An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase.
Agents used to prevent or reverse the pathological events leading to sickling of erythrocytes in sickle cell conditions.
A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S.
The major component of hemoglobin in the fetus. This HEMOGLOBIN has two alpha and two gamma polypeptide subunits in comparison to normal adult hemoglobin, which has two alpha and two beta polypeptide subunits. Fetal hemoglobin concentrations can be elevated (usually above 0.5%) in children and adults affected by LEUKEMIA and several types of ANEMIA.
Compounds that inhibit cell production of DNA or RNA.
Ribonucleotide Reductases are enzymes that catalyze the conversion of ribonucleotides to deoxyribonucleotides, which is a crucial step in DNA synthesis and repair, utilizing a radical mechanism for this conversion.
The process by which a DNA molecule is duplicated.
A myeloproliferative disorder of unknown etiology, characterized by abnormal proliferation of all hematopoietic bone marrow elements and an absolute increase in red cell mass and total blood volume, associated frequently with splenomegaly, leukocytosis, and thrombocythemia. Hematopoiesis is also reactive in extramedullary sites (liver and spleen). In time myelofibrosis occurs.
An antineoplastic agent that acts by alkylation.
Phase of the CELL CYCLE following G1 and preceding G2 when the entire DNA content of the nucleus is replicated. It is achieved by bidirectional replication at multiple sites along each chromosome.
A cytostatic triazole derivative which is not to be confused with guanazolo, the generic name for 8-azaguanine.
A clinical syndrome characterized by repeated spontaneous hemorrhages and a remarkable increase in the number of circulating platelets.
An antiviral antibiotic produced by Cephalosporium aphidicola and other fungi. It inhibits the growth of eukaryotic cells and certain animal viruses by selectively inhibiting the cellular replication of DNA polymerase II or the viral-induced DNA polymerases. The drug may be useful for controlling excessive cell proliferation in patients with cancer, psoriasis or other dermatitis with little or no adverse effect upon non-multiplying cells.
Thymidine is a pyrimidine nucleoside, consisting of a thymine base linked to a deoxyribose sugar by a β-N1-glycosidic bond, which plays a crucial role in DNA replication and repair processes as one of the four nucleosides in DNA.
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
A purine or pyrimidine base bonded to a DEOXYRIBOSE containing a bond to a phosphate group.
An alkylating agent in cancer therapy that may also act as a mutagen by interfering with and causing damage to DNA.
An abnormal hemoglobin resulting from the substitution of valine for glutamic acid at position 6 of the beta chain of the globin moiety. The heterozygous state results in sickle cell trait, the homozygous in sickle cell anemia.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
Enzyme activated in response to DNA DAMAGE involved in cell cycle arrest. The gene is located on the long (q) arm of chromosome 22 at position 12.1. In humans it is encoded by the CHEK2 gene.
A genus of ascomycetous fungi of the family Schizosaccharomycetaceae, order Schizosaccharomycetales.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite.
A disorder characterized by reduced synthesis of the beta chains of hemoglobin. There is retardation of hemoglobin A synthesis in the heterozygous form (thalassemia minor), which is asymptomatic, while in the homozygous form (thalassemia major, Cooley's anemia, Mediterranean anemia, erythroblastic anemia), which can result in severe complications and even death, hemoglobin A synthesis is absent.

Caffeine can override the S-M checkpoint in fission yeast. (1/1655)

The replication checkpoint (or 'S-M checkpoint') control prevents progression into mitosis when DNA replication is incomplete. Caffeine has been known for some time to have the capacity to override the S-M checkpoint in animal cells. We show here that caffeine also disrupts the S-M checkpoint in the fission yeast Schizosaccharomyces pombe. By contrast, no comparable effects of caffeine on the S. pombe DNA damage checkpoint were seen. S. pombe cells arrested in early S phase and then exposed to caffeine lost viability rapidly as they attempted to enter mitosis, which was accompanied by tyrosine dephosphorylation of Cdc2. Despite this, the caffeine-induced loss of viability was not blocked in a temperature-sensitive cdc2 mutant incubated at the restrictive temperature, although catastrophic mitosis was prevented under these conditions. This suggests that, in addition to S-M checkpoint control, a caffeine-sensitive function may be important for maintenance of cell viability during S phase arrest. The lethality of a combination of caffeine with the DNA replication inhibitor hydroxyurea was suppressed by overexpression of Cds1 or Chk1, protein kinases previously implicated in S-M checkpoint control and recovery from S phase arrest. In addition, the same combination of drugs was specifically tolerated in cells overexpressing either of two novel S. pombe genes isolated in a cDNA library screen. These findings should allow further molecular investigation of the regulation of S phase arrest, and may provide a useful system with which to identify novel drugs that specifically abrogate the checkpoint control.  (+info)

Increased sensitivity of hydroxyurea-resistant leukemic cells to gemcitabine. (2/1655)

Tumor cell resistance to certain chemotherapeutic agents may result in cross-resistance to related antineoplastic agents. To study cross-resistance among inhibitors of ribonucleotide reductase, we developed hydroxyurea-resistant (HU-R) CCRF-CEM cells. These cells were 6-fold more resistant to hydroxyurea than the parent hydroxyurea-sensitive (HU-S) cell line and displayed an increase in the mRNA and protein of the R2 subunit of ribonucleotide reductase. We examined whether HU-R cells were cross-resistant to gemcitabine, a drug that blocks cell proliferation by inhibiting ribonucleotide reductase and incorporating itself into DNA. Contrary to our expectation, HU-R cells had an increased sensitivity to gemcitabine. The IC50 of gemcitabine was 0.061 +/- 0.03 microM for HU-R cells versus 0.16 +/- 0.02 microM for HU-S cells (P = 0.005). The cellular uptake of [3H]gemcitabine and its incorporation into DNA were increased in HU-R cells. Over an 18-h incubation with radiolabeled gemcitabine (0.25 microM), gemcitabine uptake was 286 +/- 37.3 fmol/10(6) cells for HU-R cells and 128 +/- 8.8 fmol/10(6) cells for HU-S cells (P = 0.03). The incorporation of gemcitabine into DNA was 75 +/- 6.7 fmol/10(6) cells for HU-R cells versus 22 +/- 0.6 fmol/10(6) cells for HU-S cells (P < 0.02). Our studies suggest that the increased sensitivity of HU-R cells to gemcitabine results from increased drug uptake by these cells. This, in turn, favors the incorporation of gemcitabine into DNA, resulting in enhanced cytotoxicity. The increased sensitivity of malignant cells to gemcitabine after the development of hydroxyurea resistance may be relevant to the design of chemotherapeutic trials with these drugs.  (+info)

RAD53 regulates DBF4 independently of checkpoint function in Saccharomyces cerevisiae. (3/1655)

The Cdc7p and Dbf4p proteins form an active kinase complex in Saccharomyces cerevisiae that is essential for the initiation of DNA replication. A genetic screen for mutations that are lethal in combination with cdc7-1 led to the isolation of seven lsd (lethal with seven defect) complementation groups. The lsd7 complementation group contained two temperature-sensitive dbf4 alleles. The lsd1 complementation group contained a new allele of RAD53, which was designated rad53-31. RAD53 encodes an essential protein kinase that is required for the activation of DNA damage and DNA replication checkpoint pathways, and that is implicated as a positive regulator of S phase. Unlike other RAD53 alleles, we demonstrate that the rad53-31 allele retains an intact checkpoint function. Thus, the checkpoint function and the DNA replication function of RAD53 can be functionally separated. The activation of DNA replication through RAD53 most likely occurs through DBF4. Two-hybrid analysis indicates that the Rad53p protein binds to Dbf4p. Furthermore, the steady-state level of DBF4 message and Dbf4p protein is reduced in several rad53 mutant strains, indicating that RAD53 positively regulates DBF4. These results suggest that two different functions of the cell cycle, initiation of DNA replication and the checkpoint function, can be coordinately regulated through the common intermediate RAD53.  (+info)

Sustained induction of fetal hemoglobin by pulse butyrate therapy in sickle cell disease. (4/1655)

High levels of fetal hemoglobin (Hb F) protect from many of the complications of sickle cell disease and lead to improved survival. Butyrate and other short chain fatty acids were previously shown to increase Hb F production in erythroid cells in vitro and in animal models in vivo. However, butyrates are also known to inhibit the proliferation of many cell types, including erythroid cells. Experience with the use of butyrate in animal models and in early clinical trials demonstrated that the Hb F response may be lost after prolonged administration of high doses of butyrate. We hypothesized that this loss of response may be a result of the antiproliferative effects of butyrate. We designed a regimen consisting of intermittent or pulse therapy in which butyrate was administered for 4 days followed by 10 to 24 days with no drug exposure. This pulse regimen induced fetal globin gene expression in 9 of 11 patients. The mean Hb F in this group increased from 7.2% to 21.0% (P <.002) after intermittent butyrate therapy for a mean duration of 29.9 weeks. This was associated with a parallel increase in the number of F cells and F reticulocytes. The total hemoglobin levels also increased from a mean of 7.8 g/dL to a mean of 8.8 g/dL (P <.006). The increased levels of Hb F were sustained in all responders, including 1 patient who has been on pulse butyrate therapy for more than 28 months. This regimen, which resulted in a marked and sustained increase in Hb F levels in more than two thirds of the adult sickle cell patients enrolled in this study, was well tolerated without adverse side effects. These encouraging results require confirmation along with an appropriate evaluation of clinical outcomes in a larger number of patients with sickle cell disease.  (+info)

Radiation therapy with concomitant hydroxyurea and fluorouracil in stage II and III head and neck cancer. (5/1655)

