1
Cyclopentenone prostaglandins
Enzyme inhibitor
Histone methyltransferase
SNX8
STAT6
PTK2
H19 (gene)
List of skin conditions
Interleukin 11
Granulocyte colony-stimulating factor
Interleukin 6
Janus kinase 3 deficiency
X-linked severe combined immunodeficiency
FYN
Prostasomes
Interferon tau
Atopic dermatitis
Hes3 signaling axis
Interleukin 13
SOCS3
Lestaurtinib
Biochemical cascade
FERM domain
Ankylosing spondylitis
Janus kinase-2 inhibitor fedratinib in patients with myelofibrosis previously treated with ruxolitinib (JAKARTA-2): a single...
Author Page for Carolyn Rochester :: SSRN
JAK2 gene: MedlinePlus Genetics
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JAK210
- In 2005, researchers discovered a mutation in the Janus Tyrosine Kinase 2 gene (JAK2 (V617F)), which plays a pivotal role in the regulation of blood cell production (Levine et al. (cdc.gov)
- He recently examined a causal SNP for inflammatory bowel disease (IBD) in the promoter region of the Janus kinase 2 (JAK2) gene. (chop.edu)
- Activating alleles of Janus kinase 2 (JAK2) such as JAK2 V617F are central to the pathogenesis of myeloproliferative neoplasms (MPN), suggesting that small molecule inhibitors targeting JAK2 may be therapeutically useful. (elsevierpure.com)
- We have identified an aminopyrimidine derivative (CYT387), which inhibits JAK1, JAK2, and tyrosine kinase 2 (TYK2) at low nanomolar concentrations, with few additional targets. (elsevierpure.com)
- While the clinical benefit of JAK2 inhibitors may be substantial, not the least due to reduction of inflammatory cytokines and symptomatic improvement, our data add to increasing evidence that kinase inhibitor monotherapy of malignant disease is not curative, suggesting a need for drug combinations to optimally target the malignant cells. (elsevierpure.com)
- Janus kinase 2 (JAK2) methylation and obesity: A Mendelian randomization study. (cdc.gov)
- Polycythemia vera (PV) as a primary condition is a type of clonal disorder of bone marrow stem cells which is often caused by a mutation in exon 12 of the janus kinase 2 ( JAK2 ) tyrosine kinase gene [ 4 , 5 ]. (biomedcentral.com)
- Increased secretion of both GH and IGF-1 activates pathways, such as Janus kinase 2/signal transducer and activator of transcription 5 (JAK2/STAT5), and mitogen-activated protein kinase (MAPK), involved in the development of tumors. (bvsalud.org)
- It is an oral kinase inhibitor with activity against wild type and mutationally activated Janus Associated Kinase 2 (JAK2) and FMS-like tyrosine kinase 3 (FLT3). (mpn-advocates.net)
- The intact receptor lacks tyrosine kinase activity, but binding of GH and dimerization results in association with JAK2, a member of the Janus kinase family, which results in self-phosphorylation of the JAK2 and a cascade of phosphorylation of cellular proteins. (medscape.com)
Inhibitors12
- We report disseminated T. marneffei infection in 4 hematology patients without AIDS who received targeted therapy with monoclonal antibodies against CD20 or kinase inhibitors during the past 2 years. (cdc.gov)
- Oral Janus kinase inhibitors are known to be effective treating hypereosinophilic syndrome. (biomedcentral.com)
- Janus kinase inhibitors have also demonstrated efficacy in alopecia. (biomedcentral.com)
- This study demonstrates that longer eyelashes may be another effect of oral Janus kinase inhibitors. (biomedcentral.com)
- Physicians and patients should be aware of the side effect of these Janus kinase inhibitors. (biomedcentral.com)
- Las Vega (Nevada), United States //- As per DelveInsight's assessment, globally, Janus kinase (JAK) Inhibitors pipeline constitutes key companies continuously working towards developing Janus kinase (JAK) Inhibitors treatment therapies, analysis of Clinical Trials, Therapies, Mechanism of Action, Route of Administration, and Developments analyzes DelveInsight. (saurashtranews.com)
- Janus kinase (JAK) inhibitors are small molecules approximately 400 Da that could be administered as oral medicines. (saurashtranews.com)
- " Janus kinase (JAK) Inhibitors Pipeline Insight, 2023 " report by DelveInsight outlines comprehensive insights into the present clinical development scenario and growth prospects across the Janus kinase (JAK) Inhibitors Market. (saurashtranews.com)
