Thioguanine
6-Mercaptopurine
Hypoxanthine Phosphoribosyltransferase
Azaguanine
Methylthioinosine
Azathioprine
Daunorubicin
Cytarabine
Methyltransferases
Azauridine
Guanine Nucleotides
Hypoxanthines
Purines
DCMP Deaminase
Mitolactol
Mutagens
Guanine
Drug Resistance
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Purine Nucleotides
Leukemia, Myeloid, Acute
Adenine Phosphoribosyltransferase
Biotransformation
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Internship, Nonmedical
5-azacytidine induces transgene silencing by DNA methylation in Chinese hamster cells. (1/428)
The cytosine analog 5-azacytidine (5-AzaC) is a demethylating agent that is also known to induce mutagenesis in mammalian cells. In this study, the mutagenic potential of this drug was tested in the G10 and G12 transgenic Chinese hamster cell lines, which have a single bacterial gpt gene integrated into the genome at different sites, with its expression driven by a simian virus 40 (SV40) promoter. We show that the mutation frequencies following a 48-h exposure to different concentrations of 5-AzaC were 10 to 20 times higher than those of any of the other numerous mutagens that have been tested in the G10-G12 system. Moreover, the mutation frequencies were much higher in the G10 cell line than in the G12 cells. Detailed molecular analysis of the 6-thioguanine (6-TG)-resistant variants demonstrated that transgene silencing by de novo DNA methylation and increased chromatin condensation in the SV40 promoter was the major factor responsible for this high level of 6-TG resistance. As would be expected, exposure to 5-AzaC lowered the overall genomic DNA methylation levels, but it unexpectedly caused hypermethylation and increased chromatin condensation of the transgene in both the G10 and G12 cell lines. These results provide the first evidence that 5-AzaC may also induce transgene-specific DNA methylation, a phenomenon that can further be used for the elucidation of the mechanism that controls silencing of foreign DNA. (+info)The mismatch repair protein, hMLH1, mediates 5-substituted halogenated thymidine analogue cytotoxicity, DNA incorporation, and radiosensitization in human colon cancer cells. (2/428)
Deficiency in DNA mismatch repair (MMR) is found in some hereditary (hereditary nonpolyposis colorectal cancer) and sporadic colon cancers as well as other common solid cancers. MMR deficiency has recently been shown to impart cellular resistance to multiple chemical agents, many of which are commonly used in cancer chemotherapy. It is therefore of interest to find an approach that selectively targets cells that have lost the ability to perform MMR. In this study, we examine the response of MMR-proficient (hMLH1+) and MMR-deficient (hMLH1-) colon carcinoma cell lines to the halogenated thymidine (dThd) analogues iododeoxyuridine (IdUrd) and bromodeoxyuridine (BrdUrd) before and after irradiation. These dThd analogues are used clinically as experimental sensitizing agents in radioresistant human cancers, and there is a direct correlation between the levels of dThd analogue DNA incorporation and tumor radiosensitization. In contrast to the well-characterized, marked increase in cytotoxicity (> 1 log cell kill) found with 6-thioguanine exposures in HCT116/3-6 (hMLH1+) cells compared to HCT116 (hMLH1-) cells, we found only modest cytotoxicity (10-20% cell kill) in both cell lines when treated with IdUrd or BrdUrd for 1 population doubling. Upon further analysis, the levels of halogenated dThd analogues in DNA were significantly lower (two to three times lower) in HCT116/3-6 cells than in HCT116 cells, and similar results were found in Mlh1+/+ spontaneously immortalized murine embryonic fibroblasts and fibroblasts from Mlh1 knockout mice. As a result of the higher levels of the dThd analogue in DNA, there was an increase in radiation sensitivity in HCT116 cells but not in HCT116/3-6 cells after pretreatment with IdUrd or BrdUrd when compared to treatment with radiation alone. Additionally, we found no differences in the cellular metabolic pathways for dThd analogue DNA incorporation because the enzyme activities of dThd kinase and thymidylate synthase, as well as the levels of triphosphate pools, were similar in HCT116 and HCT116/3-6 cells. These data suggest that the hMLH1 protein may participate in the recognition and subsequent removal of halogenated dThd analogues from DNA. Consequently, whereas MMR-deficient cells and tumor xenografts have shown intrinsic resistance to a large number of chemotherapeutic agents, the 5-halogenated dThd analogues appear to selectively target such cells for potential enhanced radiation sensitivity. (+info)Double induction strategy for acute myeloid leukemia: the effect of high-dose cytarabine with mitoxantrone instead of standard-dose cytarabine with daunorubicin and 6-thioguanine: a randomized trial by the German AML Cooperative Group. (3/428)
Early intensification of chemotherapy with high-dose cytarabine either in the postremission or remission induction phase has recently been shown to improve long-term relapse-free survival (RFS) in patients with acute myeloid leukemia (AML). Comparable results have been produced with the double induction strategy. The present trial evaluated the contribution of high-dose versus standard-dose cytarabine to this strategy. Between March 1985 and November 1992, 725 eligible patients 16 to 60 years of age with newly diagnosed primary AML entered the trial. Before treatment started, patients were randomized between two versions of double induction: 2 courses of standard-dose cytarabine (ara-C) with daunorubicin and 6-thioguanine (TAD) were compared with 1 course of TAD followed by high-dose cytarabine (3 g/m2 every 12 hours for 6 times) with mitoxantrone (HAM). Second courses started on day 21 before remission criteria were reached, regardless of the presence or absence of blast cells in the bone marrow. Patients in remission received consolidation by TAD and monthly maintenance with reduced TAD courses for 3 years. The complete remission (CR) rate in the TAD-TAD compared with the TAD-HAM arm was 65% versus 71% (not significant [NS]), and the early and hypoplastic death rate was 18% versus 14% (NS). The corresponding RFS after 5 years was 29% versus 35% (NS). An explorative analysis identified a subgroup of 286 patients with a poor prognosis representing 39% of the entire population; they included patients with more than 40% residual blasts in the day-16 bone marrow, patients with unfavorable karyotype, and those with high levels of serum lactate dehydrogenase. Their CR rate was 65% versus 49% (p =.004) in favor of TAD-HAM and was associated with a superior event-free survival (median, 7 v 3 months; 5 years, 17% v 12%; P =.012) and overall survival (median, 13 v 8 months; 5 years, 24% v 18%; P =.009). This suggests that the incorporation of high-dose cytarabine with mitoxantrone may contribute a specific benefit to poor-risk patients that, however, requires further substantiation. Double induction, followed by consolidation and maintenance, proved a safe and effective strategy and a new way of delivering early intensification treatment for AML. (+info)6-Thioguanine alters the structure and stability of duplex DNA and inhibits quadruplex DNA formation. (4/428)