PURPOSE: In 1986, a multi-institutional phase II trial was begun to study the use of chemotherapy with concomitant radiation in patients with stage II and III head and neck cancer. End points were overall survival, progression-free survival, local/regional control, and toxicity in the setting of organ preservation with concomitant treatment. METHODS: Eligible patients with stage II or III disease received chemotherapy and radiation on a 2-week cycle. Chemotherapy consisted of continuous infusion fluorouracil (5-FU) at 800 mg/m2/d for 5 consecutive days (days 1 to 5) and hydroxyurea (HU) at 1 g orally every 12 hours for 13 doses starting the evening before the start of irradiation. Radiation therapy was given as single 1.8- to 2.0-Gy fractions for 5 consecutive days (days 1 to 5) with chemotherapy. Each 5 days of treatment was followed by a 9-day break (days 6 to 14), during which no additional treatment was given. Treatment cycles were repeated until the completion of the planned radiation dose (six to eight cycles). RESULTS: Between 1989 and 1996, 60 patients were enrolled. All patients were eligible for analysis, with a median follow-up of 52 months for surviving patients and 42 months for all patients. Grade 3 to 4 mucositis occurred in 57% of patients. The 5 year-actuarial overall survival, progression-free survival, and local/regional control were 65%, 82%, and 86%, respectively. Eight patients developed local and/or regional recurrence after treatment. Surgical salvage was possible in three of these patients. Thus, the ultimate 5-year local/ regional control was 91%. CONCLUSION: Concomitant radiation and chemotherapy with 5-FU and HU is an effective regimen in patients with stage II and III head and neck cancer. Progression-free survival and local/regional control appear to be superior to expected rates in patients treated with surgery and radiation. Further testing of this regimen in a phase III setting is indicated.  (+info)

Cell cycle-dependent sequencing of cell fate decisions in Caenorhabditis elegans vulva precursor cells. (6/1655)

In Caenorhabditis elegans, the fates of the six multipotent vulva precursor cells (VPCs) are specified by extracellular signals. One VPC expresses the primary (1 degrees ) fate in response to a Ras-mediated inductive signal from the gonad. The two VPCs flanking the 1 degrees cell each express secondary (2 degrees ) fates in response to lin-12-mediated lateral signaling. The remaining three VPCs each adopt the non-vulval tertiary (3 degrees ) fate. Here I describe experiments examining how the selection of these vulval fates is affected by cell cycle arrest and cell cycle-restricted lin-12 activity. The results suggest that lin-12 participates in two developmental decisions separable by cell cycle phase: lin-12 must act prior to the end of VPC S phase to influence a 1 degrees versus 2 degrees cell fate choice, but must act after VPC S phase to influence a 3 degrees versus 2 degrees cell fate choice. Coupling developmental decisions to cell cycle transitions may provide a mechanism for prioritizing or ordering choices of cell fates for multipotential cells.  (+info)

Randomized trial of zileuton in patients with moderate asthma: effect of reduced dosing frequency and amounts on pulmonary function and asthma symptoms. Zileuton Study Group. (7/1655)

This 6-month, randomized, multicenter study was designed to determine whether patients who had been treated with the leukotriene pathway inhibitor zileuton 600 mg four times daily (QID) for 2 months could be maintained at the same level of pulmonary function, symptom control, and beta-agonist use with less frequent dosing--first 600 or 800 mg three times daily (TID) and then twice daily (BID). A total of 278 patients with chronic asthma, ages 16 to 70, participated at 25 US centers. All had a 1-second forced expiratory volume (FEV1) of 35%-75%, reversible airway disease, and a nonsmoking history of 1 year. An 8-week open-label period (zileuton 600 mg QID) was followed by a 16-week double-blind period, in which patients who responded to the QID treatment were randomized to receive zileuton 600 or 800 mg TID for 8 weeks and then rerandomized to receive zileuton 600 or 800 mg BID for another 8 weeks. Primary outcomes were FEV1 and asthma symptom scores; secondary outcomes were peak expiratory flow rate, beta-agonist use, and asthma exacerbations requiring steroid rescue. Patients who showed improvements in lung function when treated with zileuton 600 mg QID demonstrated minimal decreases in FEV1 and comparable peak expiratory flow rates, symptom control, beta-agonist use, and systemic corticosteroid rescue when being treated with lower doses and/or less frequent doses of zileuton. Patients who demonstrate improved asthma control with zileuton 600 mg QID may be able to reduce their daily dosage and/or frequency while still maintaining the same level of symptom control.  (+info)

Safety and clinical efficacy of zileuton in patients with chronic asthma. (8/1655)

Zileuton, a leukotriene pathway inhibitor used to treat asthma, improves lung function, relieves symptoms, and is well tolerated. The purpose of this 12-month, parallel-group, open-label study was to assess the efficacy of zileuton and evaluate liver function in patients treated with this drug (approximately 2% of patients treated with zileuton in controlled trials had reversible liver enzyme elevations). A total of 2,947 patients at 233 centers in the United States were randomly assigned in a 5:1 ratio to treatment with zileuton plus usual asthma care or usual asthma care alone. Efficacy variables included asthma exacerbations; need for alternative treatment, steroid rescue, emergency care, and hospitalizations; forced expiratory volume in 1 second (FEV1); and asthma symptom scores. The safety evaluation included measurement of alanine aminotransferase levels. Patients treated with zileuton had significantly fewer corticosteroid rescues (P < 0.001), required less emergency care (P < 0.05), had fewer hospitalizations, and had greater increases in FEV1 (P = 0.048). They also had significantly greater improvements in asthma symptoms. Increases in alanine aminotransferase levels to three times or more the upper limit of normal occurred in 4.6% of patients treated with zileuton and 1.1% of those receiving usual care (P < 0.001); most increases occurred during the first 2 to 3 months. Alanine aminotransferase levels decreased to less than two times the upper limit of normal or to baseline levels during zileuton treatment or after drug cessation. Jaundice or chronic liver disease did not develop in any patient. Adding zileuton to the therapeutic regimens of patients with asthma is likely to improve asthma control and lower utilization of healthcare resources.  (+info)

Hydroxyurea is an antimetabolite drug that is primarily used in the treatment of myeloproliferative disorders such as chronic myelogenous leukemia (CML), essential thrombocythemia, and polycythemia vera. It works by interfering with the synthesis of DNA, which inhibits the growth of cancer cells.

In addition to its use in cancer therapy, hydroxyurea is also used off-label for the management of sickle cell disease. In this context, it helps to reduce the frequency and severity of painful vaso-occlusive crises by increasing the production of fetal hemoglobin (HbF), which decreases the formation of sickled red blood cells.

The medical definition of hydroxyurea is:

A hydantoin derivative and antimetabolite that inhibits ribonucleoside diphosphate reductase, thereby interfering with DNA synthesis. It has been used as an antineoplastic agent, particularly in the treatment of myeloproliferative disorders, and more recently for the management of sickle cell disease to reduce the frequency and severity of painful vaso-occlusive crises by increasing fetal hemoglobin production.

Antisickling agents are medications or substances that help prevent or reduce the sickling of red blood cells in individuals with sickle cell disease. Sickling is a pathological process where the normally disc-shaped red blood cells become crescent-shaped due to abnormal hemoglobin (HbS). This change in shape can lead to blockages in small blood vessels, causing tissue damage and various complications such as pain crises, acute chest syndrome, and stroke.

Antisickling agents work by either inhibiting the polymerization of HbS or improving the oxygen-carrying capacity of red blood cells. The most commonly used antisickling agent is hydroxyurea, which increases the production of fetal hemoglobin (HbF) in red blood cells. HbF has a higher affinity for oxygen than HbS and can prevent the polymerization of HbS, thereby reducing sickling. Other antisickling agents include:

1. L-glutamine: An amino acid that helps maintain the structural integrity of red blood cells and reduces oxidative stress.
2. Arginate: A salt of arginine, an amino acid that helps improve nitric oxide production and vasodilation, reducing sickling.
3. Senicapoc: A drug that inhibits the formation of HbS polymers by blocking the interaction between HbS molecules.
4. Voxelotor (Oxbryta): A medication that binds to HbS and stabilizes it in its oxygenated state, reducing sickling.

These antisickling agents can help alleviate symptoms, decrease the frequency of pain crises, and improve the quality of life for individuals with sickle cell disease. However, they should be used under the supervision of a healthcare professional, as each has its benefits, risks, and potential side effects.

Sickle cell anemia is a genetic disorder that affects the hemoglobin in red blood cells. Hemoglobin is responsible for carrying oxygen throughout the body. In sickle cell anemia, the hemoglobin is abnormal and causes the red blood cells to take on a sickle shape, rather than the normal disc shape. These sickled cells are stiff and sticky, and they can block blood vessels, causing tissue damage and pain. They also die more quickly than normal red blood cells, leading to anemia.

People with sickle cell anemia often experience fatigue, chronic pain, and jaundice. They may also have a higher risk of infections and complications such as stroke, acute chest syndrome, and priapism. The disease is inherited from both parents, who must both be carriers of the sickle cell gene. It primarily affects people of African descent, but it can also affect people from other ethnic backgrounds.

There is no cure for sickle cell anemia, but treatments such as blood transfusions, medications to manage pain and prevent complications, and bone marrow transplantation can help improve quality of life for affected individuals. Regular medical care and monitoring are essential for managing the disease effectively.

Fetal hemoglobin (HbF) is a type of hemoglobin that is produced in the fetus and newborn babies. It is composed of two alpha-like globin chains and two gamma-globin chains, designated as α2γ2. HbF is the primary form of hemoglobin during fetal development, replacing the embryonic hemoglobin (HbG) around the eighth week of gestation.

The unique property of HbF is its higher affinity for oxygen compared to adult hemoglobin (HbA), which helps ensure adequate oxygen supply from the mother to the developing fetus. After birth, as the newborn starts breathing on its own and begins to receive oxygen directly, the production of HbF gradually decreases and is usually replaced by HbA within the first year of life.

