A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
Polyacenes with four ortho-fused benzene rings in a straight linear arrangement. This group is best known for the subclass called TETRACYCLINES.
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)
An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.
A 170-kDa transmembrane glycoprotein from the superfamily of ATP-BINDING CASSETTE TRANSPORTERS. It serves as an ATP-dependent efflux pump for a variety of chemicals, including many ANTINEOPLASTIC AGENTS. Overexpression of this glycoprotein is associated with multidrug resistance (see DRUG RESISTANCE, MULTIPLE).
Organic compounds that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
Simultaneous resistance to several structurally and functionally distinct drugs.
An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.
A calcium channel blocker that is a class IV anti-arrhythmia agent.
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.
A group of closely related cyclic undecapeptides from the fungi Trichoderma polysporum and Cylindocarpon lucidum. They have some antineoplastic and antifungal action and significant immunosuppressive effects. Cyclosporins have been proposed as adjuvants in tissue and organ transplantation to suppress graft rejection.
An anthracycline produced by Streptomyces galilaeus. It has potent antineoplastic activity.
A transplantable, poorly differentiated malignant tumor which appeared originally as a spontaneous breast carcinoma in a mouse. It grows in both solid and ascitic forms.
An antimitotic agent with immunosuppressive properties.
Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.
Therapeutic act or process that initiates a response to a complete or partial remission level.
An anthracenedione-derived antineoplastic agent.
A genus of bacteria that form a nonfragmented aerial mycelium. Many species have been identified with some being pathogenic. This genus is responsible for producing a majority of the ANTI-BACTERIAL AGENTS of practical value.
An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.)
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
A hydrolase enzyme that converts L-asparagine and water to L-aspartate and NH3. EC 3.5.1.1.
Artificial, single or multilaminar vesicles (made from lecithins or other lipids) that are used for the delivery of a variety of biological molecules or molecular complexes to cells, for example, drug delivery and gene transfer. They are also used to study membranes and membrane proteins.
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
Compounds with a five-membered heterocyclic ring with two nitrogens and a keto OXYGEN. Some are inhibitors of TNF-ALPHA production.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Compounds based on ANTHRACENES which contain two KETONES in any position. Substitutions can be in any position except on the ketone groups.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Phenomena and pharmaceutics of compounds that selectively bind to a specific receptor and trigger a response. They mimic the action of endogenous biochemical molecules. Their effect can be countered by antagonists (DRUG ANTAGONISM).
Drug treatment designed to further diminish the disease toward complete remission following INDUCTION CHEMOTHERAPY. It helps to consolidate the gains during induction chemotherapy and may be followed by MAINTENANCE CHEMOTHERAPY.
An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.
Genes for MEMBRANE TRANSPORT PROTEINS that confer resistance to toxic compounds. Several superfamilies of these multidrug export proteins are known and found in both prokaryotes and eukaryotes.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
A sequence-related subfamily of ATP-BINDING CASSETTE TRANSPORTERS that actively transport organic substrates. Although considered organic anion transporters, a subset of proteins in this family have also been shown to convey drug resistance to neutral organic drugs. Their cellular function may have clinical significance for CHEMOTHERAPY in that they transport a variety of ANTINEOPLASTIC AGENTS. Overexpression of proteins in this class by NEOPLASMS is considered a possible mechanism in the development of multidrug resistance (DRUG RESISTANCE, MULTIPLE). Although similar in function to P-GLYCOPROTEINS, the proteins in this class share little sequence homology to the p-glycoprotein family of proteins.
A fluorescent probe with low toxicity which is a potent substrate for P-glycoprotein and the bacterial multidrug efflux transporter. It is used to assess mitochondrial bioenergetics in living cells and to measure the efflux activity of P-glycoprotein in both normal and malignant cells. (Leukemia 1997;11(7):1124-30)
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
ISOQUINOLINES with a benzyl substituent.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
Disease having a short and relatively severe course.
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
Inorganic compounds that contain silicon as an integral part of the molecule.

Daunorubicin-induced apoptosis in rat cardiac myocytes is inhibited by dexrazoxane. (1/1295)

-The clinical efficacy of anthracycline antineoplastic agents is limited by a high incidence of severe and usually irreversible cardiac toxicity, the cause of which remains controversial. In primary cultures of neonatal and adult rat ventricular myocytes, we found that daunorubicin, at concentrations /=10 micromol/L induced necrotic cell death within 24 hours, with no changes characteristic of apoptosis. To determine whether reactive oxygen species play a role in daunorubicin-mediated apoptosis, we monitored the generation of hydrogen peroxide with dichlorofluorescein (DCF). However, daunorubicin (1 micromol/L) did not increase DCF fluorescence, nor were the antioxidants N-acetylcysteine or the combination of alpha-tocopherol and ascorbic acid able to prevent apoptosis. In contrast, dexrazoxane (10 micromol/L), known clinically to limit anthracycline cardiac toxicity, prevented daunorubicin-induced myocyte apoptosis, but not necrosis induced by higher anthracycline concentrations (>/=10 micromol/L). The antiapoptotic action of dexrazoxane was mimicked by the superoxide-dismutase mimetic porphyrin manganese(II/III)tetrakis(1-methyl-4-peridyl)porphyrin (50 micromol/L). The recognition that anthracycline-induced cardiac myocyte apoptosis, perhaps mediated by superoxide anion generation, occurs at concentrations well below those that result in myocyte necrosis, may aid in the design of new therapeutic strategies to limit the toxicity of these drugs.  (+info)

The ras oncogene-mediated sensitization of human cells to topoisomerase II inhibitor-induced apoptosis. (2/1295)

BACKGROUND: Among the inhibitors of the enzyme topoisomerase II (an important target for chemotherapeutic drugs) tested in the National Cancer Institute's In Vitro Antineoplastic Drug Screen, NSC 284682 (3'-hydroxydaunorubicin) and NSC 659687 [9-hydroxy-5,6-dimethyl-1-(N-[2(dimethylamino)ethyl]carbamoyl)-6H-pyrido -(4,3-b)carbazole] were the only compounds that were more cytotoxic to tumor cells harboring an activated ras oncogene than to tumor cells bearing wild-type ras alleles. Expression of the multidrug resistance proteins P-glycoprotein and MRP (multidrug resistance-associated protein) facilitates tumor cell resistance to topoisomerase II inhibitors. We investigated whether tumor cells with activated ras oncogenes showed enhanced sensitivity to other topoisomerase II inhibitors in the absence of the multidrug-resistant phenotype. METHODS: We studied 20 topoisomerase II inhibitors and individual cell lines with or without activated ras oncogenes and with varying degrees of multidrug resistance. RESULTS: In the absence of multidrug resistance, human tumor cell lines with activated ras oncogenes were uniformly more sensitive to most topoisomerase II inhibitors than were cell lines containing wild-type ras alleles. The compounds NSC 284682 and NSC 659687 were especially effective irrespective of the multidrug resistant phenotype. The ras oncogene-mediated sensitization to topoisomerase II inhibitors was far more prominent with the non-DNA-intercalating epipodophyllotoxins than with the DNA-intercalating inhibitors. This difference in sensitization appears to be related to a difference in apoptotic sensitivity, since the level of DNA damage generated by etoposide (an epipodophyllotoxin derivative) in immortalized human kidney epithelial cells expressing an activated ras oncogene was similar to that in the parental cells, but apoptosis was enhanced only in the former cells. CONCLUSIONS: Activated ras oncogenes appear to enhance the sensitivity of human tumor cells to topoisomerase II inhibitors by potentiating an apoptotic response. Epipodophyllotoxin-derived topoisomerase II inhibitors should be more effective than the DNA-intercalating inhibitors against tumor cells with activated ras oncogenes.  (+info)