The ability to chemically synthesize biomolecules has opened up the opportunity to observe changes in structure and activity that occur upon single atom substitution. In favorable cases this can provide information about the roles of individual atoms. The substitution of 6-thioguanine (6SG) for guanine is a potentially very useful single atom substitution as 6SG has optical, photocrosslinking, metal ion binding and other properties of potential utility. In addition, 6-mercaptopurine is a clinically important pro-drug that is activated by conversion into 6SG by cells. The results presented here indicate that the presence of 6SG blocks the formation of quadruplex DNA. The presence of 6SG alters the structure and lowers the thermal stability of duplex DNA, but duplex DNA can be formed in the presence of 6SG. These results indicate that some of the cytotoxic activity of 6SG may be due to disruption of the quadruplex structures formed by telomere and other DNAs. This additional mode of action is consistent with the delayed onset of cytotoxicity. (+info)Thioguanine administered as a continuous intravenous infusion to pediatric patients is metabolized to the novel metabolite 8-hydroxy-thioguanine. (5/428)
Thiopurine antimetabolites have been in clinical use for more than 40 years, yet the metabolism of thiopurines remains only partially understood. Data from our previous pediatric phase 1 trial of continuous i.v. infusion of thioguanine (CIVI-TG) suggested that TG was eliminated by saturable mechanism, with conversion of the drug to an unknown metabolite. In this study we have identified this metabolite as 8-hydroxy-thioguanine (8-OH-TG). The metabolite coeluted with the 8-OH-TG standard on HPLC and had an identical UV spectrum, with a lambda(max) of 350 nm. On mass spectroscopy, the positive ion, single quad scan of 8-OH-TG yielded a protonated molecular ion at 184 Da and contained diagnostic ions at m/z 167, 156, 142, and 125 Da. Incubation of TG in vitro with partially purified aldehyde oxidase resulted in 8-OH-TG formation. 8-OH-TG is the predominant circulating metabolite found in patients receiving CIVI-TG and is likely generated by the action of aldehyde oxidase. (+info)Neutrophil alkaline phosphatase score in chronic granulocytic leukaemia: effects of splenectomy and antileukaemic drugs. (6/428)
Staining with naphthol AS phosphate and Fast Blue BB salt has been used for the estimation of neutrophil alkaline phosphatase (NAP) scores in patients with chronic granulocytic leukaemia (CGL). The very low scores found at diagnosis rise when the disease is treated, and there is some inverse correlation between the NAP score and the absolute neutrophil count. Patients treated intensively developed high NAP scores. Elective splenectomy performed during the chronic phase of CGL is followed by a pronounced but transient neutrophilia and a concurrent striking rise in the NAP score. Similar changes were observed in patients without CGL who underwent splenectomy. These observations can be explained by assuming that newly formed neutrophils in CGL have a normal content of NAP but are rapidly sequestered in non-circulating extramedullary pools, whereas the circulating neutrophil with a typically low NAP content is a relatively aged cell which has lost enzyme activity. In subjects with or without CGL, removal of the spleen, a major site of such pooling, temporarily permits the circulation of newly formed neutrophils but eventually other organs assume the sequestering functions of the spleen. Thus the aberrations of NAP score seen in CGL might be attributable not to an intrinsic cellular defect but to an exaggeration of the granulocyte storage phenomena which also occur in subjects without CGL. (+info)Non-Hodgkin's lymphoma in children: results of treatment with LSA2-L2 protocol. (7/428)
The results obtained with very intensive treatment in previously untreated patients early in the disease are encouraging, and we hope will change the philosophy of most investigators that even in far advanced disease such as those with marrow metastases or multiple primary sites, one can still obtain complete regression at all tumour sites within 1 to 1 1/2 months from onset of therapy by combined treatment with multiple chemotherapeutic agents and radiation therapy to one or more sites. (+info)Acute lymphoblastic leukaemia: cyclical chemotherapy with three combinations of four drugs (COAP-POMP-CART regimen). (8/428)
Forty-two adults and children with previously untreated acute lymphoblastic leukaemia (ALL) were entered into a programme of chemotherapy in which three combinations, each of four drugs were administered in a predetermined cyclical rotation together with cranial irradiation and intrathecal injections of methotrexate. Forty-one patients (98%) entered remission and no patient developed neuroleukaemia. Relapse of ALL occurred in 10 patients, and three patients died during remission, while eight patients stopped treatment after two and a half years and have remained in remission for two to 26 months. Comparison of remission and survival experience in this mixed group of children and adults with the experience of children treated at Memphis and in the Medical Research Council's UKALL-I trial showed no significant differences. On the other hand, analysis by prognostic factors showed that neither age nor blast cell count at presentation had any adverse effect in patients treated in this study. No relapses occurred in nine patients with blast cell counts greater than 20 x 109/1 at presentation. This regimen is effective treatment for ALL and may be of special value in patients with poor prognoses. The regiment has not as yet proved superior for the treatment of children with ALL who do not have adverse prognostic features. (+info)Thioguanine is a medication that belongs to a class of drugs called antimetabolites. It is primarily used in the treatment of acute myeloid leukemia (AML) and other various types of cancer.
In medical terms, thioguanine is a purine analogue that gets metabolically converted into active thiopurine nucleotides, which then get incorporated into DNA and RNA, thereby interfering with the synthesis of genetic material in cancer cells. This interference leads to inhibition of cell division and growth, ultimately resulting in cell death (apoptosis) of the cancer cells.
It is important to note that thioguanine can also affect normal cells in the body, leading to various side effects. Therefore, it should be administered under the close supervision of a healthcare professional who can monitor its effectiveness and potential side effects.
6-Mercaptopurine (6-MP) is a medication used primarily in the treatment of cancer, specifically acute lymphoblastic leukemia (ALL), and to prevent rejection in organ transplantation. It is an antimetabolite that works by interfering with the synthesis of DNA and RNA, thereby inhibiting cell division and growth.
6-MP is a prodrug, meaning it requires metabolic activation in the body to exert its therapeutic effects. Once absorbed, 6-MP is converted into several active metabolites, including thioguanine nucleotides (TGN), which are incorporated into DNA and RNA, leading to cytotoxicity and cell death.
Common side effects of 6-MP include nausea, vomiting, diarrhea, mouth sores, and increased susceptibility to infections. Long-term use of the medication can also lead to liver toxicity, pancreatitis, and anemia. Regular monitoring of blood counts, liver function tests, and TGN levels is necessary during treatment with 6-MP to minimize potential side effects and ensure safe and effective dosing.
Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) is an enzyme that plays a crucial role in the salvage pathway of nucleotide synthesis. This enzyme catalyzes the conversion of hypoxanthine and guanine to their respective nucleotides, inosine monophosphate (IMP) and guanosine monophosphate (GMP), by transferring the phosphoribosyl group from 5-phosphoribosyl-1 pyrophosphate (PRPP) to the purine bases.