In some genetic disorders like sickle cell disease and beta-thalassemia, persistence of HbF into adulthood can be beneficial as it reduces the severity of symptoms due to its higher oxygen-carrying capacity and less polymerization tendency compared to HbS (in sickle cell disease) or unpaired alpha chains (in beta-thalassemia). Treatments like hydroxyurea are used to induce HbF production in these patients as a therapeutic approach.

Nucleic acid synthesis inhibitors are a class of antimicrobial, antiviral, or antitumor agents that block the synthesis of nucleic acids (DNA or RNA) by interfering with enzymes involved in their replication. These drugs can target various stages of nucleic acid synthesis, including DNA transcription, replication, and repair, as well as RNA transcription and processing.

Examples of nucleic acid synthesis inhibitors include:

1. Antibiotics like quinolones (e.g., ciprofloxacin), rifamycins (e.g., rifampin), and trimethoprim, which target bacterial DNA gyrase, RNA polymerase, or dihydrofolate reductase, respectively.
2. Antiviral drugs like reverse transcriptase inhibitors (e.g., zidovudine, lamivudine) and integrase strand transfer inhibitors (e.g., raltegravir), which target HIV replication by interfering with viral enzymes required for DNA synthesis.
3. Antitumor drugs like antimetabolites (e.g., methotrexate, 5-fluorouracil) and topoisomerase inhibitors (e.g., etoposide, doxorubicin), which interfere with DNA replication and repair in cancer cells.

These drugs have been widely used for treating various bacterial and viral infections, as well as cancers, due to their ability to selectively inhibit the growth of target cells without affecting normal cellular functions significantly. However, they may also cause side effects related to their mechanism of action or off-target effects on non-target cells.

Ribonucleotide Reductases (RNRs) are enzymes that play a crucial role in DNA synthesis and repair. They catalyze the conversion of ribonucleotides to deoxyribonucleotides, which are the building blocks of DNA. This process involves the reduction of the 2'-hydroxyl group of the ribose sugar to a hydrogen, resulting in the formation of deoxyribose.

RNRs are highly regulated and exist in various forms across different species. They are divided into three classes (I, II, and III) based on their structure, mechanism, and cofactor requirements. Class I RNRs are further divided into two subclasses (Ia and Ib), which differ in their active site architecture and regulation.

Class Ia RNRs, found in eukaryotes and some bacteria, contain a stable tyrosyl radical that acts as the catalytic center for hydrogen abstraction. Class Ib RNRs, found in many bacteria, use a pair of iron centers to perform the same function. Class II RNRs are present in some bacteria and archaea and utilize adenosine triphosphate (ATP) as a cofactor for reduction. Class III RNRs, found in anaerobic bacteria and archaea, use a unique mechanism involving a radical S-adenosylmethionine (SAM) cofactor to facilitate the reduction reaction.

RNRs are essential for DNA replication and repair, and their dysregulation has been linked to various diseases, including cancer and neurodegenerative disorders. Therefore, understanding the structure, function, and regulation of RNRs is of great interest in biochemistry, molecular biology, and medicine.

DNA replication is the biological process by which DNA makes an identical copy of itself during cell division. It is a fundamental mechanism that allows genetic information to be passed down from one generation of cells to the next. During DNA replication, each strand of the double helix serves as a template for the synthesis of a new complementary strand. This results in the creation of two identical DNA molecules. The enzymes responsible for DNA replication include helicase, which unwinds the double helix, and polymerase, which adds nucleotides to the growing strands.

Polycythemia Vera is a type of myeloproliferative neoplasm, a group of rare blood cancers. In Polycythemia Vera, the body produces too many red blood cells, leading to an increased risk of blood clots and thickening of the blood, which can cause various symptoms such as fatigue, headache, dizziness, and itching. It can also lead to enlargement of the spleen. The exact cause of Polycythemia Vera is not known, but it is associated with genetic mutations in the JAK2 gene in most cases. It is a progressive disease that can lead to complications such as bleeding, thrombosis, and transformation into acute leukemia if left untreated.

Pipobroman is an antineoplastic agent, which means it is used to treat cancer. It's a type of alkylating agent, specifically a nitrogen mustard. Alkylating agents work by disrupting the DNA of cancer cells, which can prevent them from dividing and growing. Pipobroman has been used in the treatment of chronic myelogenous leukemia (CML), although it's not widely used today due to the availability of more effective treatments.

Please note that medical definitions can vary based on the source, and this definition is intended to be a general overview. Always refer to the most current prescribing information for any medication.

In the context of cell biology, "S phase" refers to the part of the cell cycle during which DNA replication occurs. The "S" stands for synthesis, reflecting the active DNA synthesis that takes place during this phase. It is preceded by G1 phase (gap 1) and followed by G2 phase (gap 2), with mitosis (M phase) being the final stage of the cell cycle.

During S phase, the cell's DNA content effectively doubles as each chromosome is replicated to ensure that the two resulting daughter cells will have the same genetic material as the parent cell. This process is carefully regulated and coordinated with other events in the cell cycle to maintain genomic stability.

I'm sorry for any confusion, but "Guanazole" does not have a widely recognized medical definition or use. It is possible that you may be referring to "Guanzone," which is an obsolete term for a class of medications known as guanidines. These were once used in the treatment of heart conditions, but their use has been largely discontinued due to safer and more effective alternatives.

If you meant something else or if this doesn't answer your question, please provide more context or clarify your request.

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

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

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

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

Aphidicolin is an antimicrotubule agent that is specifically a inhibitor of DNA polymerase alpha. It is an antibiotic that is produced by the fungus Cephalosporium aphidicola and is used in research to study the cell cycle and DNA replication. In clinical medicine, it has been explored as a potential anticancer agent, although its use is not currently approved for this indication.

Thymidine is a pyrimidine nucleoside that consists of a thymine base linked to a deoxyribose sugar by a β-N1-glycosidic bond. It plays a crucial role in DNA replication and repair processes as one of the four nucleosides in DNA, along with adenosine, guanosine, and cytidine. Thymidine is also used in research and clinical settings for various purposes, such as studying DNA synthesis or as a component of antiviral and anticancer therapies.

Cytarabine is a chemotherapeutic agent used in the treatment of various types of cancer, including leukemias and lymphomas. Its chemical name is cytosine arabinoside, and it works by interfering with the DNA synthesis of cancer cells, which ultimately leads to their death.

Cytarabine is often used in combination with other chemotherapy drugs and may be administered through various routes, such as intravenous (IV) or subcutaneous injection, or orally. The specific dosage and duration of treatment will depend on the type and stage of cancer being treated, as well as the patient's overall health status.

Like all chemotherapy drugs, cytarabine can cause a range of side effects, including nausea, vomiting, diarrhea, hair loss, and an increased risk of infection. It may also cause more serious side effects, such as damage to the liver, kidneys, or nervous system, and it is important for patients to be closely monitored during treatment to minimize these risks.

It's important to note that medical treatments should only be administered under the supervision of a qualified healthcare professional, and this information should not be used as a substitute for medical advice.

DNA damage refers to any alteration in the structure or composition of deoxyribonucleic acid (DNA), which is the genetic material present in cells. DNA damage can result from various internal and external factors, including environmental exposures such as ultraviolet radiation, tobacco smoke, and certain chemicals, as well as normal cellular processes such as replication and oxidative metabolism.

Examples of DNA damage include base modifications, base deletions or insertions, single-strand breaks, double-strand breaks, and crosslinks between the two strands of the DNA helix. These types of damage can lead to mutations, genomic instability, and chromosomal aberrations, which can contribute to the development of diseases such as cancer, neurodegenerative disorders, and aging-related conditions.

The body has several mechanisms for repairing DNA damage, including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. However, if the damage is too extensive or the repair mechanisms are impaired, the cell may undergo apoptosis (programmed cell death) to prevent the propagation of potentially harmful mutations.

The cell cycle is a series of events that take place in a cell leading to its division and duplication. It consists of four main phases: G1 phase, S phase, G2 phase, and M phase.

During the G1 phase, the cell grows in size and synthesizes mRNA and proteins in preparation for DNA replication. In the S phase, the cell's DNA is copied, resulting in two complete sets of chromosomes. During the G2 phase, the cell continues to grow and produces more proteins and organelles necessary for cell division.

The M phase is the final stage of the cell cycle and consists of mitosis (nuclear division) and cytokinesis (cytoplasmic division). Mitosis results in two genetically identical daughter nuclei, while cytokinesis divides the cytoplasm and creates two separate daughter cells.

The cell cycle is regulated by various checkpoints that ensure the proper completion of each phase before progressing to the next. These checkpoints help prevent errors in DNA replication and division, which can lead to mutations and cancer.

Deoxyribonucleotides are the building blocks of DNA (deoxyribonucleic acid). They consist of a deoxyribose sugar, a phosphate group, and one of four nitrogenous bases: adenine (A), guanine (G), cytosine (C), or thymine (T). A deoxyribonucleotide is formed when a nucleotide loses a hydroxyl group from its sugar molecule. In DNA, deoxyribonucleotides link together to form a long, double-helix structure through phosphodiester bonds between the sugar of one deoxyribonucleotide and the phosphate group of another. The sequence of these nucleotides carries genetic information that is essential for the development and function of all known living organisms and many viruses.

Methyl methanesulfonate (MMS) is not a medication, but rather a chemical compound with the formula CH3SO3CH3. It's an alkylating agent that is used in laboratory settings for various research purposes, including as a methylating agent in biochemical and genetic studies.

MMS works by transferring its methyl group (CH3) to other molecules, which can result in the modification of DNA and other biological macromolecules. This property makes it useful in laboratory research, but it also means that MMS is highly reactive and toxic. Therefore, it must be handled with care and appropriate safety precautions.