Stable incorporation of a lipophilic daunorubicin prodrug into apolipoprotein E-exposing liposomes induces uptake of prodrug via low-density lipoprotein receptor in vivo. (3/1295)

Many tumors express elevated levels of low-density lipoprotein (LDL) receptors. Therefore, native LDL and synthetic LDL-like particles have been proposed as carriers for antineoplastic drugs. We demonstrated earlier that small apolipoprotein E (apoE)-exposing liposomes were specifically recognized by the LDL receptor. In this study, we incorporated a lipophilic derivative of daunorubicin (LAD) into the apoE liposomes. Up to 11 molecules of LAD could be incorporated per particle without significantly changing the size, lipid composition, and ability to bind apoE of the liposomes. The biological fate of the prodrug was largely determined by its carrier (70% of the initially incorporated LAD was still associated to the liposomes after 4 h of circulation in mice). Compared with free daunorubicin, the circulation half-life of the liposome-associated prodrug was substantially prolonged and undesired tissue disposition was reduced. The role of the LDL receptor in the metabolism of LAD-loaded apoE liposomes was demonstrated in rats with up-regulated hepatic LDL receptors. In these rats, the liver uptake of the prodrug and carrier was increased 5-fold. The addition of apoE was essential for LDL receptor-mediated uptake of the drug-carrier complex. In LDL receptor-deficient mice, the circulation time of both the prodrug and the carrier increased approximately 2-fold compared with wild-type mice. We conclude that LAD-loaded apoE liposomes constitute a stable drug-carrier complex that is well suited for LDL receptor-mediated selective drug delivery to tumors.  (+info)

Metabolism of daunorubicin by a barbiturate-sensitive aldehyde reductase from rat liver. (4/1295)

A barbiturate-sensitive aldehyde reductase was purified to homogeneity from rat liver and shown to metabolize the cancer-chemotherapeutic antibiotic daunorubicin. The aldehyde reductase may have important roles in the metabolism of exogeneous drugs as well as the aldehyde derivatives of the biogenic amines.  (+info)

Sodium salicylate activates caspases and induces apoptosis of myeloid leukemia cell lines. (5/1295)

Nonsteroidal antiinflammatory agents (NSAIA) have been shown to exert potent chemopreventive activity against colon, lung, and breast cancers. In this study, we show that at pharmacological concentrations (1 to 3 mmol/L) sodium salicylate (Na-Sal) can potently induce programmed cell death in several human myeloid leukemia cell lines, including TF-1, U937, CMK-1, HL-60, and Mo7e. TF-1 cells undergo rapid apoptosis on treatment with Na-Sal, as indicated by increased annexin V binding capacity, cpp-32 (caspase-3) activation, and cleavage of poly (ADP-ribose) polymerase (PARP) and gelsolin. In addition, the expression of MCL-1, an antiapoptotic member of the BCL-2 family, is downregulated during Na-Sal-induced cell death, whereas the expression of BCL-2, BAX, and BCL-XL is unchanged. Z-VAD, a potent caspase inhibitor, prevents the cleavage of PARP and gelsolin and rescues cells from Na-Sal-induced apoptosis. In addition, we show that Na-Sal accelerates growth factor withdrawal-induced apoptosis and synergizes with daunorubicin to induce apoptosis in TF-1 cells. Thus, our data provide a potential mechanism for the chemopreventive activity of NSAIA and suggest that salicylates may have therapeutic potential for the treatment of human leukemia.  (+info)

Selective inhibition of MDR1 P-glycoprotein-mediated transport by the acridone carboxamide derivative GG918. (6/1295)

The acridone carboxamide derivative GG918 (N-{4-[2-(1,2,3,4-tetrahydro-6,7-dimethoxy-2-isoquinolinyl)-ethyl]-pheny l}-9,10dihydro-5-methoxy-9-oxo-4-acridine carboxamide) is a potent inhibitor of MDR1 P-glycoprotein-mediated multidrug resistance. Direct measurements of ATP-dependent MDR1 P-glycoprotein-mediated transport in plasma membrane vesicles from human and rat hepatocyte canalicular membranes indicated 50% inhibition at GG918 concentrations between 8 nM and 80 nM using N-pentyl-[3H]quinidinium, ['4C]doxorubicin and [3H]daunorubicin as substrates. The inhibition constant K for GG918 was 35 nM in rat hepatocyte canalicular membrane vesicles with [3H]daunorubicin as the substrate. Photoaffinity labelling of canalicular and recombinant rat Mdr1b P-glycoprotein by [3H]azidopine was suppressed by 10 muM and 40 muM GG918. The high selectivity of GG918-induced inhibition was demonstrated in canalicular membrane vesicles and by analysis of the hepatobiliary elimination in rats using [3H]daunorubicin, [3H]taurocholate and [3H]cysteinyl leukotrienes as substrates for three distinct ATP-dependent export pumps. Almost complete inhibition of [3H]daunorubicin transport was observed at GG918 concentrations that did not affect the other hepatocyte canalicular export pumps. The high potency and selectivity of GG918 for the inhibition of human MDR1 and rat Mdr1b P-glycoprotein may serve to interfere with this type of multidrug resistance and provides a tool for studies on the function of these ATP-dependent transport proteins.  (+info)

Dual mechanism of daunorubicin-induced cell death in both sensitive and MDR-resistant HL-60 cells. (7/1295)

Exposure of some acute myeloid leukaemia (AML) cells to daunorubicin leads to rapid cell death, whereas other AML cells show natural drug resistance. This has been attributed to expression of functional P-glycoprotein resulting in reduced drug accumulation. However, it has also been proposed that P-glycoprotein-expressing multidrug-resistant (MDR) cells are inherently defective for apoptosis. To distinguish between these different possibilities, we have compared the cell death process in a human AML cell line (HL-60) with a MDR subline (HL-60/Vinc) at doses that yield either similar intracellular daunorubicin concentrations or comparable cytotoxicity. Adjustment of the dose to obtain the same intracellular drug accumulation in the two cell lines did not result in equal cytotoxicity, suggesting the presence of additional resistance mechanisms in the P-glycoprotein-expressing HL-60/Vinc cells. However, at equitoxic doses, similar cell death pathways were observed. In HL-60 cells, daunorubicin induced rapid apoptosis at 0.5-1 microM and delayed mitotic cell death at 0.1 microM. These concentrations are within the clinical dose range. Similarly, HL-60/Vinc cells underwent apoptosis at 50-100 microM daunorubicin and mitotic cell death at 10 microM. These results show, for the first time, that anthracyclines can induce cell death by a dual mechanism in both sensitive and MDR cells. Our results also show that not only the cytotoxicity, but also the kinetics and mechanism of cell death, are dose dependent. Interestingly, regrowth was observed only in association with delayed cell death and the formation of enlarged, often polyploid, cells with micronucleation, suggesting that morphological criteria may be useful to evaluate treatment efficacy in patients with myeloid leukaemias.  (+info)