HGPRT deficiency is a genetic disorder known as Lesch-Nyhan syndrome, which is characterized by mental retardation, self-mutilation, spasticity, and uric acid overproduction due to the accumulation of hypoxanthine and guanine. This disorder is caused by mutations in the HPRT1 gene, leading to a decrease or absence of HGPRT enzyme activity.
Azaguanine is a type of antimetabolite drug that is used in medical research and treatment. It is a purine analogue, which means it has a similar chemical structure to the natural purine bases adenine and guanine, which are building blocks of DNA and RNA. Azaguanine can be incorporated into the genetic material of cells, interfering with their normal function and replication. It is used in research to study the effects of such interference on cell growth and development.
In clinical medicine, azaguanine has been used as an anticancer drug, although it is not widely used today due to its toxicity and the availability of more effective treatments. It may also have some activity against certain types of parasitic infections, such as leishmaniasis and malaria.
It's important to note that azaguanine is not a commonly used medication and its use should be under the supervision of a medical professional with experience in its administration and management of potential side effects.
Methylthioinosine is not a widely recognized or used term in medicine, and it does not have a specific medical definition. It is a chemical compound that is formed by the addition of a methylthio group (-CH3S-) to the nucleoside inosine. Inosine is a purine nucleoside that is formed from the deamination of adenosine.
Methylthioinosine has been studied in some laboratory experiments, but it is not commonly used in clinical medicine or treatment. Therefore, it is not a term that most medical professionals would be familiar with.
Azathioprine is an immunosuppressive medication that is used to prevent the rejection of transplanted organs and to treat autoimmune diseases such as rheumatoid arthritis, lupus, and inflammatory bowel disease. It works by suppressing the activity of the immune system, which helps to reduce inflammation and prevent the body from attacking its own tissues.
Azathioprine is a prodrug that is converted into its active form, 6-mercaptopurine, in the body. This medication can have significant side effects, including decreased white blood cell count, increased risk of infection, and liver damage. It may also increase the risk of certain types of cancer, particularly skin cancer and lymphoma.
Healthcare professionals must carefully monitor patients taking azathioprine for these potential side effects. They may need to adjust the dosage or stop the medication altogether if serious side effects occur. Patients should also take steps to reduce their risk of infection and skin cancer, such as practicing good hygiene, avoiding sun exposure, and using sunscreen.
Thionucleosides are a type of modified nucleoside where the oxygen atom in the sugar component (ribose or deoxyribose) is replaced by a sulfur atom. This modification can occur naturally or be introduced synthetically. The resulting compounds have been studied for their potential biological activity, including antiviral and anticancer properties. However, they are not typically used as a standard medical treatment at this time.
Daunorubicin is an anthracycline antibiotic used in the treatment of various types of cancer, including leukemia, Hodgkin's lymphoma, and breast cancer. It works by intercalating with DNA and inhibiting topoisomerase II, which results in DNA damage and ultimately cell death.
The drug is administered intravenously and may cause side effects such as nausea, vomiting, hair loss, mouth sores, and damage to the heart muscle (cardiotoxicity) with long-term use. Regular monitoring of cardiac function is recommended during treatment with daunorubicin.
It's important to note that this medication should only be used under the supervision of a qualified healthcare professional, as it can have serious and potentially life-threatening consequences if not used correctly.
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.
Methyltransferases are a class of enzymes that catalyze the transfer of a methyl group (-CH3) from a donor molecule to an acceptor molecule, which is often a protein, DNA, or RNA. This transfer of a methyl group can modify the chemical and physical properties of the acceptor molecule, playing a crucial role in various cellular processes such as gene expression, signal transduction, and DNA repair.
In biochemistry, methyltransferases are classified based on the type of donor molecule they use for the transfer of the methyl group. The most common methyl donor is S-adenosylmethionine (SAM), a universal methyl group donor found in many organisms. Methyltransferases that utilize SAM as a cofactor are called SAM-dependent methyltransferases.
Abnormal regulation or function of methyltransferases has been implicated in several diseases, including cancer and neurological disorders. Therefore, understanding the structure, function, and regulation of these enzymes is essential for developing targeted therapies to treat these conditions.
Antimetabolites are a class of antineoplastic (chemotherapy) drugs that interfere with the metabolism of cancer cells and inhibit their growth and proliferation. These agents are structurally similar to naturally occurring metabolites, such as amino acids, nucleotides, and folic acid, which are essential for cellular replication and growth. Antimetabolites act as false analogs and get incorporated into the growing cells' DNA or RNA, causing disruption of the normal synthesis process, leading to cell cycle arrest and apoptosis (programmed cell death).
Examples of antimetabolite drugs include:
1. Folate antagonists: Methotrexate, Pemetrexed
2. Purine analogs: Mercaptopurine, Thioguanine, Fludarabine, Cladribine
3. Pyrimidine analogs: 5-Fluorouracil (5-FU), Capecitabine, Cytarabine, Gemcitabine
These drugs are used to treat various types of cancers, such as leukemias, lymphomas, breast, ovarian, and gastrointestinal cancers. Due to their mechanism of action, antimetabolites can also affect normal, rapidly dividing cells in the body, leading to side effects like myelosuppression (decreased production of blood cells), mucositis (inflammation and ulceration of the gastrointestinal tract), and alopecia (hair loss).
Azacitidine is a chemotherapeutic agent that is used in the treatment of myelodysplastic syndrome, a type of cancer where the bone marrow does not produce enough healthy blood cells. It is an antimetabolite that inhibits DNA methylation and RNA synthesis, which can help to restore normal cell function and reduce the production of abnormal cells in the bone marrow. Azacitidine is administered by injection or infusion and is typically given in cycles, with treatment repeated every 4 weeks. Common side effects include nausea, vomiting, diarrhea, constipation, and fatigue.
Guanine nucleotides are molecules that play a crucial role in intracellular signaling, cellular regulation, and various biological processes within cells. They consist of a guanine base, a sugar (ribose or deoxyribose), and one or more phosphate groups. The most common guanine nucleotides are GDP (guanosine diphosphate) and GTP (guanosine triphosphate).
GTP is hydrolyzed to GDP and inorganic phosphate by certain enzymes called GTPases, releasing energy that drives various cellular functions such as protein synthesis, signal transduction, vesicle transport, and cell division. On the other hand, GDP can be rephosphorylated back to GTP by nucleotide diphosphate kinases, allowing for the recycling of these molecules within the cell.
In addition to their role in signaling and regulation, guanine nucleotides also serve as building blocks for RNA (ribonucleic acid) synthesis during transcription, where they pair with cytosine nucleotides via hydrogen bonds to form base pairs in the resulting RNA molecule.
Hypoxanthine is not a medical condition but a purine base that is a component of many organic compounds, including nucleotides and nucleic acids, which are the building blocks of DNA and RNA. In the body, hypoxanthine is produced as a byproduct of normal cellular metabolism and is converted to xanthine and then uric acid, which is excreted in the urine.