It's important to note that MMS is not used as a therapeutic agent in medicine due to its high toxicity and potential to cause serious harm if mishandled or misused.

Hemoglobin S (HbS) is a genetic variant of hemoglobin, which is the oxygen-carrying protein in red blood cells. This abnormal form of hemogllobin results from a mutation in the beta-globin gene, leading to the substitution of valine for glutamic acid at position six of the beta-globin chain.

In individuals with sickle cell disease (a group of inherited red blood cell disorders), both copies of their beta-globin genes carry this mutation, causing the majority of their hemoglobin to be HbS. When deoxygenated, HbS molecules have a tendency to polymerize and form long, rigid rods within the red blood cells, distorting their shape into a characteristic sickle or crescent form.

These sickled red blood cells are less flexible and more prone to rupture (hemolysis), leading to chronic anemia, vaso-occlusive crises, and other disease complications. Sickle cell disease primarily affects people of African, Mediterranean, Middle Eastern, and Indian ancestry, but it can also be found in other populations worldwide.

Cell cycle proteins are a group of regulatory proteins that control the progression of the cell cycle, which is the series of events that take place in a eukaryotic cell leading to its division and duplication. These proteins can be classified into several categories based on their functions during different stages of the cell cycle.

The major groups of cell cycle proteins include:

1. Cyclin-dependent kinases (CDKs): CDKs are serine/threonine protein kinases that regulate key transitions in the cell cycle. They require binding to a regulatory subunit called cyclin to become active. Different CDK-cyclin complexes are activated at different stages of the cell cycle.
2. Cyclins: Cyclins are a family of regulatory proteins that bind and activate CDKs. Their levels fluctuate throughout the cell cycle, with specific cyclins expressed during particular phases. For example, cyclin D is important for the G1 to S phase transition, while cyclin B is required for the G2 to M phase transition.
3. CDK inhibitors (CKIs): CKIs are regulatory proteins that bind to and inhibit CDKs, thereby preventing their activation. CKIs can be divided into two main families: the INK4 family and the Cip/Kip family. INK4 family members specifically inhibit CDK4 and CDK6, while Cip/Kip family members inhibit a broader range of CDKs.
4. Anaphase-promoting complex/cyclosome (APC/C): APC/C is an E3 ubiquitin ligase that targets specific proteins for degradation by the 26S proteasome. During the cell cycle, APC/C regulates the metaphase to anaphase transition and the exit from mitosis by targeting securin and cyclin B for degradation.
5. Other regulatory proteins: Several other proteins play crucial roles in regulating the cell cycle, such as p53, a transcription factor that responds to DNA damage and arrests the cell cycle, and the polo-like kinases (PLKs), which are involved in various aspects of mitosis.

Overall, cell cycle proteins work together to ensure the proper progression of the cell cycle, maintain genomic stability, and prevent uncontrolled cell growth, which can lead to cancer.

Checkpoint Kinase 2 (Chk2) is a serine/threonine protein kinase that plays a crucial role in the DNA damage response and the regulation of the cell cycle. It is activated by various types of DNA damage, including double-strand breaks, and phosphorylates several downstream targets involved in cell cycle arrest, DNA repair, and apoptosis. Chk2 is a key player in the G2/M checkpoint, which prevents cells with damaged DNA from entering mitosis and dividing. Mutations in the Chk2 gene have been associated with increased risk of cancer.

I apologize for any confusion, but "Schizosaccharomyces" is not a medical term. It is a genus name in the field of microbiology and genetics, referring to a group of budding, tear-shaped yeasts that are widely used as model organisms in scientific research. The most well-known species within this genus is Schizosaccharomyces pombe, which has been extensively studied for its cell cycle regulation, DNA repair mechanisms, and other fundamental biological processes.

If you have any questions related to medical terminology or health-related topics, I would be happy to help.

Deoxyribonucleic acid (DNA) is the genetic material present in the cells of organisms where it is responsible for the storage and transmission of hereditary information. DNA is a long molecule that consists of two strands coiled together to form a double helix. Each strand is made up of a series of four nucleotide bases - adenine (A), guanine (G), cytosine (C), and thymine (T) - that are linked together by phosphate and sugar groups. The sequence of these bases along the length of the molecule encodes genetic information, with A always pairing with T and C always pairing with G. This base-pairing allows for the replication and transcription of DNA, which are essential processes in the functioning and reproduction of all living organisms.

Didanosine is a medication used to treat HIV (human immunodeficiency virus) infection. It is an antiretroviral drug, specifically a nucleoside reverse transcriptase inhibitor (NRTI), that works by interfering with the replication of the virus in the body. Didanosine is often used in combination with other antiretroviral drugs as part of highly active antiretroviral therapy (HAART) to help control HIV infection and reduce the risk of HIV-related illnesses.

The medical definition of 'Didanosine' is:

A synthetic nucleoside analogue that inhibits the reverse transcriptase activity of the human immunodeficiency virus (HIV). It is converted in vivo to the active metabolite dideoxyadenosine triphosphate, which competitively inhibits HIV DNA polymerase and has antiviral properties. The drug is used in the treatment of HIV infection and AIDS.

Beta-thalassemia is a genetic blood disorder that affects the production of hemoglobin, a protein in red blood cells that carries oxygen throughout the body. Specifically, beta-thalassemia is caused by mutations in the beta-globin gene, which leads to reduced or absent production of the beta-globin component of hemoglobin.

There are two main types of beta-thalassemia:

1. Beta-thalassemia major (also known as Cooley's anemia): This is a severe form of the disorder that typically becomes apparent in early childhood. It is characterized by a significant reduction or absence of beta-globin production, leading to anemia, enlarged spleen and liver, jaundice, and growth retardation.
2. Beta-thalassemia intermedia: This is a milder form of the disorder that may not become apparent until later in childhood or even adulthood. It is characterized by a variable reduction in beta-globin production, leading to mild to moderate anemia and other symptoms that can range from nonexistent to severe.

Treatment for beta-thalassemia depends on the severity of the disorder and may include blood transfusions, iron chelation therapy, and/or bone marrow transplantation. In some cases, genetic counseling and prenatal diagnosis may also be recommended for families with a history of the disorder.