ATP- and glutathione-dependent transport of chemotherapeutic drugs by the multidrug resistance protein MRP1. (8/1295)

The present study was performed to investigate the ability of the multidrug resistance protein (MRPI) to transport different cationic substrates in comparison with MDR1-P-glycoprotein (MDR1). Transport studies were performed with isolated membrane vesicles from in vitro selected multidrug resistant cell lines overexpressing MDR1 (A2780AD) or MRP1 (GLC4/Adr) and a MRP1-transfected cell line (S1(MRP)). As substrates we used 3H-labelled derivatives of the hydrophilic monoquaternary cation N-(4',4'-azo-in-pentyl)-21-deoxy-ajmalinium (APDA), the basic drug vincristine and the more hydrophobic basic drug daunorubicin. All three are known MDR1-substrates. MRP1 did not mediate transport of these substrates per se. In the presence of reduced glutathione (GSH), there was an ATP-dependent uptake of vincristine and daunorubicin, but not of APDA, into GLC4/Adr and S1(MRP) membrane vesicles which could be inhibited by the MRP1-inhibitor MK571. ATP- and GSH-dependent transport of daunorubicin and vincristine into GLC4/Adr membrane vesicles was inhibited by the MRP1-specific monoclonal antibody QCRL-3. MRP1-mediated daunorubicin transport rates were dependent on the concentration of GSH and were maximal at concentrations > or = 10 mM. The apparent KM value for GSH was 2.7 mM. Transport of daunorubicin in the presence of 10 mM GSH was inhibited by MK571 with an IC50 of 0.4 microM. In conclusion, these results demonstrate that MRP1 transports vincristine and daunorubicin in an ATP- and GSH-dependent manner. APDA is not a substrate for MRP1.  (+info)

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.

Antibiotics are a type of medication used to treat infections caused by bacteria. They work by either killing the bacteria or inhibiting their growth.

Antineoplastics, also known as chemotherapeutic agents, are a class of drugs used to treat cancer. These medications target and destroy rapidly dividing cells, such as cancer cells, although they can also affect other quickly dividing cells in the body, such as those in the hair follicles or digestive tract, which can lead to side effects.

Antibiotics and antineoplastics are two different classes of drugs with distinct mechanisms of action and uses. It is important to use them appropriately and under the guidance of a healthcare professional.

Naphthacenes are hydrocarbon compounds that consist of a naphthalene ring fused to two additional benzene rings. They belong to the class of polycyclic aromatic hydrocarbons (PAHs) and have been studied for their potential carcinogenic properties. Naphthacenes can be found in various environmental sources, including air pollution from vehicle emissions and cigarette smoke. However, it's important to note that specific medical definitions related to diseases or conditions are not typically associated with naphthacenes.

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.

Idarubicin is an anthracycline antibiotic used in the treatment of various types of cancer, including leukemia and lymphoma. It works by interfering with the DNA of cancer cells, which prevents them from dividing and growing. Idarubicin is often administered intravenously in a hospital or clinic setting. Common side effects include nausea, vomiting, hair loss, and an increased risk of infection due to lowered white blood cell counts. It can also cause damage to the heart muscle, so regular monitoring of cardiac function is necessary during treatment.

P-glycoprotein (P-gp) is a type of membrane transport protein that plays a crucial role in the efflux (extrusion) of various substrates, including drugs and toxins, out of cells. It is also known as multidrug resistance protein 1 (MDR1).

P-gp is encoded by the ABCB1 gene and is primarily located on the apical membrane of epithelial cells in several tissues, such as the intestine, liver, kidney, and blood-brain barrier. Its main function is to protect these organs from harmful substances by actively pumping them out of the cells and back into the lumen or bloodstream.

In the context of pharmacology, P-gp can contribute to multidrug resistance (MDR) in cancer cells. When overexpressed, P-gp can reduce the intracellular concentration of various anticancer drugs, making them less effective. This has led to extensive research on inhibitors of P-gp as potential adjuvants for cancer therapy.

In summary, P-glycoprotein is a vital efflux transporter that helps maintain homeostasis by removing potentially harmful substances from cells and can impact drug disposition and response in various tissues, including the intestine, liver, kidney, and blood-brain barrier.

Anthracyclines are a class of chemotherapeutic agents that are derived from the bacterium Streptomyces peucetius var. caesius. These drugs include daunorubicin, doxorubicin, epirubicin, and idarubicin. They work by intercalating into DNA and inhibiting the enzyme topoisomerase II, which leads to DNA damage and ultimately cell death. Anthracyclines are used in the treatment of a variety of cancers, including leukemias, lymphomas, breast cancer, and sarcomas. However, they can also cause cardiotoxicity, which limits their long-term use.

Doxorubicin is a type of chemotherapy medication known as an anthracycline. It works by interfering with the DNA in cancer cells, which prevents them from growing and multiplying. Doxorubicin is used to treat a wide variety of cancers, including leukemia, lymphoma, breast cancer, lung cancer, ovarian cancer, and many others. It may be given alone or in combination with other chemotherapy drugs.

Doxorubicin is usually administered through a vein (intravenously) and can cause side effects such as nausea, vomiting, hair loss, mouth sores, and increased risk of infection. It can also cause damage to the heart muscle, which can lead to heart failure in some cases. For this reason, doctors may monitor patients' heart function closely while they are receiving doxorubicin treatment.

It is important for patients to discuss the potential risks and benefits of doxorubicin therapy with their healthcare provider before starting treatment.

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.

"Multiple drug resistance" (MDR) is a term used in medicine to describe the condition where a patient's infection becomes resistant to multiple antimicrobial drugs. This means that the bacteria, virus, fungus or parasite that is causing the infection has developed the ability to survive and multiply despite being exposed to medications that were originally designed to kill or inhibit its growth.

In particular, MDR occurs when an organism becomes resistant to at least one drug in three or more antimicrobial categories. This can happen due to genetic changes in the microorganism that allow it to survive in the presence of these drugs. The development of MDR is a significant concern for public health because it limits treatment options and can make infections harder, if not impossible, to treat.

MDR can develop through several mechanisms, including mutations in the genes that encode drug targets or enzymes involved in drug metabolism, as well as the acquisition of genetic elements such as plasmids and transposons that carry resistance genes. The overuse and misuse of antimicrobial drugs are major drivers of MDR, as they create selective pressure for the emergence and spread of resistant strains.

MDR infections can occur in various settings, including hospitals, long-term care facilities, and communities. They can affect people of all ages and backgrounds, although certain populations may be at higher risk, such as those with weakened immune systems or chronic medical conditions. Preventing the spread of MDR requires a multifaceted approach that includes surveillance, infection control, antimicrobial stewardship, and research into new therapies and diagnostics.