However, abnormally high levels of hypoxanthine in the body can indicate tissue damage or disease. For example, during intense exercise or hypoxia (low oxygen levels), cells may break down ATP (adenosine triphosphate) rapidly, releasing large amounts of hypoxanthine. Similarly, in some genetic disorders such as Lesch-Nyhan syndrome, there is an accumulation of hypoxanthine due to a deficiency of the enzyme that converts it to xanthine. High levels of hypoxanthine can lead to the formation of kidney stones and other complications.
Purines are heterocyclic aromatic organic compounds that consist of a pyrimidine ring fused to an imidazole ring. They are fundamental components of nucleotides, which are the building blocks of DNA and RNA. In the body, purines can be synthesized endogenously or obtained through dietary sources such as meat, seafood, and certain vegetables.
Once purines are metabolized, they are broken down into uric acid, which is excreted by the kidneys. Elevated levels of uric acid in the body can lead to the formation of uric acid crystals, resulting in conditions such as gout or kidney stones. Therefore, maintaining a balanced intake of purine-rich foods and ensuring proper kidney function are essential for overall health.
Thionucleotides are chemical compounds that are analogs of nucleotides, which are the building blocks of DNA and RNA. In thionucleotides, one or more of the oxygen atoms in the nucleotide's chemical structure is replaced by a sulfur atom. This modification can affect the way the thionucleotide interacts with other molecules, including enzymes that work with nucleotides and nucleic acids.
Thionucleotides are sometimes used in research to study the biochemistry of nucleic acids and their interactions with other molecules. They can also be used as inhibitors of certain enzymes, such as reverse transcriptase, which is an important target for HIV/AIDS therapy. However, thionucleotides are not normally found in natural biological systems and are not themselves components of DNA or RNA.
DCMP deaminase is an enzyme that catalyzes the deamination of deoxycytidine monophosphate (dCMP) to deoxyuridine monophosphate (dUMP). This reaction is a part of the pyrimidine nucleotide biosynthesis pathway. The enzyme's systematic name is "deoxycytidine monophosphate deaminase." It plays a crucial role in DNA synthesis and maintenance by providing the necessary precursor (dUMP) for thymidylate synthesis, which is essential for the production of thymidine triphosphate (dTTP), one of the four building blocks of DNA.
I'm sorry for any confusion, but "Mitolactol" is not a recognized term in medical terminology or pharmacology. It's possible that there may be a spelling error or it could be a brand name of a medication that is not widely known or used internationally. If you have more context or information about where this term was found, I'd be happy to help further research the term for you.
Mutagens are physical or chemical agents that can cause permanent changes in the structure of genetic material, including DNA and chromosomes, leading to mutations. These mutations can be passed down to future generations and may increase the risk of cancer and other diseases. Examples of mutagens include ultraviolet (UV) radiation, tobacco smoke, and certain chemicals found in industrial settings. It is important to note that not all mutations are harmful, but some can have negative effects on health and development.
Guanine is not a medical term per se, but it is a biological molecule that plays a crucial role in the body. Guanine is one of the four nucleobases found in the nucleic acids DNA and RNA, along with adenine, cytosine, and thymine (in DNA) or uracil (in RNA). Specifically, guanine pairs with cytosine via hydrogen bonds to form a base pair.
Guanine is a purine derivative, which means it has a double-ring structure. It is formed through the synthesis of simpler molecules in the body and is an essential component of genetic material. Guanine's chemical formula is C5H5N5O.
While guanine itself is not a medical term, abnormalities or mutations in genes that contain guanine nucleotides can lead to various medical conditions, including genetic disorders and cancer.
Drug resistance, also known as antimicrobial resistance, is the ability of a microorganism (such as bacteria, viruses, fungi, or parasites) to withstand the effects of a drug that was originally designed to inhibit or kill it. This occurs when the microorganism undergoes genetic changes that allow it to survive in the presence of the drug. As a result, the drug becomes less effective or even completely ineffective at treating infections caused by these resistant organisms.
Drug resistance can develop through various mechanisms, including mutations in the genes responsible for producing the target protein of the drug, alteration of the drug's target site, modification or destruction of the drug by enzymes produced by the microorganism, and active efflux of the drug from the cell.
The emergence and spread of drug-resistant microorganisms pose significant challenges in medical treatment, as they can lead to increased morbidity, mortality, and healthcare costs. The overuse and misuse of antimicrobial agents, as well as poor infection control practices, contribute to the development and dissemination of drug-resistant strains. To address this issue, it is crucial to promote prudent use of antimicrobials, enhance surveillance and monitoring of resistance patterns, invest in research and development of new antimicrobial agents, and strengthen infection prevention and control measures.
2-Aminopurine is a fluorescent purine analog, which means it is a compound that is similar in structure to the naturally occurring molecule called purines, which are building blocks of DNA and RNA. 2-Aminopurine is used in research to study the structure and function of nucleic acids (DNA and RNA) due to its fluorescent properties. It can be incorporated into oligonucleotides (short stretches of nucleic acids) to allow for the monitoring of interactions between nucleic acids, such as during DNA replication or transcription. The fluorescence of 2-Aminopurine changes upon excitation with light and can be used to detect structural changes in nucleic acids or to measure the distance between two fluorophores.
Precursor Cell Lymphoblastic Leukemia-Lymphoma (previously known as Precursor T-lymphoblastic Leukemia/Lymphoma) is a type of cancer that affects the early stages of T-cell development. It is a subtype of acute lymphoblastic leukemia (ALL), which is characterized by the overproduction of immature white blood cells called lymphoblasts in the bone marrow, blood, and other organs.
In Precursor Cell Lymphoblastic Leukemia-Lymphoma, these abnormal lymphoblasts accumulate primarily in the lymphoid tissues such as the thymus and lymph nodes, leading to the enlargement of these organs. This subtype is more aggressive than other forms of ALL and has a higher risk of spreading to the central nervous system (CNS).
The medical definition of Precursor Cell Lymphoblastic Leukemia-Lymphoma includes:
1. A malignant neoplasm of immature T-cell precursors, also known as lymphoblasts.
2. Characterized by the proliferation and accumulation of these abnormal cells in the bone marrow, blood, and lymphoid tissues such as the thymus and lymph nodes.
3. Often associated with chromosomal abnormalities, genetic mutations, or aberrant gene expression that contribute to its aggressive behavior and poor prognosis.
4. Typically presents with symptoms related to bone marrow failure (anemia, neutropenia, thrombocytopenia), lymphadenopathy (swollen lymph nodes), hepatosplenomegaly (enlarged liver and spleen), and potential CNS involvement.
5. Diagnosed through a combination of clinical evaluation, imaging studies, and laboratory tests, including bone marrow aspiration and biopsy, immunophenotyping, cytogenetic analysis, and molecular genetic testing.
6. Treated with intensive multi-agent chemotherapy regimens, often combined with radiation therapy and/or stem cell transplantation to achieve remission and improve survival outcomes.