... is caused by chronic use of hydroxyurea for chronic myelogenous leukemia, thrombocytosis, or psoriasis, ...
This method of hydroxyurea synthesis was patented by Hussain et al. (2015). Hydroxyurea is a monohydroxyl-substituted urea ( ... offering potential synergy between hydroxyurea and radiation or alkylating agents. Hydroxyurea has many pharmacological ... Hydroxyurea lay dormant for more than fifty years until it was studied as part of an investigation into the toxicity of protein ... "Hydroxyurea". PubChem. U.S. National Library of Medicine. Archived from the original on 2017-05-18. Koç A, Wheeler LJ, Mathews ...
Hydroxyurea (HU) is a small molecule drug that inhibits the enzyme ribonucleotide reductase (RNR), preventing the catalysis of ... Koç A, Wheeler LJ, Mathews CK, Merrill GF (January 2004). "Hydroxyurea arrests DNA replication by a mechanism that preserves ... Xu YJ, Singh A, Alter GM (November 2016). "Hydroxyurea Induces Cytokinesis Arrest in Cells Expressing a Mutated Sterol-14α- ... Platt OS (March 2008). "Hydroxyurea for the treatment of sickle cell anemia". The New England Journal of Medicine. 358 (13): ...
He was prescribed an unusual combination therapy: didanosine, indinavir and hydroxyurea. Hydroxyurea was the most unusual of ... Gibbs MA, Sorensen SJ (January 2000). "Hydroxyurea in the treatment of HIV-1". The Annals of Pharmacotherapy. 34 (1): 89-93. ...
Newton HB (2007). "Hydroxyurea chemotherapy in the treatment of meningiomas". Neurosurgical Focus. 23 (4): E11. doi:10.3171/foc ... A 2007 study of whether hydroxyurea has the capacity to shrink unresectable or recurrent meningiomata is being further ...
Hydroxyurea is the only FDA approved drug for thalassemia. Patients who took 10 mg/kg of hydroxyurea every day for a year had ... Thalassemia patients who do not respond well to blood transfusions can take hydroxyurea or thalidomide, and sometimes a ... Keikhaei, Bijan (2015). "Clinical and Haematological Effects of Hydroxyurea in β -Thalassemia Intermedia Patients". Journal of ... The combination of thalidomide and hydroxyurea resulted in hemoglobin levels increasing significantly in transfusion-dependent ...
In the early 1980s a team led by Charache began testing a few patients at Hopkins to see if hydroxyurea, a cancer drug, would ... They found that hydroxyurea treatment could increase recipients' blood levels of hemoglobin F, a form of hemoglobin primarily ... Subsequent investigation of the beneficial effects hydroxyurea in people with sickle cell disease has revealed multiple ... Agrawal, Rohit Kumar; Patel, Rakesh Kantilal; Shah, Varsha; Nainiwal, Lalit; Trivedi, Bhadra (June 2014). "Hydroxyurea in ...
These include hydroxyurea and interferon therapy, among others. The tendency of some practitioners to avoid chemotherapy if ... While hydroxyurea is considered a safer chemotherapy in this aspect, there is still some debate about its long-term safety. ...
Hydroxyurea administration - Hydroxyurea is a drug that can be used as an alternative method of increasing fetal haemoglobin ... Hydroxyurea also provides the benefit of reducing inflammation. Haematopoetic stem cell transplantation - This process is more ...
Tripathi, K; Mor, V; Bairwa, NK; Del Poeta, M; Mohanty, BK (2012). "Hydroxyurea treatment inhibits proliferation of ...
The hydroxyurea arm had a lower likelihood of myelofibrosis, arterial thrombosis, and bleeding, but it had a slightly higher ... July 2005). "Hydroxyurea compared with anagrelide in high-risk essential thrombocythemia". The New England Journal of Medicine ... Anagrelide can be useful in times when hydroxyurea proves ineffective. Common side effects are headache, diarrhea, unusual ... Stopping anagrelide (and switching patients to hydroxyurea) appeared to reverse the degree of marrow fibrosis. Thus, patients ...
July 2005). "Hydroxyurea compared with anagrelide in high-risk essential thrombocythemia". The New England Journal of Medicine ... Extremely high platelet counts can be treated with hydroxyurea (a cytoreducing agent) or anagrelide (Agrylin). In Janus kinase ...
Inhibition of the enzyme by hydroxyurea, hydroxylamine, and acetohydroxamic acid". J Biol Chem. 240: 2407-2414. doi:10.1016/ ...
Inhibition of the Enzyme by Hydroxyurea, Hydroxylamine, and Acetohydroxamic Acid". The Journal of Biological Chemistry. 240: ...
Hydroxycarbamide (hydroxyurea) was shown effective in mouse models and subsequently commercially researched by Novo Nordisk, ... Grzeschik SM, Ganta M, Prior TW, Heavlin WD, Wang CH (August 2005). "Hydroxyurea enhances SMN2 gene expression in spinal ... placebo-controlled trial of hydroxyurea in spinal muscular atrophy". Neurology. 75 (24): 2190-7. doi:10.1212/WNL. ...
For example, it is used to prepare the drug hydroxyurea. It is also used for the heat treatment of metals (e.g., Ferritic ...
Brawley, Otis W. (2008-06-17). "National Institutes of Health Consensus Development Conference Statement: Hydroxyurea Treatment ... hydroxyurea treatment for sickle cell disease." "Introduction to special issue: advancing the ethics of community-based ... "NIH consensus development statement on hydroxyurea treatment for sickle cell disease". NIH Consensus and State-of-the-science ... "NIH consensus development statement on hydroxyurea treatment for sickle cell disease." "National Institutes of Health Consensus ...
Examples of substances under this schedule: Testolactone, Hydroxyurea, Carbutamide, Primidone etc. Schedule H: The drug label ...
Hydroxyurea had previously been used as a chemotherapy agent, and some concern exists that long-term use may be harmful, but ... Hydroxyurea and phlebotomy combined may be more effective than transfusion and chelation combined in terms of pain, life- ... Hydroxyurea, also known as hydroxycarbamide, probably reduces the frequency of painful episodes and the risk of life- ... Guidelines from NIH published in 2014 state that all children and adolescents should take hydroxyurea, as should adults with ...
The primary treatment consists of anagrelide or hydroxyurea to lower platelet levels. Congenital amegakaryocytic ...
The starting dose was lower for participants who were transitioning from hydroxyurea. The trial was conducted at six sites ...
Rodgers G. "Hydroxyurea and other disease-modifying therapies in sickle cell disease". UpToDate. Archived from the original on ...
"1-{4-[3-(4-Fluorophenoxy)phenyl]-3-butyn-2-yl}-1-hydroxyurea". Retrieved 24 December 2015. Marr KA, Lees P, ...
Cytokinetic analysis of L1210 leukemia after continuous infusion of hydroxyurea in vivo Straus, Marc J., Vivian Sege, and Sung ... "Synchronization of L1210 leukemia with hydroxyurea infusion and the effect of subsequent pulse dose chemotherapy." Cancer Treat ... "Cytokinetic analysis of L1210 leukemia after continuous infusion of hydroxyurea in vivo." Cancer research 39.5 (1979): 1616- ...
Hydroxyurea is also used to treat certain types of cancer and blood disorders. Aphidocolin is a fungus-derived tetracyclic ... Hydroxyurea decreases the production of dNTPs by inhibiting the enzyme ribonucleotide reductase. This serves to halt DNA ... "Hydroxyurea Arrests DNA Replication by a Mechanism That Preserves Basal dNTP Pools". Journal of Biological Chemistry. 279 (1): ...
Hydroxyurea is used to increase the amount of fetal hemoglobin in an adult. The fetal hemoglobin levels drop within 6 months of ...
Najean Y, Rain JD (November 1997). "Treatment of polycythemia vera: the use of hydroxyurea and pipobroman in 292 patients under ... Dexamethasone, alpha-interferon and hydroxyurea (also known as hydroxycarbamide) may play a role. Lenalidomide and thalidomide ... the development of myelofibrosis following these disorders may be accelerated by the oral chemotherapy drug hydroxyurea. The ...
The drugs hydroxyurea and Motexafin gadolinium interfere with the action of this enzyme. Elledge SJ, Zhou Z, Allen JB (March ... "Mutations in the R2 subunit of ribonucleotide reductase that confer resistance to hydroxyurea". The Journal of Biological ...
Patients may receive hydroxyurea to induce the protective effects of increased fetal hemoglobin production. They may also ...
Noguchi has studied hydroxyurea and hemoglobin, showing that hydroxyurea can increase a form of fetal hemoglobin in sickle cell ... "Hydroxyurea induces fetal hemoglobin by the nitric oxide-dependent activation of soluble guanylyl cyclase". Journal of Clinical ...
Hydroxyurea dermopathy is caused by chronic use of hydroxyurea for chronic myelogenous leukemia, thrombocytosis, or psoriasis, ...
Hydroxyurea: learn about side effects, dosage, special precautions, and more on MedlinePlus ... When hydroxyurea is used to treat certain types of cancer, it may be taken once every third day. Take hydroxyurea at around the ... Before taking hydroxyurea,. *tell your doctor and pharmacist if you are allergic to hydroxyurea, any other medications, or any ... Hydroxyurea treats cancer by slowing or stopping the growth of cancer cells in your body. Hydroxyurea treats sickle cell anemia ...
Hydroxyurea is mutagenic in vitro to bacteria, fungi, protozoa, and mammalian cells. Hydroxyurea is clastogenic in vitro ( ... Hydroxyurea Capsules USP is an antimetabolite available for oral use as capsules containing 500 mg hydroxyurea, USP. Inactive ... Swallow hydroxyurea capsule whole. Do NOT open, break, or chew capsule because hydroxyurea is a cytotoxic drug. ... Hydroxyurea capsules is contraindicated in patients who have demonstrated a previous hypersensitivity to hydroxyurea or any ...
CanMED: NDC. The Cancer Medications Enquiry Database (CanMED) is a two-part resource for cancer drug treatment related studies.
Hydroxyurea fights cancer by preventing the growth of cancer cells, which eventually results in their destruction. It is ... When treating these types of cancers, hydroxyurea is usually used at the same time as radiation therapy, as these two methods ... Hydroxyurea belongs to the group of cancer-fighting medications known as antineoplastics, and specifically to the group of ... Anemia: Hydroxyurea may cause low levels of red blood cells. If you experience symptoms of reduced red blood cell count (anemia ...
Receive NAPRA updates of interest directly to your inbox: general NAPRA news, NDS updates and/or updates on practice resources.. ...
Hydrea (hydroxyurea, is also known as Cytodrox) is a medication that is able to affect certain cells within the human body. The ...
... Author(s): Rana S(1), Houston PE(2), Wang WC(3), Iyer RV(4 ... Hydrea Umecta PD Droxia Hydroxyurea Labetalol Nadolol Phentolamine Sulfadiazine Bleomycin Cyanocobalamin Injection Estazolam ... Effects of hydroxyurea (HU) on growth in very young children are not known. METHODS: Height, weight, BMI, and head ...
Data for 82,960 patients with PV were extracted: 3852 patients were treated with hydroxyurea (HU) only, while 130 patients were ... Hydroxyurea (HU) is a commonly used first-line cytoreductive therapy for high-risk patients with PV [4]. However, even with HU ... De Stefano, V.; Rossi, E.; Carobbio, A.; Ghirardi, A.; Betti, S.; Finazzi, G.; Vannucchi, A.M.; Barbui, T. Hydroxyurea prevents ... Data for 82,960 patients with PV were extracted: 3852 patients were treated with hydroxyurea (HU) only, while 130 patients were ...