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

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

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

Verapamil is a calcium channel blocker medication that is primarily used to treat hypertension (high blood pressure), angina (chest pain), and certain types of cardiac arrhythmias (irregular heart rhyats). It works by relaxing the smooth muscle cells in the walls of blood vessels, which causes them to dilate or widen, reducing the resistance to blood flow and thereby lowering blood pressure. Verapamil also slows down the conduction of electrical signals within the heart, which can help to regulate the heart rate and rhythm.

In addition to its cardiovascular effects, verapamil is sometimes used off-label for the treatment of other conditions such as migraine headaches, Raynaud's phenomenon, and certain types of tremors. It is available in various forms, including immediate-release tablets, extended-release capsules, and intravenous (IV) injection.

It is important to note that verapamil can interact with other medications, so it is essential to inform your healthcare provider about all the drugs you are taking before starting this medication. Additionally, verapamil should be used with caution in people with certain medical conditions, such as heart failure, liver disease, and low blood pressure.

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.

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.

Cyclosporins are a group of cyclic undecapeptides that have immunosuppressive properties. The most well-known and widely used cyclosporin is cyclosporine A, which is commonly used in organ transplantation to prevent rejection. It works by inhibiting the activation of T-cells, a type of white blood cell that plays a central role in the immune response. By suppressing the activity of T-cells, cyclosporine A reduces the risk of an immune response against the transplanted organ.

Cyclosporins are also used in the treatment of autoimmune diseases, such as rheumatoid arthritis and psoriasis, where they help to reduce inflammation and prevent damage to tissues. Like all immunosuppressive drugs, cyclosporins can increase the risk of infection and cancer, so they must be used with caution and under close medical supervision.

Aclarubicin is an anthracycline antibiotic used in cancer chemotherapy. It works by interfering with the DNA in cancer cells, preventing them from dividing and growing. Aclarubicin is often used to treat acute leukemias, lymphomas, and solid tumors.

Like other anthracyclines, aclarubicin can cause significant side effects, including damage to the heart muscle, suppression of bone marrow function, and hair loss. It may also cause nausea, vomiting, and mouth sores. Aclarubicin is usually given by injection into a vein.

It's important to note that the use of aclarubicin should be under the supervision of a healthcare professional, as its administration requires careful monitoring due to potential toxicities.

I'm sorry for any confusion, but "Carcinoma, Ehrlich Tumor" is not a recognized medical term or a valid medical definition. The term "Ehrlich tumor" is sometimes used to refer to a type of transplantable tumor that was first developed by the German physician Paul Ehrlich in the early 20th century for cancer research purposes. However, it's important to note that this type of tumor is not a naturally occurring cancer and is typically used only in laboratory experiments.

Carcinoma, on the other hand, is a medical term that refers to a type of cancer that starts in cells that line the inner or outer surfaces of organs. Carcinomas can develop in various parts of the body, including the lungs, breasts, colon, and skin.

If you have any specific questions about cancer or a particular medical condition, I would be happy to try to help answer them for you.

I'm sorry for any confusion, but "Razoxane" is not a medical term that has a widely accepted or specific definition in the field of medicine. It is possible that you may be referring to "razoxane," which is a medication used in the treatment of certain types of cancer. Razoxane is an antineoplastic agent, which means it is a drug that is used to treat cancer. It works by interfering with the formation of blood vessels that supply tumors, which can help to slow or stop the growth of the tumor.

It is important to note that the use of razoxane is not widely accepted and it is not a commonly used cancer treatment. It is typically used only in certain specific circumstances and when other treatments have not been effective. As with any medication, razoxane should be used under the close supervision of a healthcare professional, and it is important to be aware of the potential risks and benefits.

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

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

Remission induction is a treatment approach in medicine, particularly in the field of oncology and hematology. It refers to the initial phase of therapy aimed at reducing or eliminating the signs and symptoms of active disease, such as cancer or autoimmune disorders. The primary goal of remission induction is to achieve a complete response (disappearance of all detectable signs of the disease) or a partial response (a decrease in the measurable extent of the disease). This phase of treatment is often intensive and may involve the use of multiple drugs or therapies, including chemotherapy, immunotherapy, or targeted therapy. After remission induction, patients may receive additional treatments to maintain the remission and prevent relapse, known as consolidation or maintenance therapy.

Mitoxantrone is a synthetic antineoplastic anthracenedione drug, which means it is used to treat cancer. Its medical definition can be found in various authoritative sources such as the Merck Manual or Stedman's Medical Dictionary. Here's a brief version of the definition from MedlinePlus, a service of the US National Library of Medicine:

"Mitoxantrone is used to treat certain types of cancer (e.g., breast cancer, leukemia, non-Hodgkin's lymphoma). It works by slowing or stopping the growth of cancer cells. Mitoxantrone belongs to a class of drugs known as antitumor antibiotics."

Please note that this is a simplified definition meant for general information purposes and does not include all the details that might be present in a comprehensive medical definition. Always consult a healthcare professional or refer to authoritative resources for accurate, detailed, and up-to-date information.

Streptomyces is a genus of Gram-positive, aerobic, saprophytic bacteria that are widely distributed in soil, water, and decaying organic matter. They are known for their complex morphology, forming branching filaments called hyphae that can differentiate into long chains of spores.

Streptomyces species are particularly notable for their ability to produce a wide variety of bioactive secondary metabolites, including antibiotics, antifungals, and other therapeutic compounds. In fact, many important antibiotics such as streptomycin, neomycin, tetracycline, and erythromycin are derived from Streptomyces species.

Because of their industrial importance in the production of antibiotics and other bioactive compounds, Streptomyces have been extensively studied and are considered model organisms for the study of bacterial genetics, biochemistry, and ecology.

Vincristine is an antineoplastic agent, specifically a vinca alkaloid. It is derived from the Madagascar periwinkle plant (Catharanthus roseus). Vincristine binds to tubulin, a protein found in microtubules, and inhibits their polymerization, which results in disruption of mitotic spindles leading to cell cycle arrest and apoptosis (programmed cell death). It is used in the treatment of various types of cancer including leukemias, lymphomas, and solid tumors. Common side effects include peripheral neuropathy, constipation, and alopecia.

Drug resistance in neoplasms (also known as cancer drug resistance) refers to the ability of cancer cells to withstand the effects of chemotherapeutic agents or medications designed to kill or inhibit the growth of cancer cells. This can occur due to various mechanisms, including changes in the cancer cell's genetic makeup, alterations in drug targets, increased activity of drug efflux pumps, and activation of survival pathways.

Drug resistance can be intrinsic (present at the beginning of treatment) or acquired (developed during the course of treatment). It is a significant challenge in cancer therapy as it often leads to reduced treatment effectiveness, disease progression, and poor patient outcomes. Strategies to overcome drug resistance include the use of combination therapies, development of new drugs that target different mechanisms, and personalized medicine approaches that consider individual patient and tumor characteristics.