Purine nucleotides are fundamental units of life that play crucial roles in various biological processes. A purine nucleotide is a type of nucleotide, which is the basic building block of nucleic acids such as DNA and RNA. Nucleotides consist of a nitrogenous base, a pentose sugar, and at least one phosphate group.
In purine nucleotides, the nitrogenous bases are either adenine (A) or guanine (G). These bases are attached to a five-carbon sugar called ribose in the case of RNA or deoxyribose for DNA. The sugar and base together form the nucleoside, while the addition of one or more phosphate groups creates the nucleotide.
Purine nucleotides have several vital functions within cells:
1. Energy currency: Adenosine triphosphate (ATP) is a purine nucleotide that serves as the primary energy currency in cells, storing and transferring chemical energy for various cellular processes.
2. Genetic material: Both DNA and RNA contain purine nucleotides as essential components of their structures. Adenine pairs with thymine (in DNA) or uracil (in RNA), while guanine pairs with cytosine.
3. Signaling molecules: Purine nucleotides, such as adenosine monophosphate (AMP) and cyclic adenosine monophosphate (cAMP), act as intracellular signaling molecules that regulate various cellular functions, including metabolism, gene expression, and cell growth.
4. Coenzymes: Purine nucleotides can also function as coenzymes, assisting enzymes in catalyzing biochemical reactions. For example, nicotinamide adenine dinucleotide (NAD+) is a purine nucleotide that plays a critical role in redox reactions and energy metabolism.
In summary, purine nucleotides are essential biological molecules involved in various cellular functions, including energy transfer, genetic material formation, intracellular signaling, and enzyme cofactor activity.
Acute myeloid leukemia (AML) is a type of cancer that originates in the bone marrow, the soft inner part of certain bones where new blood cells are made. In AML, the immature cells, called blasts, in the bone marrow fail to mature into normal blood cells. Instead, these blasts accumulate and interfere with the production of normal blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia).
AML is called "acute" because it can progress quickly and become severe within days or weeks without treatment. It is a type of myeloid leukemia, which means that it affects the myeloid cells in the bone marrow. Myeloid cells are a type of white blood cell that includes monocytes and granulocytes, which help fight infection and defend the body against foreign invaders.
In AML, the blasts can build up in the bone marrow and spread to other parts of the body, including the blood, lymph nodes, liver, spleen, and brain. This can cause a variety of symptoms, such as fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss.
AML is typically treated with a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the type and stage of the leukemia.
Adenine Phosphoribosyltransferase (APRT) is an enzyme that plays a crucial role in the metabolism of purines, specifically adenine, in the body. The enzyme catalyzes the conversion of adenine to AMP (adenosine monophosphate) by transferring a phosphoribosyl group from 5-phosphoribosyl-1-pyrophosphate (PRPP) to adenine.
Deficiency in APRT can lead to a rare genetic disorder known as Adenine Phosphoribosyltransferase Deficiency or APRT Deficiency. This condition results in the accumulation of 2,8-dihydroxyadenine (DHA) crystals in the renal tubules, which can cause kidney stones and chronic kidney disease. Proper diagnosis and management, including dietary modifications and medication, are essential to prevent complications associated with APRT Deficiency.
Biotransformation is the metabolic modification of a chemical compound, typically a xenobiotic (a foreign chemical substance found within an living organism), by a biological system. This process often involves enzymatic conversion of the parent compound to one or more metabolites, which may be more or less active, toxic, or mutagenic than the original substance.
In the context of pharmacology and toxicology, biotransformation is an important aspect of drug metabolism and elimination from the body. The liver is the primary site of biotransformation, but other organs such as the kidneys, lungs, and gastrointestinal tract can also play a role.
Biotransformation can occur in two phases: phase I reactions involve functionalization of the parent compound through oxidation, reduction, or hydrolysis, while phase II reactions involve conjugation of the metabolite with endogenous molecules such as glucuronic acid, sulfate, or acetate to increase its water solubility and facilitate excretion.
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MedlinePlus offers information on various health topics, including conditions, diseases, tests, treatments, and wellness. It also provides access to drug information, medical dictionary, and encyclopedia, as well as links to clinical trials, medical news, and patient organizations. The website is available in both English and Spanish and can be accessed for free.
Copyright is a legal concept that gives the creator of an original work exclusive rights to its use and distribution, usually for a limited period of time. In the medical field, copyright protection can apply to various works such as medical textbooks, journal articles, educational materials, software, and multimedia presentations. It is important to note that copyright law seeks to strike a balance between protecting the rights of creators and promoting the progress of science and knowledge by allowing for limited use of copyrighted material under certain circumstances, such as fair use.
It's worth mentioning that while copyright protection can apply to medical works, there are also exceptions and limitations to copyright law that may allow for the use of copyrighted material without permission from the copyright owner in certain situations. For example, in the United States, the "fair use" doctrine allows for limited use of copyrighted material without obtaining permission from the copyright owner, depending on factors such as the purpose and character of the use, the nature of the copyrighted work, the amount and substantiality of the portion used, and the effect of the use upon the potential market for or value of the copyrighted work.
When using medical works that are protected by copyright, it is important to obtain permission from the copyright owner or ensure that the use falls under an exception or limitation to copyright law, such as fair use, in order to avoid infringing on the exclusive rights of the copyright owner.
Patient medication knowledge, also known as patient medication literacy or medication adherence, refers to the ability of a patient to understand and effectively communicate about their medications, including what they are for, how and when to take them, potential side effects, and other important information. This is an essential component of medication management, as it allows patients to properly follow their treatment plans and achieve better health outcomes. Factors that can affect patient medication knowledge include age, education level, language barriers, and cognitive impairments. Healthcare providers play a key role in promoting patient medication knowledge by providing clear and concise instructions, using visual aids when necessary, and regularly assessing patients' understanding of their medications.
Drug Information Services (DIS) are specialized resources within healthcare systems, typically staffed by clinical pharmacists and pharmacy residents, that provide evidence-based information and analysis about medications to healthcare professionals and patients. The primary goal of DIS is to optimize medication use and improve patient outcomes through the provision of accurate, unbiased, and timely information on drug therapy.
DIS commonly provide a range of services, including:
1. Answering medication-related questions from healthcare providers, such as physicians, nurses, and other pharmacists, regarding drug interactions, dosing, adverse effects, and therapeutic alternatives.
2. Developing and maintaining formulary management systems to ensure the safe and cost-effective use of medications within a healthcare institution or system.
3. Providing patient education materials and resources on medication therapy, including proper administration techniques, potential side effects, and storage requirements.
4. Conducting ongoing literature evaluations and synthesizing evidence-based recommendations for medication use in various clinical scenarios.
5. Collaborating with healthcare teams to develop and implement guidelines, policies, and procedures related to medication management and safety.
6. Offering educational programs and resources for healthcare professionals and students to enhance their knowledge of pharmacotherapy and medication safety practices.