- The Janus kinase (JAK) Inhibitors Pipeline report embraces in-depth commercial and clinical assessment of the pipeline products from the pre-clinical developmental phase to the marketed phase. (saurashtranews.com)
- Companies across the globe are diligently working toward developing novel Janus kinase (JAK) Inhibitors treatment therapies with a considerable amount of success over the years. (saurashtranews.com)
- Janus kinase (JAK) Inhibitors pipeline report provides the therapeutic assessment of the pipeline drugs by the Route of Administration. (saurashtranews.com)
- With an increased worldwide focus on treating axial spondyloarthritis, the major market players are developing novel therapeutics, such as anti-janus kinase therapy, anti-interleukin therapy, and anti-tumor necrosis factor therapy, which is significantly impacting the growth of axial spondyloarthritis market.Due to the introduction of tumor necrosis factor inhibitors and interleukin 17 inhibitors, a new era of drug therapy was initiated for previously largely incurable diseases. (storiescover.com)
Inhibitor2
- We aimed to evaluate the use of baricitinib, a Janus kinase (JAK) 1-2 inhibitor, for the treatment of patients admitted to hospital with COVID-19. (ebsco.com)
- BackgroundWe aimed to evaluate the use of baricitinib, a Janus kinase (JAK) 1-2 inhibitor, for the treatment of patients admitted to hospital with COVID-19.MethodsThis randomised, controlled, open-label, platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple possible treatments in patients hospitalised with COVID-19 in the UK. (ox.ac.uk)
Protein3
- Janus was the Roman god of gates and this protein regulates the production of red bloods cells. (gboncology.com)
- In the present study, we characterized the E3 orthologues from sheeppox virus, yaba monkey tumor virus, swinepox virus, and myxoma virus for their ability to modulate protein kinase R (PKR) function, cytokine responses and virus pathogenicity. (mdm2-receptor.com)
- TCDD for every step of the mechanism described for 2,3,7,8-TCDD carcinogenesis in humans including receptor binding, gene expression, protein activity changes, cellular replication, oxidative stress, promotion in initiation-promotion studies and complete carcinogenesis in laboratory animals. (who.int)
20231
- 24(2): 1-10, 2023. (bvsalud.org)
20222
- Methodology: Between September 2021 and February 2022, oropharyngeal and/or nasopharyngeal swab samples of consecutively selected COVID-19 symptomatic and apparently healthy workers from the Wahgnion mining site in the South-western Burkina Faso who consented to the study were collected according to the two weeks shift program and tested for SARS-CoV-2 using RT-PCR assay. (bvsalud.org)
- Méthodologie: Entre septembre 2021 et février 2022, des écouvillonnages oropharyngés et/ou nasopharyngés de travailleurs symptomatiques COVID-19 et apparemment en bonne santé sélectionnés consécutivement du site minier de Wahgnion dans le sud-ouest du Burkina Faso qui ont consenti à l'étude ont été prélevés selon les deux programme de quart de semaines et testé pour le SRAS-CoV-2 à l'aide d'un test RT-PCR. (bvsalud.org)
Receptor3
- Casirivimab and imdevimab are non-competing monoclonal antibodies that bind to two different sites on the receptor binding domain of the SARS-CoV-2 spike glycoprotein, blocking viral entry into host cells. (ebsco.com)
- The GH molecule binds to its specific cell surface receptor (GHR), which dimerizes with another GHR molecule so that the single GH molecule is enveloped by 2 GHR molecules. (medscape.com)
- IGF binding involves 3 basic types of receptors: the structurally homologous insulin receptor and type 1 IGF receptor and the distinctive type 2 IGF-II/mannose-6-phosphate receptor. (medscape.com)
20211
- The RECOVERY trial is registered with ISRCTN (50189673) and ClinicalTrials.gov (NCT04381936) and is ongoing.FindingsBetween Feb 2 and Dec 29, 2021, from 10 852 enrolled, 8156 patients were randomly allocated to receive usual care plus baricitinib versus usual care alone. (ox.ac.uk)
Immune2
- For instance, the tumor microenvironment modulates the immune response by selectively attracting and repolarizing immune cells (e.g. macrophages and neutrophils) from an anti-tumorigenic to a pro-tumorigenic phenotype ( 2 , 3 ). (frontiersin.org)