Antineoplastic combined chemotherapy protocols refer to a treatment plan for cancer that involves the use of more than one antineoplastic (chemotherapy) drug given in a specific sequence and schedule. The combination of drugs is used because they may work better together to destroy cancer cells compared to using a single agent alone. This approach can also help to reduce the likelihood of cancer cells becoming resistant to the treatment.

The choice of drugs, dose, duration, and frequency are determined by various factors such as the type and stage of cancer, patient's overall health, and potential side effects. Combination chemotherapy protocols can be used in various settings, including as a primary treatment, adjuvant therapy (given after surgery or radiation to kill any remaining cancer cells), neoadjuvant therapy (given before surgery or radiation to shrink the tumor), or palliative care (to alleviate symptoms and prolong survival).

It is important to note that while combined chemotherapy protocols can be effective in treating certain types of cancer, they can also cause significant side effects, including nausea, vomiting, hair loss, fatigue, and an increased risk of infection. Therefore, patients undergoing such treatment should be closely monitored and managed by a healthcare team experienced in administering chemotherapy.

Asparaginase is a medication that is used in the treatment of certain types of cancer, such as acute lymphoblastic leukemia (ALL) and non-Hodgkin lymphoma (NHL). It is an enzyme that breaks down the amino acid asparagine, which is a building block of proteins. Some cancer cells are unable to produce their own asparagine and rely on obtaining it from the bloodstream. By reducing the amount of asparagine in the blood, asparaginase can help to slow or stop the growth of these cancer cells.

Asparaginase is usually given as an injection into a muscle (intramuscularly) or into a vein (intravenously). It may be given alone or in combination with other chemotherapy drugs. The specific dosage and duration of treatment will depend on the individual's medical history, the type and stage of cancer being treated, and how well the person tolerates the medication.

Like all medications, asparaginase can cause side effects. Common side effects include nausea, vomiting, loss of appetite, and changes in liver function tests. Less common but more serious side effects may include allergic reactions, pancreatitis, and blood clotting problems. It is important for patients to discuss the potential risks and benefits of asparaginase with their healthcare provider before starting treatment.

Liposomes are artificially prepared, small, spherical vesicles composed of one or more lipid bilayers that enclose an aqueous compartment. They can encapsulate both hydrophilic and hydrophobic drugs, making them useful for drug delivery applications in the medical field. The lipid bilayer structure of liposomes is similar to that of biological membranes, which allows them to merge with and deliver their contents into cells. This property makes liposomes a valuable tool in delivering drugs directly to targeted sites within the body, improving drug efficacy while minimizing side effects.

HL-60 cells are a type of human promyelocytic leukemia cell line that is commonly used in scientific research. They are named after the hospital where they were first isolated, the Hospital of the University of Pennsylvania (HUP) and the 60th culture attempt to grow these cells.

HL-60 cells have the ability to differentiate into various types of blood cells, such as granulocytes, monocytes, and macrophages, when exposed to certain chemical compounds or under specific culturing conditions. This makes them a valuable tool for studying the mechanisms of cell differentiation, proliferation, and apoptosis (programmed cell death).

HL-60 cells are also often used in toxicity studies, drug discovery and development, and research on cancer, inflammation, and infectious diseases. They can be easily grown in the lab and have a stable genotype, making them ideal for use in standardized experiments and comparisons between different studies.

Pyrazolones are a group of non-steroidal anti-inflammatory drugs (NSAIDs) that contain a pyrazole ring in their chemical structure. They have analgesic, antipyretic, and anti-inflammatory properties. Pyrazolones include drugs such as phenylbutazone, oxyphenbutazone, and aminopyrine. However, due to their potential for serious side effects, including agranulocytosis (a severe decrease in white blood cells), pyrazolones are rarely used in modern clinical practice.

Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.

Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.

It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.

Anthraquinones are a type of organic compound that consists of an anthracene structure (a chemical compound made up of three benzene rings) with two carbonyl groups attached to the central ring. They are commonly found in various plants and have been used in medicine for their laxative properties. Some anthraquinones also exhibit antibacterial, antiviral, and anti-inflammatory activities. However, long-term use of anthraquinone-containing laxatives can lead to serious side effects such as electrolyte imbalances, muscle weakness, and liver damage.

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

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

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

Drug agonism is a concept in pharmacology that refers to the ability of a drug to bind to and activate a specific receptor in the body, leading to a physiological response. When a drug agonist binds to its target receptor, it causes a conformational change in the receptor's structure, which activates a signaling pathway that ultimately leads to a biological response.

The strength of the interaction between the drug and the receptor is often described in terms of affinity and efficacy. Affinity refers to the ability of the drug to bind to the receptor, while efficacy refers to the drug's ability to activate the receptor and cause a response. A full agonist has both high affinity and high efficacy for its target receptor, meaning that it can fully activate the receptor and produce a maximal response.

Partial agonists, on the other hand, have lower efficacy than full agonists, meaning that they can only partially activate the receptor and produce a submaximal response. Antagonists, in contrast, bind to the receptor without activating it, thereby blocking the effects of both full and partial agonists.

Understanding drug agonism is important for developing drugs with desired therapeutic effects while minimizing unwanted side effects. By carefully selecting drugs that target specific receptors with known affinity and efficacy profiles, researchers can design more effective treatments for a wide range of medical conditions.

Consolidation chemotherapy is a type of cancer treatment that is given after the initial or primary treatment, called induction therapy, to consolidate or strengthen the response and increase the chance of a cure. It typically involves the use of one or more anticancer drugs to target any remaining cancer cells in the body following remission. This approach is often used in the treatment of acute leukemias, such as acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), where the goal is to eliminate residual disease and reduce the risk of relapse. The specific drugs, doses, and schedules used in consolidation chemotherapy may vary depending on the type and stage of cancer being treated.

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

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

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

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

"MDR" is an abbreviation for "Multidrug Resistance." In the context of genetics, MDR genes are those that encode for proteins, typically transmembrane pumps, which can actively transport various drugs out of cells. This results in reduced drug accumulation within cells and decreased effectiveness of these drugs.

MDR genes play a crucial role in conferring resistance to chemotherapy agents in cancer cells, making treatment more challenging. One well-known MDR gene is the ABCB1 (ATP Binding Cassette Subfamily B Member 1) gene, which encodes for the P-glycoprotein efflux pump. Overexpression of such MDR genes can lead to cross-resistance to multiple drugs, further complicating treatment strategies.

Etoposide is a chemotherapy medication used to treat various types of cancer, including lung cancer, testicular cancer, and certain types of leukemia. It works by inhibiting the activity of an enzyme called topoisomerase II, which is involved in DNA replication and transcription. By doing so, etoposide can interfere with the growth and multiplication of cancer cells.

Etoposide is often administered intravenously in a hospital or clinic setting, although it may also be given orally in some cases. The medication can cause a range of side effects, including nausea, vomiting, hair loss, and an increased risk of infection. It can also have more serious side effects, such as bone marrow suppression, which can lead to anemia, bleeding, and a weakened immune system.

Like all chemotherapy drugs, etoposide is not without risks and should only be used under the close supervision of a qualified healthcare provider. It is important for patients to discuss the potential benefits and risks of this medication with their doctor before starting treatment.