7. Participating in multidisciplinary committees focused on improving medication use processes, reducing medication errors, and promoting patient safety.
DIS are essential components of modern healthcare systems, as they help ensure the safe, effective, and efficient use of medications for improved patient outcomes.
A pharmaceutical society is a professional organization that represents and serves the interests of pharmacists and the pharmaceutical industry in a given society or country. The primary objective of these societies is to promote the advancement of the profession of pharmacy, including education, research, and practice. They also work to ensure the safe and effective use of medications, advocate for evidence-based policies and practices, and provide resources and support to their members.
Pharmaceutical societies may engage in various activities, such as:
1. Developing guidelines and standards for pharmacy education and practice.
2. Providing continuing education programs for pharmacists.
3. Conducting research and disseminating knowledge related to pharmacy and medication use.
4. Advocating for policies that promote the safe and effective use of medications.
5. Collaborating with other healthcare professionals, regulatory bodies, and industry partners to improve patient outcomes.
6. Providing resources and support to members, including career development opportunities and networking events.
Examples of pharmaceutical societies include the American Pharmacists Association (APhA), the Royal Pharmaceutical Society (RPS) in the UK, and the International Pharmaceutical Federation (FIP).
A non-medical internship is not specifically related to the field of medicine. It generally refers to an organized period of work experience, often temporary, in which a person typically a student or trainee, gains practical knowledge and skills in a particular industry or profession. The intern is supervised and mentored by experienced professionals in the field. Non-medical internships can be found in various sectors such as business, engineering, law, education, media, technology, and many others. They provide an opportunity to apply theoretical knowledge gained in the classroom to real-world situations and help interns develop professional competencies and networks.
I'm sorry for any confusion, but "Maryland" is a proper noun and does not have a medical definition. It is a state located in the Mid-Atlantic region of the United States. However, if you are referring to a specific medical term or concept that includes "Maryland," could you please provide more context? I'll do my best to help with accurate information based on the provided context.
Gertrude B. Elion
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Tioguanine
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George H. Hitchings
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National Cancer Institute
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Thioguanine (Thioguanine)
Thioguanine (Tabloid) | Davis's Drug Guide
Association between 6-thioguanine nucleotide levels and preventing production of antibodies to infliximab in patients with...
Table of Pharmacogenetic Associations | FDA
Tioguanine - Side Effects, Precautions and Contraindications
The continuous rediscovery and the benefit-risk ratio of thioguanine, a comprehensive review<...
Gertrude B. Elion - Wikipedia
Table 2 - Analysis of MarketScan Data for Immunosuppressive Conditions and Hospitalizations for Acute Respiratory Illness,...
Search for a Test by Disorder | Molecular Genetics Laboratory
Prognosis
6‐thioguanine nucleotide monitoring in azathioprine and mercaptopurine monotherapy for the treatment of inflammatory bowel...
Thioguanine used in maintenance therapy of chronic myeloid leukaemia causes non-cirrhotic portal hypertension. Results from MRC...
MeSH Browser
Remicade - Uses, Side Effects, Interactions - MedBroadcast.com
Drugs beginning with T: MedlinePlus Drug Information
Drugs - Drug and supplement information - MayoClinic.org
Chemotherapy in Children | CureSearch
Registration Dossier - ECHA
Pharmacogenomic Screening
Sodium Nitroprusside inhibits HEK293 Cell Growth by cGMP-Dependent and Independent Mechanisms
Psoriasis - Dermatologic Disorders - Merck Manuals Professional Edition
Trp-P-2 Summary Report | CureHunter
Registration Dossier - ECHA
Combination Chemotherapy in Treating Children or Adolescents With Newly Diagnosed Stage III or Stage IV Lymphoblastic Lymphoma
BW5147.G.1.4.OUA/R.1 85082302 | Sigma-Aldrich
Registration Dossier - ECHA
Drug Summary
Clinical Professor Murray Barclay, Our people, University of Otago, Christchurch | University of Otago
Mercaptopurine3
- Introduction: In the 1950s, thioguanine (TG), a thiopurine-derivative together with azathioprine (AZA) and mercaptopurine (MP), were developed for the treatment of childhood leukemia. (amsterdamumc.org)
- Should thiopurine methyltransferase (TPMT) activity be determined before prescribing azathioprine, mercaptopurine, or thioguanine? (ccjm.org)
- It is necessary to test TPMT because it is an important enzyme which metabolizes thiopurine drugs such as azathioprine, mercaptopurine, and thioguanine. (bookwormlab.com)
Nucleotide2
- Serial clinical response, thiopurine methyl transferase (TPMT) activity and thioguanine nucleotide (TGN) concentrations were measured over 6 months. (nih.gov)
- a polymorphism, 6-thioguanine nucleotide (6-TGN) concentration and toxicity. (bvsalud.org)
20231
- 2023. https://www.drugguide.com/ddo/view/Davis-Drug-Guide/51736/all/thioguanine. (drugguide.com)
Purine1
- Thioguanine is a purine analog with antineoplastic and antimetabolite properties. (medscape.com)
Tioguanine2
- What side effects can Thioguanine (Tioguanine) cause? (nni.com.sg)
- Before taking Thioguanine (Tioguanine) , what precautions must I follow? (nni.com.sg)
Mutagenicity1
- The same welding fume sample was used for a mutagenicity test (resistance to 6-thioguanine) with V 79 hamster cells. (sjweh.fi)
Gene mutation1
- Diesel exhaust particulate matter dispersed in a phospholipid surfactant induces chromosomal aberrations and micronuclei but not 6-thioguanine-resistant gene mutation in V79 cells. (cdc.gov)
Toxicity1
- Thioguanine toxicity, especially myelotoxicity, and hepatotoxicity, including nodular regenerative hyperplasia (NRH) of the liver, is limited when dosed adequately. (amsterdamumc.org)
Clinical1
- Expert opinion: Thioguanine has shown beneficial clinical effects in hematological (particularly leukemia) and several immune-inflammatory diseases including psoriasis, SLE, polycythemia vera, Churg-Strauss syndrome, IBD, collagenous sprue, refractory celiac disease, and autoimmune hepatitis. (amsterdamumc.org)
Resistant2
- The cells are resistant to 100μM thioguanine and 1mM ouabain. (sigmaaldrich.com)
- In Chinese hamster cells, arsenite did not induce ouabain-resistant mutants or thioguanine-resistant mutants. (europa.eu)
Patients1
- Portal hypertension with varices developed in 18/675 patients with chronic myeloid leukaemia (CML) in a randomized trial comparing busulphan with busulphan and thioguanine. (ox.ac.uk)