- Research on Ebola survivors has documented long-lasting inflammation and severe immune dysfunction 2 years after infection, for instance. (medscape.com)
Regulate1
- Muscle subjected to functional overload mobilizes the mitotically-active satellite cells, in turn increasing myonuclei number of the recipient muscle cells and facilitating hypertrophy [2] -- an adaptation that will allow each nucleus to regulate more cytoplasm [3], and ultimately the enlarged muscles to undergo more forceful contractions (lift heavier loads). (bodybuilding.com)
Years4
- Distinguishing between the two became much easier about ten years ago with the discovery and testing for Janus Kinase 2 (JAK-2) mutations. (gboncology.com)
- The patients underwent bariatric surgery at a single center in France and were followed for 2 years. (bvsalud.org)
- The average time in years from symptom onset to start of first treatment, and from first to second added treatment was 2;7/2;9 (females) and 5;1/5;2 (males). (braincirculation.org)
- OPZELURA was studied in 2 double-blind, randomized, vehicle-controlled trials of identical design that enrolled 674 adult and adolescent patients with nonsegmental vitiligo ≥12 years of age. (opzelurahcp.com)
Infection3
- Real time polymerase chain reaction (RT-PCR) assay is the recommended confirmatory method for the diagnosis of SARS-CoV-2 infection. (bvsalud.org)
- The aim of this study was to determine the prevalence of SARSCoV-2 infection in Burkina Faso and to use the initial cycle threshold (Ct) values of RT-PCR as a tool to monitor the dynamics of the viral load. (bvsalud.org)
- The overall prevalence of SARS-CoV-2 infection was 14.3% (216/1506). (bvsalud.org)
Treatment3
- Table 2 Plasma concentration of MP-10 and estimated target occupancy of PDE10A in monkeys 7.9, p 0.01,) and cortical (6, p 0.02) regions compared to vehicle treatment (Figure 1A-B). The magnitude of the increase was not different between the two doses of MP-10 despite a predicted 6-fold change in 7.9) or cortical (6) ROIs. (bioskinrevive.com)
- INREBIC® (fedratinib) is indicated for the treatment of adult patients with intermediate-2 or high-risk primary or secondary (post-polycythemia vera or post-essential thrombocythemia) myelofibrosis (MF). (mpn-advocates.net)
- In both trials, patients were randomized 2:1 to treatment with OPZELURA or vehicle cream twice daily (BID) for 24 weeks followed by a 28-week open-label extension, wherein patients originally assigned to vehicle could switch to OPZELURA. (opzelurahcp.com)
Severe1
- Background: To control the spread of coronavirus disease-19 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), it is necessary to adequately identify and isolate infectious patients particularly at the work place. (bvsalud.org)
Disease2
- Pregnant women are no more likely to contract coronavirus disease 2019 (COVID-19) than the background population and two-thirds of those testing positive are asymptomatic [ 1 , 2 ]. (ersjournals.com)
- An estimated 2 million people in the United States are living with what's called posttreatment Lyme disease (PTLD) - a subset of patients with persistent or chronic Lyme disease - and an estimated 1.7-3.3 million people in the United States have diagnoses of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). (medscape.com)
Plasma2
- Wet/dry mass ratio (W/D) of lung tissue of rats in each group was measured, and ELISA was used to assay interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), IL-6 content and rat plasma angiopoietin 2 (Ang2) content in bronchoalveolar lavage fluid (BALF). (bvsalud.org)
- Many patients with COVID-19 have been treated with plasma containing anti-SARS-CoV-2 antibodies. (ebsco.com)
Patients1
- Contexte: Pour contrôler la propagation de la maladie à coronavirus 19 (COVID-19) causée par le syndrome respiratoire aigu sévère coronavirus-2 (SRAS-CoV-2), il est nécessaire d'identifier et d'isoler de manière adéquate les patients infectieux, en particulier sur le lieu de travail. (bvsalud.org)
Medical1
- 25 kg·m −2 , having a medical comorbidity, being in the Black, Asian and Minority Ethnicity (BAME) population, and socioeconomic deprivation [ 1 ]. (ersjournals.com)