Multidrug Resistance-Associated Proteins (MRPs) are a subfamily of ATP-binding cassette (ABC) transporter proteins that play a crucial role in the efflux of various substrates, including drugs and organic anions, out of cells. They are located in the plasma membrane of many cell types, including epithelial cells in the liver, intestine, kidney, and blood-brain barrier.

MRPs are known to transport a wide range of molecules, such as glutathione conjugates, bilirubin, bile acids, and various clinical drugs. One of the most well-known MRPs is MRP1 (ABCC1), which was initially identified in drug-resistant tumor cells. MRP1 can confer resistance to chemotherapeutic agents by actively pumping them out of cancer cells, thereby reducing their intracellular concentration and effectiveness.

The activity of MRPs can have significant implications for the pharmacokinetics and pharmacodynamics of drugs, as they can affect drug absorption, distribution, metabolism, and excretion (ADME). Understanding the function and regulation of MRPs is essential for developing strategies to overcome multidrug resistance in cancer therapy and optimizing drug dosing regimens in various clinical settings.

Rhodamine 123 is not a medical term, but a chemical compound. It's a fluorescent dye used in various scientific and research applications, particularly in the field of cell biology. Rhodamine 123 has an affinity for mitochondria, the energy-producing structures in cells, making it useful as a marker to study mitochondrial function and distribution within cells.

In summary, Rhodamine 123 is not a medical definition itself, but it can be used in medical research contexts to investigate cellular processes.

Drug screening assays for antitumor agents are laboratory tests used to identify and evaluate the effectiveness of potential drugs or compounds that can inhibit the growth of tumor cells or induce their death. These assays are typically performed in vitro (in a test tube or petri dish) using cell cultures of various types of cancer cells.

The assays measure different parameters such as cell viability, proliferation, apoptosis (programmed cell death), and cytotoxicity to determine the ability of the drug to kill or inhibit the growth of tumor cells. The results of these assays can help researchers identify promising antitumor agents that can be further developed for clinical use in cancer treatment.

There are different types of drug screening assays for antitumor agents, including high-throughput screening (HTS) assays, which allow for the rapid and automated testing of a large number of compounds against various cancer cell lines. Other types of assays include phenotypic screening assays, target-based screening assays, and functional screening assays, each with its own advantages and limitations.

Overall, drug screening assays for antitumor agents play a critical role in the development of new cancer therapies by providing valuable information on the activity and safety of potential drugs, helping to identify effective treatments and reduce the time and cost associated with bringing new drugs to market.

Benzylisoquinolines are a type of naturally occurring organic compounds found in various plants. These compounds are derived from the combination of a benzyl group and an isoquinoline ring, hence the name "benzylisoquinolines." They are known to have diverse biological activities, including anti-inflammatory, antispasmodic, and antimicrobial properties. Some well-known examples of benzylisoquinoline alkaloids include papaverine, found in the opium poppy, and berberine, found in various medicinal plants such as goldenseal and barberry. These compounds have been used in traditional medicine for centuries and continue to be studied for their potential therapeutic uses.

Experimental leukemia refers to the stage of research or clinical trials where new therapies, treatments, or diagnostic methods are being studied for leukemia. Leukemia is a type of cancer that affects the blood and bone marrow, leading to an overproduction of abnormal white blood cells.

In the experimental stage, researchers investigate various aspects of leukemia, such as its causes, progression, and potential treatments. They may conduct laboratory studies using cell cultures or animal models to understand the disease better and test new therapeutic approaches. Additionally, clinical trials may be conducted to evaluate the safety and efficacy of novel treatments in human patients with leukemia.

Experimental research in leukemia is crucial for advancing our understanding of the disease and developing more effective treatment strategies. It involves a rigorous and systematic process that adheres to ethical guidelines and scientific standards to ensure the validity and reliability of the findings.

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

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

Examples of acute diseases include:

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

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

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

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

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

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

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

Silicon compounds refer to chemical substances that contain the element silicon (Si) combined with other elements. Silicon is a Group 14 semimetal in the periodic table, and it often forms compounds through covalent bonding. The most common silicon compound is silicon dioxide (SiO2), also known as silica, which is found in nature as quartz, sand, and other minerals.

Silicon can form compounds with many other elements, including hydrogen, oxygen, halogens, sulfur, nitrogen, and carbon. For example:

* Silanes (SiHn) are a series of silicon-hydrogen compounds where n ranges from 1 to 6.
* Silicones are synthetic polymers made up of alternating silicon and oxygen atoms with organic groups attached to the silicon atoms.
* Silicates are a class of minerals that contain silicon, oxygen, and one or more metal cations. They have a wide range of structures and uses, including as building materials, ceramics, and glass.
* Siloxanes are a group of compounds containing alternating silicon-oxygen bonds with organic groups attached to the silicon atoms.

Silicon compounds have various applications in industry, medicine, and daily life. For instance, silicones are used in medical devices such as breast implants, contact lenses, and catheters due to their biocompatibility and flexibility. Silicates are found in pharmaceuticals, cosmetics, and food additives. Silicon-based materials are also used in dental restorations, bone cement, and drug delivery systems.