Side1
- Possible side effects from Thioguanine and their management are listed below. (nni.com.sg)
Portal2
Side effects of thioguanine1
- you should know that the risk that you will develop serious side effects of thioguanine may be higher if you have a genetic (inherited) risk factor. (medlineplus.gov)
Azathioprine3
- This form of hepatotoxicity appears to be idiosyncratic and a class effect of the thiopurines, although more typical of azathioprine than thioguanine or mercaptopurine. (nih.gov)
- There is a growing interest in the use of thiopurines (azathioprine, 6-mercaptopurine and 6-thioguanine) for the management of inflammatory bowel disease. (eur.nl)
- On theoretical basis, 6-thioguanine might therefore have a more predictable profile than azathioprine and 6-mercaptopurine. (eur.nl)
Nucleotides2
- The median 6-thioguanine nucleotides and thiopurine methyltransferase levels were 953 (IQR, 145-1761) pmoL/8×10 5 RBC and 47 (IQR, 34.5-96) mU/L, respectively. (medscape.com)
- Observations included regular measures of ANC, as well as erythrocyte concentrations of MTX (E-MTX) and thioguanine nucleotides (E-TGN). (news-medical.net)
Hepatotoxicity3
- As with other thiopurines, thioguanine has been associated with several forms of hepatotoxicity, including mild, transient and asymptomatic rises in serum aminotransferase levels, an acute hepatic injury developing during the first year of starting therapy, and a chronic hepatic injury marked by variable degrees of peliosis hepatis, veno-occlusive disease and/or nodular regenerative hyperplasia. (nih.gov)
- The chronic thioguanine hepatotoxicity typically presents with fatigue and signs and symptoms of portal hypertension with mild liver enzyme abnormalities and minimal jaundice arising 6 months to many years after starting thioguanine. (nih.gov)
- 16. Hepatotoxicity during 6-thioguanine treatment in inflammatory bowel disease and childhood acute lymphoblastic leukaemia: A systematic review. (nih.gov)
Thiopurine methyltransferase3
- Two enzymes in the body called thiopurine methyltransferase (TPMT) and nudix type motif 15 (NUDT15) have the ability to break down certain medicines, including thioguanine. (stjude.org)
- For information about both TPMT and NUDT15 and their effect on thioguanine, talk with your doctor or pharmacist, and see " Do You Know… Thiopurine methyltransferase (TPMT) and medicines . (stjude.org)
- 15. The thiopurine methyltransferase genetic polymorphism is associated with thioguanine-related veno-occlusive disease of the liver in children with acute lymphoblastic leukemia. (nih.gov)
Inflammatory bowel d2
- Other topics discussed in this review are the utilisation of therapeutic drug monitoring and the experimental use of 6-thioguanine in the treatment of inflammatory bowel disease. (eur.nl)
- Further research is warranted before 6-thioguanine can be considered as a treatment option for inflammatory bowel disease. (eur.nl)
Veno-occlusi2
- 14. Oral 6-mercaptopurine versus oral 6-thioguanine and veno-occlusive disease in children with standard-risk acute lymphoblastic leukemia: report of the Children's Oncology Group CCG-1952 clinical trial. (nih.gov)
- However, the use of 6-thioguanine has been associated with an increased risk of nodular regenerative hyperplasia of the liver and veno-occlusive disease. (eur.nl)
Efficacy and Safety2
- Efficacy and Safety of Thioguanine as Maintenance Treatment for IBD - Medscape - 16 September 2020. (medscape.com)
- 1. Clinical efficacy and safety of 6-thioguanine in the treatment of childhood acute lymphoblastic leukemia: A protocol for systematic review and meta-analysis. (nih.gov)
Guanine4
- Thioguanine, known chemically as 2-amino-1,7-dihydro-6 H -purine-6-thione, is an analogue of the nucleic acid constituent guanine, and is closely related structurally and functionally to PURINETHOL ® (mercaptopurine). (nih.gov)
- With the 5-dose schedule, from one-half to virtually all of the guanine in the residual DNA was replaced by thioguanine. (nih.gov)
- Thioguanine competes with hypoxanthine and guanine for the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) and is itself converted to 6-thioguanylic acid (TGMP). (nih.gov)
- The end point used was the induction of mutations in the hypoxanthine-guanine phosphoribosyltransferase (HGPRT) locus, selected using 6-thioguanine resistance (TGr). (nih.gov)
Anticancer3
- Thioguanine (also called 6-TG or 6-thioguanine) is an anticancer medicine. (stjude.org)
- Anticancer nucleobase analogues 6-mercaptopurine and 6-thioguanine are novel substrates for equilibrative nucleoside transporter 2. (bvsalud.org)
- Mercaptopurine and thioguanine are anticancer and immunosuppressive agents that exert their primary cytotoxic effects via incorporation of deoxythioguanosine (dG s ) into DNA, but the precise mechanism(s) by which this causes cytotoxicity remains unknown. (aspetjournals.org)
TABLOID4
- TABLOID brand Thioguanine is a potent drug. (nih.gov)
- TABLOID brand Thioguanine was synthesized and developed by Hitchings, Elion, and associates at the Wellcome Research Laboratories. (nih.gov)
- TABLOID brand Thioguanine is available in tablets for oral administration. (nih.gov)
- Thioguanine is available generically and under the brand name of Tabloid as tablets of 40 mg. (nih.gov)
Immunosuppressive1
- 6-Thioguanine (6-TG) is a cytotoxic agent with immunosuppressive and antitumor properties. (tcichemicals.com)
Nodular regenerativ1
- Thioguanine therapy is associated with minor, usually transient and asymptomatic elevations in serum aminotransferase levels and has also been linked to rare instances of cholestatic acute liver injury and to chronic liver injury, resulting in portal hypertension due to nodular regenerative hyperplasia. (nih.gov)
Therapeutic1
- No measurements have been made of thioguanine concentrations in human cerebrospinal fluid (CSF), but observations on tissue distribution in animals, together with the lack of CNS penetration by the closely related compound, mercaptopurine, suggest that thioguanine does not reach therapeutic concentrations in the CSF. (nih.gov)
Metabolites1
- More significantly, thioguanine enters rapidly into the anabolic and catabolic pathways for purines, and the active intracellular metabolites have appreciably longer half-lives than the parent drug. (nih.gov)
Thye1
- Thioguanine (thye" oh gwa' neen) is a thiopurine, a purine analogue and antimetabolite. (nih.gov)
Tablets2
- tell your doctor and pharmacist if you are allergic to thioguanine, any other medications, or any of the ingredients in thioguanine tablets. (medlineplus.gov)
- Store thioguanine tablets and liquid at room temperature in a dry place. (stjude.org)
Quantification1
- Quantification of thioguanine-resistant lymphocytes from mice irradiated in vivo. (nih.gov)
Metabolism3
- ALT elevations as well as myelotoxicity have been linked to higher levels of methyl-mercaptopurine, a product of one of the metabolic pathways of thioguanine metabolism. (nih.gov)