Nail pigmentation caused by hydroxyurea: report of 9 cases. J Am Acad Dermatol 2002;47:146-7. doi:10.1067/mjd.2002.120910. ... Longitudinal melanonychia induced by hydroxyurea: four case reports and review of literature. Nouv Rev Fr Hematol 1995;37:205- ... Multiple longitudinal brown bands on the toenails of digiti I-III of the right foot during treatment with hydroxyurea (A) and 6 ... Multiple longitudinal brown bands on all the toenails of the left foot during treatment with hydroxyurea (A) and 6 weeks after ...
Following cessation of hydroxyurea therapy, there was a rapid improvement of the clinical findings and complete resolution by 4 ... Editor,-Hydroxyurea is an antineoplastic agent used in the treatment of various myelproliferative conditions and severe ... 1991) Skin lesions simulating chronic dermatomyositis during long term hydroxyurea therapy. J Am Acad Dermatol 24:143-145. ... They have been speculated to result from a cumulative toxicity of hydroxyurea on the basal layer of the epidermis due to ...
Developing a risk-based composite neurologic outcome for a trial of hydroxyurea in young children with sickle cell disease ... Developing a risk-based composite neurologic outcome for a trial of hydroxyurea in young children with sickle cell disease. ... METHODS: In Study 1, investigators were surveyed about their practice regarding hydroxyurea therapy and opinions about outcomes ... Developing a risk-based composite neurologic outcome for a trial of hydroxyurea in young children with sickle cell disease. ...
Hydroxyurea (HU) has been suggested to act as a nitric oxide (NO) donor in sickle cell anemia (SCA). However, little is known ... Hydroxyurea therapy modulates sickle cell anemia red blood cell physiology: Impact on RBC deformability, oxidative stress, ... Hydroxyurea therapy modulates sickle cell anemia red blood cell physiology: Impact on RBC deformability, oxidative stress, ...
Hydroxyurea. A separate poster presented by Felipe Garcia considered if the use of hydroxyurea (HU) might be associated with ... Added value of hydroxyurea or IL-2 to STIs remains uncertain. 16 July 2000. Related: Conference reports, Intl Drug Resistance ... The hydroxyurea study varies from other STI studies in that there were set 2 week periods off treatment after the second and ... It may be that hydroxyurea might display an effect on the set-point. Loris PANDA cohort were on 2 NAs + HU only, and low level ...
Effectiveness of Hydroxyurea in the Management of Sickle Cell Disease () 2018-08-28 10:31:15 -0400. Press to Select an action * ... Effectiveness of Hydroxyurea in the Management of Sickle Cell Disease Open Access. Quarmyne, Maa-Ohui (2014) Permanent URL: ... Results: Of 1,111 patients with SCA who received care at CHOA, 127 patients started hydroxyurea during 2009-2010, and 91 met ... Background: The clinical efficacy of hydroxyurea (HU) in sickle cell anemia (SCA) has been established over the last two ...
Hydroxyurea. Hydroxyurea (hydroxycarbamate, Hydrea) is a chemo drug that has helped some patients with CMML live longer. This ... Because the main effect of hydroxyurea is to lower blood counts, anyone taking this drug will need to have their blood counts ...
Youre reviewing:Hydroxyurea Suspension Compounded. Your Rating. Quality. 1 star 2 stars 3 stars 4 stars 5 stars ... Hydroxyurea is an antimetabolite that slows the reproduction of cells, treating certain types of leukemias. It can also help ... Hydroxyurea is an antimetabolite that slows the reproduction of cells, treating certain types of leukemias. It can also help ...
"Hydroxyurea" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Hydroxyurea" by people in this website by year, and whether " ... What is the evidence that hydroxyurea improves health-related quality of life in patients with sickle cell disease? Hematology ... Therapy-related acute myelogenous leukemia in a hydroxyurea-treated patient with sickle cell anemia. Ann Intern Med. 2011 Nov ...
AdvaCare is a GMP manufacturer of Hydroxyurea Tablets, an antineoplastic used to treat myelocytic leukemia, ovarian cancer, and ... AdvaCare Hydroxyurea Tablets are GMP certified.. **AdvaCare Hydroxyurea Tablets are manufactured in our facilities located in ... AdvaCare Hydroxyurea Tablets are GMP certified.. **AdvaCare Hydroxyurea Tablets are manufactured in our facilities located in ... AdvaCare is a GMP Hydroxyurea Tablets manufacturer.. Hydroxyurea tablets, or hydroxycarbamide, in an antineoplastic drug, used ...
Additionally, hydroxyurea is used in the treatment of sickle cell disease. Hydroxyurea increases fetal hemoglobin, which is ... hydroxyurea decreases DNA synthesis and halts the cell cycle in the S phase. This property is particularly useful in targeting ... Hydroxyurea is an antimetabolite drug that inhibits RNR, or ribonucleotide reductase. RNR is an enzyme that plays a role in the ... and preventing the growth of rapidly dividing cells, which is why hydroxyurea is used to treat myeloproliferative disorders. ...
Capsule/Oblong and has been identified as Hydroxyurea 500 mg. It is supplied by Par Pharmaceutical Inc. ... Hydroxyurea. Imprint. 724 par. Strength. 500 mg. Color. Green & Pink. Size. 19.00 mm. Shape. Capsule/Oblong. Availability. ... Hydroxyurea is used in the treatment of Chronic Myelogenous Leukemia; Sickle Cell Disease; Solid Tumors and belongs to the drug ... Pill with imprint 724 par is Green & Pink, Capsule/Oblong and has been identified as Hydroxyurea 500 mg. It is supplied by Par ...
Revyuh reports on new science projects, new discoveries, health-related studies, forensics, crime, schools, policies, climate change, and a little bit about politics, business, entertainment, social media, lifestyle and sports. ...
Hydroxyurea. Hydroxyurea ICD-10-CM Drugs Index The ICD-10-CM Drugs Index is designed to allow medical coders to look up various ... Hydroxyurea poisoning accidental. poisoning intentional self harm. poisoning assault. poisoning undetermined. adverse effect. ... There are 0 terms under the parent term Hydroxyurea in the ICD-10-CM Drugs Index. ... Source: ...
Active ingredient of this drug is hydroxyurea. The exact mechanism of its action is unknown, it is supposed that it is cell ...
Hydroxyurea. CAS No.. : 127-07-1. Compare. Product No.. Description. SDS. Pricing. ...
Hydroxyurea-induced skin changes. Hydroxyurea is probably the medication most commonly used to treat polycythemia vera and ... Hydroxyurea treatment of sickle cell anemia in children can be associated with nail hyperpigmentation, longitudinal bands, and ... Salmon-Ehr et al prospectively followed 26 patients treated with hydroxyurea over 2 years. [59] All patients except 1 developed ... Skin and nail changes in children with sickle cell anemia receiving hydroxyurea therapy. J Am Acad Dermatol. 2001 May. 44(5): ...
CUADRO BÁSICO DE MEDICAMENTOS 2018. Ministerio de Salud Pública ...
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  • Hydroxyurea (Droxia, Siklos) is used to reduce the frequency of painful crises and reduce the need for blood transfusions in adults and children 2 years of age and older with sickle cell anemia (an inherited blood disorder in which the red blood cells are abnormally shaped [shaped like a sickle] and cannot bring enough oxygen to all parts of the body). (
  • Hydroxyurea treats sickle cell anemia by helping to prevent formation of sickle-shaped red blood cells. (
  • Hydroxyurea is used in less than 25% of patients with sickle cell anemia (SCA) who could benefit from it, according to results of a study published in the April 28 issue of JAMA . (
  • Hydroxyurea is also used for the management of sickle cell anemia. (
  • Hydroxyurea also increases the production of fetal hemoglobin, via an unknown mechanism of action, which increases overall hemoglobin levels and decreases sickling in patients with sickle cell anemia. (
  • Hydroxyurea was approved by the FDA for use in adults with sickle cell anemia in 1998. (
  • Hydroxyurea Capsule is a prescription medication used in the treatment of certain medical conditions, including various types of cancer and sickle cell anemia. (
  • For the REACH Investigators 2016, ' Hydroxyurea Therapy for Children With Sickle Cell Anemia in Sub-Saharan Africa: Rationale and Design of the REACH Trial ', Pediatric Blood and Cancer , vol. 63, no. 1, pp. 98-104. (
  • Longitudinal analysis of cardiac abnormalities in pediatric patients with sickle cell anemia and effect of hydroxyurea therapy. (
  • Evaluation of the concentration of malondialdehyde and nitrite in patients with sickle cell anemia treated or not with hydroxyurea. (
  • To determine the serum levels of malondialdehyde and nitrite in patients with sickle cell anemia treated or not with hydroxyurea in outpatient 's setting. (
  • Of the 65 patients with sickle cell anemia selected for the study, 51 were not treated with hydroxyurea (Group 1), 14 made chronic use of hydroxyurea (Group 2) and 20 individuals had no hemoglobinopathies ( Control Group ). (
  • Hydrea (Hydroxyurea) is used to treat melanoma, chronic myelocytic leukemia, ovarian and primary squamous cell cancer, carcinoma of the head and neck (excluding the lip), chronic myelogenous leukemia, sickle cell anemia. (
  • Hydroxyurea is also used in adult patients with sickle cell anemia to prevent painful episodes and reduce the need for blood transfusions. (
  • Hydroxyurea is available in capsules of 200, 300, 400 and 500 mg generically and under brand names as Droxia (for sickle cell disease) and Hydrea (for cancer). (
  • Hydroxyurea (hydroxycarbamate, Hydrea) is a chemo drug that has helped some patients with CMML live longer. (
  • Buy Hydrea 'Hydroxyurea' Online Without Prescriptions. (
  • Order Hydrea 'Hydroxyurea' Online Without Prescriptions. (
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  • Hydroxyurea comes as a capsule and tablet to take by mouth. (
  • Hydroxyurea is available in capsule form. (
  • With its proven effectiveness and safety profile, Hydroxyurea Capsule plays a crucial role in managing specific diseases and improving patients' quality of life. (
  • Q: How does Hydroxyurea Capsule work? (
  • A: Hydroxyurea Capsule works by inhibiting the growth and reproduction of certain cells in the body. (
  • Q: What medical conditions are treated with Hydroxyurea Capsule? (
  • A: Hydroxyurea Capsule is primarily used in the treatment of several conditions, including certain types of cancer such as chronic myelogenous leukemia, ovarian cancer, and melanoma. (
  • Q: Is Hydroxyurea Capsule safe to use? (
  • A: Hydroxyurea Capsule is a prescription medication and should only be used under the guidance of a healthcare professional. (
  • Q: How should I take Hydroxyurea Capsule? (
  • A: The dosage and administration of Hydroxyurea Capsule will be determined by your healthcare provider based on your specific medical condition and individual factors. (
  • The second finding is that IPF is susceptible to myelosuppressive treatment, which may additionally explain the favorable effect of hydroxyurea therapy on MPN outcome as well as the associated thrombotic risk. (