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Daunorubicin Women&Cancer Magazine Liposomal daunorubicin[permanent dead link] Johns Hopkins AIDS Service - New from the Food ... Liposomal daunorubicin (trade name DaunoXome) is a chemotherapy drug that is FDA approved to treat AIDS related Kaposi's ... Liposomal daunorubicin is intravenously administered. It utilizes the liposomal carrier system that provides a favorable ...
... a daunorubicin derivative) Idarubicin is able to pass through cell membranes easier than daunorubicin and doxorubicin because ... Di Marco, A.; Cassinelli, G.; Arcamone, F. (1981). "The discovery of daunorubicin". Cancer Treatment Reports. 65 (Suppl 4): 3-8 ... Currently, there are four main anthracyclines in medical use: Doxorubicin Daunorubicin (doxorubicin precursor) Epirubicin (a ...
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"Vyxeos (cytarabine and daunorubicin) FDA Approval History". Drugs.com. Archived from the original on 2019-04-11. Retrieved 2018 ... As a result, Jazz obtained the rights to breakthrough therapy Vyxeos (liposomal daunorubicin and cytarabine) for treatment of ...
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Anthracyclines (Aclarubicin · Daunorubicin · Doxorubicin · Epirubicin · Idarubicin · Amrubicin · Pirarubicin · Valrubicin · ...
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Liu Z, Sun Y, Hong H, Zhao S, Zou X, Ma R, Jiang C, Wang Z, Li H, Liu H (2015-08-15). "3-bromopyruvate enhanced daunorubicin- ...
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AKRs have been linked to metabolism of the anthracyclines doxorubicin (DOX) and daunorubicin (DAUN), allelic variants showed ... "Two allelic variants of aldo-keto reductase 1A1 exhibit reduced in vitro metabolism of daunorubicin". Drug Metabolism and ...
Certain anticancer drugs such as doxorubicin (Doxil) and daunorubicin may be administered encapsulated in liposomes. Liposomal ...
Kwon KB, Park EK, Ryu DG, Park BH (2003). "D4-GDI is cleaved by caspase-3 during daunorubicin-induced apoptosis in HL-60 cells ...
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If you become pregnant while receiving daunorubicin and cytarabine lipid complex, call your doctor. Daunorubicin and cytarabine ... Daunorubicin and cytarabine lipid complex is used to treat certain types of acute myeloid leukemia (AML; a type of cancer of ... Daunorubicin and cytarabine lipid complex may cause side effects. Tell your doctor if any of these symptoms are severe or do ... Daunorubicin and cytarabine lipid complex comes as a powder to be mixed with liquid and injected intravenously (into a vein) by ...
CheckOrphan is a non-profit organization located in Basel, Switzerland and Santa Cruz, California that is dedicated to rare, orphan and neglected diseases. CheckOrphan offers users an interactive and dynamic platform for all these diseases. This strategy allows visitors to be updated daily on all the latest news and interact with people internationally. This is essential, because due to the nature of these diseases, there is not a large concentration of individuals within any given proximity ...
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Diatrizoate, Iopromide and Iotrolan Enhanced Cytotoxicity of Daunorubicin in Multidrug Resistant K562/adr Cells: Impaired the ... but in co-treatment with daunorubicin (DNR), diatrizoate decreased cell viability in K562/adr cells by decreasing ICso of DNR ... Iopromide and Iotrolan Enhanced Cytotoxicity of Daunorubicin in Multidrug Resistant K562/adr Cells: Impaired the Mitochondrial ...
CH$NAME: Daunorubicin. CH$COMPOUND_CLASS: N/A. CH$FORMULA: C27H29NO10. CH$EXACT_MASS: 527.17915. CH$SMILES: c(=O)(c12)c(c5O[H]) ... RECORD_TITLE: Daunorubicin; LC-ESI-QTOF; MS2; CE:30 eV; [M+H]+. DATE: 2016.01.19 (Created 2008.07.15, modified 2012.11.20). ... Daunorubicin; LC-ESI-QTOF; MS2; CE:30 eV; [M+H]+. Mass Spectrum ... Daunorubicin with the InChIKey STQGQHZAVUOBTE-UHFFFAOYSA-N. ...
Daunorubicin (Cerubidine). Doctors prescribe daunorubicin for certain types of acute myeloid leukemia (AML) and acute ... Daunorubicin. (2022.) .. https://pubchem.ncbi.nlm.nih.gov/compound/Daunorubicin. *. Doxorubicin. (2022).. https://pubchem.ncbi. ...
Daunorubicin inhibitor is a chemotherapy medication used to treat cancer. ...
Daunorubicin) injection at affordable price. It is a chemotherapy medication used to treat cancer. Know Daunorubicin ... Usage of Daunorubicin. Daunorubicin is an anti-cancer medication, which is used to treat a type of cancer that affects the red ... What is Daunorubicin? Ans. This medication is used to treat a certain type of cancer (Kaposis sarcoma). Daunorubicin belongs ... Pharmacodynamics of Daunorubicin Daunorubicin forms complexes with DNA by intercalation between base pairs. It inhibits the ...
Find information on Daunorubicin/cytarabine Liposomal (Vyxeos) in Daviss Drug Guide including dosage, side effects, ... "Daunorubicin/cytarabine Liposomal." Daviss Drug Guide, 18th ed., F.A. Davis Company, 2023. www.drugguide.com/ddo/view/Davis- ... Drug-Guide/110585/all/daunorubicin_cytarabine_liposomal. Vallerand AHA, Sanoski CAC, Quiring CC. Daunorubicin/cytarabine ... Daunorubicin/cytarabine Liposomal [Internet]. In: Daviss Drug Guide. F.A. Davis Company; 2023. [cited 2023 September 26]. ...
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Indications and Usage Daunorubicin and cytarabine is a liposomal combination of daunorubicin, an anthracycline topoisomerase ... Generic name Daunorubicin and cytarabine Brand name(s), other common name(s) Vyxeos® Drug type Antitumor antibiotic and ... Daunorubicin and cytarabine is a liposomal combination of daunorubicin, an anthracycline topoisomerase inhibitor, and ... Patients Disease Information Treatment Types of Treatment Chemotherapy and Other Drug Therapies Drug Listings Daunorubicin and ...
Ministerio de Salud Pública. / Daunorubicin Daunorubicin. Injection 50 mg Injection 2 mg/mL Injection 20mg (chlorohydrate) ...
See Safety Info & Warning about not substituting with other daunorubicin and/or cytarabine-containing medicines. ... daunorubicin and cytarabine), a treatment for adults for two types of newly-diagnosed AML. ... Do not substitute VYXEOS for other daunorubicin and/or cytarabine-containing products. VYXEOS should not be given to patients ... VYXEOS is a combination of 2 chemotherapies, daunorubicin and cytarabine, into tiny, bubble-like carriers called liposomes. ...
6.3 Anthracycline uptake (Daunorubicin): Functional assay *Adjust cells concentration to 1 x 106 cells/mL in RPMI + 10% FCS at ...
See Safety Info & Warning about not substituting with other daunorubicin and/or cytarabine-containing medicines. ... daunorubicin and cytarabine), a treatment for adults for two types of newly-diagnosed AML, t-AML and AML-MRC. ... Do not substitute VYXEOS for other daunorubicin and/or cytarabine-containing products. VYXEOS should not be given to patients ... VYXEOS has different dosage recommendations from other medications that contain daunorubicin and/or cytarabine. Do not ...
See full Prescribing Information, including BOXED Warning, about not substituting with other daunorubicin and/or ... VYXEOS has different dosage recommendations than daunorubicin hydrochloride injection, cytarabine injection, daunorubicin ... VYXEOS has different dosage recommendations than daunorubicin hydrochloride injection, cytarabine injection, daunorubicin ... VYXEOS contains daunorubicin, which has a known risk of cardiotoxicity. This risk may be increased in patients with prior ...
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Daunorubicin. Prohibited. Doxorubicin. Prohibited. 1 Wilkes & Barton-Burke, 2008 Oncology Nursing Drug Handbook 27-33 (2008) ( ...
Cerubidine (Daunorubicin). CERUBIDINE® Rh´ne-Poulenc Rorer Daunorubicin Antimitotic - Antibiotic Action And Clinical ... Pharmacology: Daunorubicin inhibits the synthesis of nucleic acids; its effect on desoxyribonucleic acid is particularly… ...