- 13. Pharmacokinetics and metabolism of thiopurines in children with acute lymphoblastic leukemia receiving 6-thioguanine versus 6-mercaptopurine. (nih.gov)
- 6-Thioguanine has a less genetically controlled metabolism and skips genetically determined metabolic steps. (eur.nl)
Dose5
- Your doctor may increase or decrease your dose of thioguanine during your treatment. (medlineplus.gov)
- Although initial plasma levels of thioguanine did correlate with the dose level, there was no correlation between the plasma half-disappearance time and the dose. (nih.gov)
- Studies with intravenous 35 S-6-thioguanine have shown that the amount of thioguanine incorporated into nucleic acids is more than 100 times higher after 5 daily doses than after a single dose. (nih.gov)
- The biochemical effects of a single dose of thioguanine are evident long after the parent drug has disappeared from plasma. (nih.gov)
- 7. Thiopurine Enhanced ALL Maintenance (TEAM): study protocol for a randomized study to evaluate the improvement in disease-free survival by adding very low dose 6-thioguanine to 6-mercaptopurine/methotrexate-based maintenance therapy in pediatric and adult patients (0-45 years) with newly diagnosed B-cell precursor or T-cell acute lymphoblastic leukemia treated according to the intermediate risk-high group of the ALLTogether1 protocol. (nih.gov)
Acute5
- Thioguanine (also referred to as 6-thioguanine and as tioguanine) is a purine analogue that is used in the therapy of acute and chronic myelogenous leukemias. (nih.gov)
- Thioguanine was approved for use in the United States in 1966 and is commonly used in the therapy of acute and chronic myelogenous (nonlymphocytic) leukemias. (nih.gov)
- The acute hepatic injury due to thioguanine usually presents with fatigue and jaundice and with a mixed hepatocellular-cholestatic pattern of serum enzyme elevations after 2 to 12 months of starting therapy. (nih.gov)
- We developed an assay to measure DNA-incorporated 6-thioguanine (DNA-TG) and validated its clinical applicability in Korean pediatric patients with acute lymphoblastic leukemia (ALL) in order to improve individualized thiopurine treatment and reduce the life-threatening cytotoxicity. (annlabmed.org)
- 5. Substitution of oral and intravenous thioguanine for mercaptopurine in a treatment regimen for children with standard risk acute lymphoblastic leukemia: a collaborative Children's Oncology Group/National Cancer Institute pilot trial (CCG-1942). (nih.gov)
Etoposide1
- Determine the presence of the promyelocyte-retinoic acid receptor alpha (PML-RARa) transcript using polymerase chain reaction (PCR) in patients with CR after 3 sequential consolidation regimens comprising cytarabine (ARA-C) plus IDA, followed by mitoxantrone plus etoposide, and then IDA, ARA-C, and thioguanine. (knowcancer.com)
Liver1
- Also tell your doctor and pharmacist about all the medications you are taking so they can check whether any of your medications may increase the risk that you will develop liver damage during your treatment with thioguanine. (medlineplus.gov)
Substitution1
- 6-thioguanine substitution in duplexes, triplexes, and tetraplexes. (ub.es)
Mice2
HGPRT1
- Do radiation-induced thioguanine-resistant mutants of cultured mammalian cells arise by HGPRT gene mutation or X-chromosome rearrangement? (wikidata.org)
Leukaemia1
- Thioguanine used in maintenance therapy of chronic myeloid leukaemia causes non-cirrhotic portal hypertension. (nih.gov)
Portal hypertension1
- Chronic injury typically arises 1 to 5 years after starting thioguanine and can present insidiously with signs and symptoms of portal hypertension. (nih.gov)
Doses2
- If your body breaks down the medicine slower than most people, you should receive lower doses of thioguanine. (stjude.org)
- Mild serum aminotransferase elevations can occur during thioguanine therapy, particularly with high doses during the first 12 weeks of therapy. (nih.gov)
Drugs1
- Gertrude is responsible for the synthesis and co-development of the first two successful drugs for the treatment of leukemia (thioguanine and mercaptopurine). (witi.com)
Diseases1
- Thioguanine has also been used off-label to treat autoimmune diseases as a steroid sparing agent. (nih.gov)
Tablet3
- Thioguanine comes as a tablet to take by mouth usually once a day. (medlineplus.gov)
- Each scored tablet contains 40 mg thioguanine and the inactive ingredients acacia, lactose monohydrate, magnesium stearate, potato starch, and stearic acid. (nih.gov)
- Thioguanine is available as a beige 40-mg tablet and as an oral liquid taken by mouth. (stjude.org)
Determine1
- In Mayo , the level of 6-thioguanine was measured to determine whether the patient needed more thiopurine drug. (patentlyo.com)
Treatment2
- Drink plenty of fluids during your treatment with thioguanine. (medlineplus.gov)
- 2. Thioguanine offers no advantage over mercaptopurine in maintenance treatment of childhood ALL: results of the randomized trial COALL-92. (nih.gov)
Drug1
- The oral administration of radiolabeled thioguanine revealed only trace quantities of parent drug in the urine. (nih.gov)
Pregnant2
- You should not become pregnant or breast-feed while you are receiving thioguanine. (medlineplus.gov)
- If you become pregnant while receiving thioguanine, call your doctor. (medlineplus.gov)
Search1
- Your search for THIOGUANINE ANHYDROUS did not return any results. (nih.gov)
Oral3
- Following oral administration of 35 S-6-thioguanine, total plasma radioactivity reached a maximum at 8 hours and declined slowly thereafter. (nih.gov)
- thioguanine decreases effects of adenovirus types 4 and 7 live, oral by pharmacodynamic antagonism. (medscape.com)
- Third consolidation:Within 4-6 weeks after initiation of second consolidation, patients receive ARA-C subcutaneously every 8 hours and oral thioguanine every 8 hours on days 1-5 and IDA IV over 15 minutes on day 1. (knowcancer.com)
Effects2
- Thioguanine may cause side effects. (medlineplus.gov)
- thioguanine decreases effects of influenza virus vaccine quadrivalent, adjuvanted by pharmacodynamic antagonism. (medscape.com)
Levels2
- Monitoring of plasma levels of thioguanine during therapy is of questionable value. (nih.gov)
- Although the link between body-levels of 6-thioguanine and thiopurine was an important discovery, that link was an unpatentable law of nature. (patentlyo.com)
Bone1
- Thioguanine is incorporated into the DNA and the RNA of human bone marrow cells. (nih.gov)
Therapy1
- This syndrome can progress to hepatic failure, particularly if thioguanine is continued, but improvement on stopping therapy is typical. (nih.gov)
Human1
- Induction of thioguanine-resistant mutations in human uroepithelial cells by 4-aminobiphenyl and its N-hydroxy derivatives. (nih.gov)
Medicine1
- The doctor can prescribe medicine to keep you from feeling sick and throwing up while you are taking thioguanine. (stjude.org)
Treat1
- tell your doctor if you have already taken thioguanine or mercaptopurine to treat your cancer. (medlineplus.gov)