  • Your doctor or pharmacist will give you the manufacturer's patient information sheet (Medication Guide) when you begin treatment with hydroxyurea and each time you refill your prescription. (
  • Before you begin treatment with hydroxyurea, you and your doctor should talk about the good this medicine will do as well as the risks of using it. (
  • The hydroxyurea 1,000-mg tablets (Siklos) are scored so that they can easily be split into halves or quarters to provide smaller doses. (
  • Here we report that low doses of hydroxyurea, an inhibitor of ribonucleotide reductase and an important drug in the treatment of sickle cell disease and other diseases induces a high frequency of de novo CNVs in cultured human cells that resemble pathogenic and aphidicolin-induced CNVs in size and breakpoint structure. (
  • Serum aminotransferase and bilirubin elevations occur in a small proportion of patients on conventional doses of hydroxyurea and a greater proportion at higher doses. (
  • The TWiTCH study sought to determine whether giving daily doses of hydroxyurea (currently the only FDA-approved drug for sickle cell disease) lowers the TCD blood velocity in children with sickle cell disease (SCD) to a similar degree as blood transfusions. (
  • Tolerability and age-dependent toxicokinetics following perinatal hydroxyurea treatment in Sprague Dawley rats. (
  • Your doctor may need to delay your treatment or adjust your dose of hydroxyurea depending on your response to treatment and any side effects that you may experience. (
  • The study defined treatment with hydroxyurea as filling at least one prescription during the 3, 6, or 12 months of continued enrollment after the third hospitalization or ED visit. (
  • The researchers hypothesize that several factors might contribute to the low use of this inexpensive and effective treatment, including clinician unfamiliarity with hydroxyurea, fear of adverse events, and absence of shared decision-making. (
  • Vasculitic toxicities: Discontinue hydroxyurea and initiate treatment if this occurs. (
  • discontinue hydroxyurea capsules, and implement treatment. (
  • Hydroxyurea treatment saves lives in Africa and other countries. (
  • Yet the study also offers promising new evidence that treatment with hydroxyurea could lead to improvement and even reversal of cardiac abnormalities in individuals with SCA. (
  • When we compared the group that had been on hydroxyurea treatment for less than one year to the group that had been on treatment for more than one year, we found that the people who had been treated for longer were less likely to have an enlarged heart or a thickened heart," said Dr. Dhar. (
  • The next phase of the study was a longitudinal analysis in which Dr. Dhar and her team assessed echocardiograms (ultrasound tests of the function of the heart's muscles and valves) performed over time on the patients receiving treatment with hydroxyurea. (
  • Even for asymptomatic individuals, screening should start at a young age so we can catch any abnormalities early and start treatment with hydroxyurea as soon as possible. (
  • An expert panel has released evidence-based guidelines for the treatment of SCD, including a strong recommendation that hydroxyurea and long-term, periodic blood transfusions should be used more often to treat patients. (
  • Hydroxyurea is an anticancer medication used for the treatment of leukemia. (
  • Expert perspectives on hydroxyurea as a staple therapy in the treatment armamentarium for sickle cell disease. (
  • Hydroxyurea is our tried-and-true treatment. (
  • Hydroxyurea is the oldest federally approved treatment for patients with sickle cell disease, and since the time of the original approval for a reduction in annual rate of pain crises, it has now proven itself as a possible substitute for transfusion in young children who have strokes. (
  • Hydroxyurea is an antimetabolite that is used in the treatment of cancer and to stimulate fetal hemoglobin production in sickle cell disease. (
  • Hydroxyurea is used in the treatment of solid tumors and myeloproliferative diseases, the latter because of its effects in reducing excessive production of red blood cells (polycythemia vera), white blood cells (chronic myelogenous leukemia) or platelets (essential thrombocythemia). (
  • What is the efficacy (results from clinical studies) of hydroxyurea treatment for patients who have sickle cell disease in three groups: infants, preadolescents, and adolescents/adults? (
  • What is the effectiveness (in everyday practice) of hydroxyurea treatment for patients who have sickle cell disease? (
  • What are the short- and long-term harms of hydroxyurea treatment? (
  • What are the barriers to hydroxyurea treatment for patients who have sickle cell disease and what are the potential solutions? (
  • Along with its benefits, hydroxyurea treatment may cause severe, sometimes fatal side effects (see also Side Effects section). (
  • The efficacy and mechanism of hydroxyurea in the treatment of atherosclerosis have rarely been reported. (
  • The goal of this study was to investigate the efficacy of hydroxyurea in high-fat diet-fed ApoE -/- mice against atherosclerosis and examine the possible mechanism underlying treatment outcomes. (
  • 16S rRNA was used to detect composition changes in the intestinal bacterial community of animals after treatment with hydroxyurea. (
  • We showed that aortic root HE staining and oil red O staining determined the therapeutic efficacy of hydroxyurea in the treatment of atherosclerosis in high-fat diet-fed ApoE -/- mice. (
  • Further histological and ELISAs verified that the protein responsible for intestinal absorption of cholesterol in mice, NPC1L1, was significantly reduced after hydroxyurea treatment. (
  • To address this point, in 46 essential thrombocythemia and 38 polycythemia vera consecutive patients, we measured IPF and correlated the results to JAK2V617F mutation and myelosuppressive treatment with hydroxyurea. (
  • By developing local expertise with the use of hydroxyurea and helping to establish treatment guidelines, the REACH trial results will have the potential to transform care for children with SCA in Africa. (
  • According to a recent study published in Blood advances, timely initiation of treatment with hydroxyurea (HU) may lead to reverse cardiac remodelling and improvement in these cardiac abnormalities. (
  • On the other hand , no changes in oxidative parameters were detected during treatment with hydroxyurea , probably due to the short period of treatment of the patients studied. (
  • Scholars@Duke publication: Treatment patterns and economic burden of sickle-cell disease patients prescribed hydroxyurea: a retrospective claims-based study. (
  • BACKGROUND: This study aimed to evaluate sickle-cell disease (SCD) treatment patterns and economic burden among patients prescribed hydroxyurea (HU) in the US, through claims data. (
  • Hydroxyurea (HU) is one of the US-FDA approved and commonly used drug for the treatment of adult SCD patients with clinical -severity. (
  • and defining the relationships between hydroxyurea treatment and fetal hemoglobin, soluble intracellular adhesion molecule-1, and nitric oxide levels, and between levels of these factors and risk of subsequent malaria. (
  • Conclusion: Treatment with hydroxyurea for 24 months did not influence GFR in young children with SCA. (
  • Evaluation of pharmacological efficacy and safety of hydroxyurea in sickle cell disease: Study of a pediatric cohort from Chhattisgarh, India. (
  • In Sub-Saharan Africa, however, the risk of malaria, hematologic toxicities, and safety of hydroxyurea in children with SCA living in malaria-endemic areas are unknown. (
  • In conclusion, our results showed significant clinical and laboratory benefits of hydroxyurea in children with SCD. (
  • Procedure: A partnership was established between investigators in North America and sub-Saharan Africa, to develop a prospective multicenter research protocol designed to provide data on the safety, feasibility, and benefits of hydroxyurea for children with SCA. (
  • Hydroxyurea (hye drox" ee ure ee' a) is a hydroxylated analogue of urea and an antimetabolite which inhibits the enzyme ribonucleotide reductase, which is necessary for DNA synthesis and cell cycle replication. (
  • I would kindly like to request information regarding the use of the drug Siklos, which contains hydroxyurea, in terms of its administration to breastfeeding mothers. (
  • It contains hydroxyurea, an active ingredient that helps regulate the production of cells in the body. (
  • These highlights do not include all the information needed to use HYDROXYUREA CAPSULES safely and effectively. (
  • See full prescribing information for HYDROXYUREA CAPSULES. (
  • Live Vaccinations: Avoid live vaccine use in a patient taking hydroxyurea capsules. (
  • Swallow hydroxyurea capsules whole. (
  • Do NOT open, break, or chew capsules because hydroxyurea is a cytotoxic drug. (
  • Monitor blood counts at least once a week during Hydroxyurea capsules therapy. (
  • Severe anemia must be corrected before initiating therapy with Hydroxyurea capsules. (
  • We used to think that hydroxyurea worked primarily by increasing the production of fetal hemoglobin, which as Dr Shah, said is naturally occurring in the Saudi Arabian population and in other populations where their disease is milder. (
  • Hydroxyurea can't quite reproduce that, but it does increase the production of the total amount of fetal hemoglobin. (
  • In 2014, the National Heart, Lung, and Blood Institute issued recommendations to treat all adults with SCA who experience at least three moderate to severe pain crises a year with hydroxyurea. (
  • Despite evidence that the drug reduces pain crises, hospitalizations, and blood transfusions, hydroxyurea is reportedly underused. (
  • The study may have underestimated the magnitude of the hydroxyurea gap in three ways: the study population was privately insured and did not include patients who could manage their pain crises at home. (
  • Cite this: Hydroxyurea Underused in Sickle Cell Pain Crises - Medscape - Apr 29, 2015. (
  • But in my mind, if they're symptomatic the way that they would be if they had hemoglobin S and have a lot of painful crises, they're going to get hydroxyurea even if they have hemoglobin SC. (
  • That means if they have a lot of crises and they're feeling poorly, and I think that it might help, I'm going to give hydroxyurea to them. (
  • In controlled clinical trials, hydroxyurea has been shown to increase hemoglobin concentrations, decrease transfusion requirements and lessen painful crises in patients with sickle cell disease. (
  • In the mid-1990s, researchers began investigating the potential of hydroxyurea to reduce the number and severity of pain crises in sickle cell patients. (
  • Hydroxyurea can cause a severe decrease in the number of blood cells in your bone marrow. (
  • The Food and Drug Administration (FDA) approved hydroxyurea for severe SCD in 1998 for adults and in 2017 for children. (
  • By increasing hemoglobin, hydroxyurea can energy. (
  • Even though the book says it's for hemoglobin SS and S beta zero thalassemia, I give hydroxyurea to whoever needs it. (
  • Although there is no cure for Sickle Cell Disease yet, but there is a drug called hydroxyurea that is used to treat the crisis and maintain blood hemoglobin level. (
  • Hydroxyurea is used alone or in conjunction with other antitumor agents or radiation therapy to treat neoplastic diseases. (
  • A study published today in the journal Blood Advances is the first to find that hydroxyurea therapy can improve or even reverse cardiac complications in individuals living with SCA. (
  • Hydroxyurea is associated with a low rate of transient serum enzyme and bilirubin elevations during therapy, and has been implicated in rare cases of clinically apparent acute liver injury with jaundice. (
  • Hydroxyurea was first approved for use in the United States in 1967 as an antineoplastic agent for therapy of melanoma, chronic myelogenous leukemia, ovarian carcinoma, and head and neck cancers. (
  • Long term hydroxyurea therapy may increase the risk of cancer. (
  • Hydroxyurea represents the only available disease-modifying therapy for SCA, and has proven safety and efficacy in high-resource countries. (
  • Hydroxyurea, the only disease-modifying therapy approved by the Food and Drug Administration for SCA, has proven to be a viable therapeutic option for SCA patients in resource-rich settings, given clinical improvements experienced while taking the medication and its once-daily oral dosing. (
  • Studies have shown hydroxyurea is one potential y prevent the blockage of blood flow of several drugs that does this. (
  • What Other Drugs Interact with Hydroxyurea? (
  • Hydroxyurea has moderate interactions with at least 115 different drugs. (
  • Hydroxyurea has no known mild interactions with other drugs. (
  • Hydroxyurea, one of the four drugs currently approved by the U.S. Food and Drug Administration to treat SCD, is believed to mitigate SCD symptoms by preventing the formation of sickled cells, but its precise mechanism of action is still not fully understood. (
  • We have 4 drugs: crizanlizumab and voxelotor are the 2 new ones, and Endari [L-glutamine] and hydroxyurea. (
  • Hydroxyurea is in a class of anti-cancer drugs and it acts to increase the overall percentage of normally structured red blood cells in the circulation. (
  • Hydroxyurea is an antineoplastic agent used to treat melanoma, leukemias, and other neoplasms. (
  • Hydroxyurea dermopathy is caused by chronic use of hydroxyurea for chronic myelogenous leukemia, thrombocytosis, or psoriasis, and presents with skin lesions characteristic of dermatomyositis. (
  • Hydroxyurea is an antineoplastic (anti-cancer) agent used to treat melanoma , resistant chronic myelocytic leukemia , and recurrent , metastatic, or inoperable carcinoma of the ovary and primary squamous cell (epidermoid) carcinomas of the head and neck. (
  • Hydroxyurea is used to treat skin cancer (melanoma), a cancer of the white blood cells called chronic myelocytic leukemia (CML), and metastatic cancer (cancer that has spread) of the ovaries. (
  • Hydroxyurea is an oral medicine that can help reduce sickle cel disease (SCD) complications. (
  • Hydroxyurea (HU) is known to decrease the frequency of vaso-occlusive complications and need for blood transfusions in severely affected individuals. (
  • Hydroxyurea is a cytotoxic drug. (
  • In this research, we investigated the cytotoxic, antiproliferative and apoptosis-inducing effects of hydroxyurea on a human cervical carcinoma cell line, HeLa. (
  • We found that hydroxyurea has cytotoxic and antiproliferative effects on HeLa cells in a dose-dependent manner. (
  • We concluded that the observed antiproliferative, cytotoxic and apoptosis inducing activities of hydroxyurea might be mediated by the induction of p53 and its transcriptional target, p21. (
  • REACH has an adaptive statistical design that allows for careful assessment of toxicities to accurately identify a safe hydroxyurea dose. (
  • Hydroxyurea is in a class of medications called antimetabolites. (
  • If you are unable to swallow hydroxyurea tablets or portion(s) of tablets, you may dissolve your dose in water. (
  • Novel use Of Hydroxyurea in an African Region with Malaria (NOHARM, NCT01976416) is a prospective, randomized, placebo-controlled, double-blinded phase III trial to compare risk of malaria with oral hydroxyurea versus placebo. (
  • The study also did not consider, "the broadened criteria described in new guidelines for the use of hydroxyurea, such as patients who have daily pain that affects their quality of life. (
  • The investigators conclude that to address the gap in hydroxyurea use, "it may be necessary to enhance patient outreach and clinician training and develop health care quality measures aimed at increasing the use of hydroxyurea for all patients who would benefit. (
  • In patients who have demonstrated a previous hypersensitivity to hydroxyurea or any other component of its formulation. (
  • Sixty of the study participants were taking hydroxyurea, and the researchers noted that there was no difference in the level of LV enlargement for that group of patients as compared to the group not taking the drug. (
  • If patients with SCD crisis are being transported by emergency medical services (EMS), they should receive supplemental oxygen and intravenous hydration en route to the hospital. (
  • Drug fever occurs in up to 1% of patients treated with hydroxyurea, typically arising within 1 to 3 weeks of starting and presenting with high fevers and mild constitutional symptoms of fatigue and nausea (Case 1 below). (
  • Thirty-seven (37) of the patients using hydroxyurea had an increase in the mean corpuscular volume (MCV). (
  • Moreover, the frequency of blood transfusion in patients using hydroxyurea was statistically significant as p-value = 0.048. (
  • Hydroxyurea has been shown to reduce the frequency of VOC and blood transfusion in patients with SCD. (
  • An overview of Genetic Toxicology Micronucleus Mice study conclusions related to Hydroxyurea (127-07-1). (
  • What Are Warnings and Precautions for Hydroxyurea? (
  • Talk with your doctor about the risks of taking hydroxyurea. (
  • Ask your healthcare provider about the potential benefits and risks, and whether hydroxyurea is right for you. (
  • These findings strengthen the beneficial effect of hydroxyurea in pediatric population also without any serious adverse effects and builds up ground for expanding its use under regular monitoring. (
  • Until relatively recently, only one drug, hydroxyurea, was approved by the US Food and Drug Administration to ameliorate disease severity. (
  • This drug is prescribed when hydroxyurea and other treatments have failed. (
  • Since 1998, doctors have used a drug called hydroxyurea to reduce symptoms, but it can cause serious side effects and increase the risk of certain cancers. (
  • Because the main effect of hydroxyurea is to lower blood counts, anyone taking this drug will need to have their blood counts checked regularly. (
  • Hydroxyurea may increase the risk that you will develop other cancers, including skin cancer. (
  • Hydroxyurea treats cancer by slowing or stopping the growth of cancer cells in your body. (
  • When hydroxyurea is used to treat certain types of cancer, it may be taken once every third day. (
  • Your doctor will order certain tests on a regular basis to check your body's response to hydroxyurea and to see if your blood count has dropped. (
  • Your doctor may need to change your dose or tell you to stop taking hydroxyurea for a period of time to allow your blood count to return to normal if it has dropped too low. (
  • Your doctor may change the dosage of Hydroxyurea depending on blood tests results. (
  • The National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health, has ended the Transcranial Doppler (TCD) with Transfusions Changing to Hydroxyurea (TWiTCH) clinical trial early in agreement with the recommendations of the Data and Safety Monitoring Board (DSMB). (
  • Children with sickle cell disease who are at a higher risk for stroke are identified by measuring the velocity of blood flow to the brain by TCD ultrasound studies.Children with the highest TCD velocities have a greater risk of strokes.The early review showed that hydroxyurea reduces TCD blood velocities to a similar degree as blood transfusions. (
  • The results of this study show that hydroxyurea is not inferior to (that is, no worse than) regular blood transfusions in lowering TCD velocities in children with sickle cell disease who are at high risk for stroke. (
  • Current management strategies include prophylactic penicillin and immunizations to decrease the occurrence of pneumococcal infections, hydroxyurea (a disease-modifying agent), blood transfusions (for symptomatic acute anemia, stroke management, preoperative optimization), and bone marrow transplant. (
  • Read the Patient Information Leaflet if available from your pharmacist before you start taking hydroxyurea and each time you get a refill. (
  • In sub-Saharan Africa, there is minimal use of hydroxyurea, due to lack of data, absence of evidence-based guidelines, and inexperience among healthcare providers. (
  • Results: The Realizing Effectiveness Across Continents with Hydroxyurea (REACH, NCT01966731) trial is a prospective, phase I/II open-label dose escalation study of hydroxyurea that will treat a total of 600 children age 1-10 years with SCA: 150 at each of four different clinical sites within sub-Saharan Africa (Angola, Democratic Republic of Congo, Kenya, and Uganda). (
  • NOHARM will be the first prospective randomized, placebo-controlled clinical trial investigating the use of hydroxyurea for children with SCA in a malaria-endemic region within Africa. (
  • SCD treatments, including hydroxyurea, may reduce symptoms and improve quality of life. (
  • The incidence of vaso-occlusive crisis (VOC) increased after hydroxyurea initiation from 4.555±4.08 to 6.288±9.80. (
  • How should I handle Hydroxyurea safely? (
  • How should I dispose of Hydroxyurea safely? (
  • The results of this trial have the potential to significantly advance understanding of how to safely and effectively use hydroxyurea in children with SCA in malaria-endemic areas. (
  • In high-fat diet-fed ApoE -/- mice, hydroxyurea effectively treated atherosclerosis, lowered serum cholesterol, modulated the gut microbiota at multiple levels and affected cholesterol absorption by reducing NPC1L1 in small intestinal epithelial cells. (
  • This study aims to determine the frequency and benefits of using hydroxyurea in treating children with SCD in King Abdulaziz University Hospital (KAUH) in Saudi Arabia. (
  • Do not use this medicine if you (or your child) is allergic to Hydroxyurea. (
  • The Phase III randomized double-blinded Clinical Trial of Hydroxyurea in Infants with SCA (BABY HUG) tested the hypothesis that hydroxyurea can prevent kidney dysfunction by reducing hyperfiltration. (
  • In addition, they point to a need for further study of the genomic consequences of the therapeutic use of hydroxyurea. (