Since the late 1960s, treatment outcomes for pediatric patients with non-Hodgkin lymphoma have steadily improved. Even for patients with advanced disease, event-free survival rates are now 65-90%.
Liposomal daunorubicin (DaunoXome®). Another chemo drug commonly used to treat KS is paclitaxel (Taxol®). Initial studies show ...
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Higher daunorubicin exposure benefits FLT3 mutated acute myeloid leukemia. Burnett AK., Russell NH., Hills RK., United Kingdom ... Acute Disease, Antibiotics, Antineoplastic, Daunorubicin, Dose-Response Relationship, Drug, Humans, Leukemia, Myeloid, Mutation ...
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Adipocytes Sequester and Metabolize the Chemotherapeutic Daunorubicin. Mol. Cancer Res. 15, 1704-1713 (2017). ... For instance, adipocytes may metabolize and inactivate the chemotherapeutic Daunorubicin21, which strongly affects the efficacy ...
Daunorubicin. - Cytarabine. Eligibility Requirements. Inclusion Criteria:. - Patients with AML who are newly diagnosed ...
  • citation needed] Daunorubicin is also used as the starting material for semi-synthetic manufacturing of doxorubicin, epirubicin and idarubicin. (wikipedia.org)
  • Similar to doxorubicin, daunorubicin interacts with DNA by intercalation and inhibition of macromolecular biosynthesis. (wikipedia.org)
  • Daunorubicin is an antineoplastic anthracycline antibiotic with actions similar to those of doxorubicin. (e-lactancia.org)
  • Liposomal formulations of daunorubicin and doxorubicin have been approved that appear to be somewhat less toxic to cardiac tissue. (wikidoc.org)
  • Anthracyclines, e. g. daunorubicin, doxorubicin, and idarubicin, consist of a tetracycline moiety linked via a glycosidic bond to a sugar residue, usually the aminosugar daunosamine. (lu.se)
  • A liposomal formulation known as liposomal daunorubicin also exists. (wikipedia.org)
  • www.drugguide.com/ddo/view/Davis-Drug-Guide/110585/all/daunorubicin_cytarabine_liposomal. (drugguide.com)
  • Vallerand AHA, Sanoski CAC, Quiring CC. Daunorubicin/cytarabine liposomal. (drugguide.com)
  • VYXEOS has different dosage recommendations than daunorubicin hydrochloride injection, cytarabine injection, daunorubicin citrate liposome injection, and cytarabine liposome injection. (vyxeospro.com)
  • Cytarabine is also available in a different form, combined with Daunorubicin Hydrochloride. (cancer.gov)
  • For more information see the Drug Information Summary for Daunorubicin Hydrochloride and Cytarabine Liposome . (cancer.gov)
  • Patients who have a history of serious hypersensitivity to daunorubicin, cytarabine or any component of the formulation should not use Vyxeos. (lls.org)
  • The prescribing information for Vyxeos includes a boxed warning not to interchange Vyxeos with other daunorubicin- and/or cytarabine-containing products. (lls.org)
  • VYXEOS is a combination of 2 chemotherapies, daunorubicin and cytarabine, into tiny, bubble-like carriers called liposomes. (vyxeos.com)
  • WARNING: VYXEOS has different dosage recommendations from other medications that contain daunorubicin and/or cytarabine. (vyxeos.com)
  • Do not substitute VYXEOS for other daunorubicin and/or cytarabine-containing products. (vyxeos.com)
  • VYXEOS should not be given to patients who have a history of serious allergic reaction to daunorubicin, cytarabine, or any of its ingredients. (vyxeos.com)
  • Presentations include clinical data from trials of Vyxeos ® (daunorubicin and cytarabine). (lls.org)
  • Daunorubicin, also known as daunomycin, is a chemotherapy medication used to treat cancer. (wikipedia.org)
  • Daunorubicin has been used with other chemotherapy agents to treat the blastic phase of chronic myelogenous leukemia. (wikipedia.org)
  • Daunorubicin injection must be given in a hospital or medical facility under the supervision of a doctor who is experienced in giving chemotherapy medications for cancer. (medlineplus.gov)
  • Daunorubicin comes as a solution (liquid) or as a powder to be mixed with liquid to be injected intravenously (into a vein) by a doctor or nurse in a medical facility along with other chemotherapy medications. (medlineplus.gov)
  • Standard chemotherapy was cytarabine 100 mg/m 2 and daunorubicin 60 mg/m 2 . (vyxeos.com)
  • Daunorubicin belongs to the group of antineoplastic (cancer-fighting medicines) known as anthracyclines. (magicinepharma.com)
  • An anthracycline antineoplastic agent, daunorubicin inhibits DNA and RNA synthesis by intercalating between DNA base pairs. (medscape.com)
  • GGP modified daunorubicin plus dioscin liposome has suitable particle size , narrow PDI, zeta potential of about -5 mV, long cycle effect, and enhanced cell uptake due to surface modification of GGP making the liposome could enter the inside of the tumor to fully exert its anti- tumor effect. (bvsalud.org)
  • Daunorubicin is in a class of medications called anthracyclines. (medlineplus.gov)
  • Lenalidomide monotherapy and in combination with cytarabine, daunorubicin and etoposide for high-risk myelodysplasia and acute myeloid leukaemia with chromosome 5 abnormalities. (ox.ac.uk)
  • Daunorubicin stabilizes the topoisomerase II complex after it has broken the DNA chain for replication, preventing the DNA double helix from being resealed and thereby stopping the process of replication. (wikipedia.org)
  • Daunorubicin also inhibits polymerase activity, affects the regulation of gene expression, and produces free radical damage to DNA. (magicinepharma.com)
  • tell your doctor and pharmacist if you are allergic to daunorubicin, any other medications, or any of the ingredients in daunorubicin injection. (medlineplus.gov)
  • A water-soluble anthracycline antibiotic medication (daunorubicin DNR) was loaded into oxidized porous silicon (pSiO2) microparticles and encapsulated using a level of polymer (poly lactide-co-glycolide PLGA) to research their synergistic results ICOS in charge of DNR discharge. (research-in-field.com)
  • Daunorubicin is in the anthracycline family of medication. (wikipedia.org)
  • Daunorubicin is an anti-cancer medication, which is used to treat a type of cancer that affects the red blood cells, platelets, and white blood cells except for lymphocytes. (magicinepharma.com)
  • Keywords: Porous silicon oxide Poly (dl-lactide-co-glycolide) Daunorubicin Ocular medication delivery Intro Proliferative vitreoretinopathy (PVR) may be the most frequent reason behind failing for retinal detachment medical procedures [1]. (research-in-field.com)
  • Doctors prescribe daunorubicin for certain types of acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) . (medicalnewstoday.com)
  • Higher daunorubicin exposure benefits FLT3 mutated acute myeloid leukemia. (ox.ac.uk)
  • However, by 1967, it was recognized that daunorubicin could produce fatal cardiac toxicity. (wikipedia.org)
  • The long infusion of daunorubicin is used to minimize the risk for cardiac toxicity. (cancercentrum.se)
  • GGP modified daunorubicin plus dioscin liposomes inhibit breast cancer by suppressing epithelial-mesenchymal transition. (bvsalud.org)
  • In this study, GGP modified daunorubicin plus dioscin liposomes are constructed and characterized. (bvsalud.org)
  • This study evaluated the in vitro effects of the combination of PKC412 and ara-C or daunorubicin, studying the effect of co-incubation, pre-incubation and sequential incubation of the drugs in patient samples and cell lines. (lu.se)
  • Daunorubicin forms complexes with DNA by intercalation between base pairs. (magicinepharma.com)
  • Since a group of French researchers discovered the same compound at about the same time, the two teams named the compound daunorubicin, combining the name Dauni, a pre-Roman tribe that occupied the area of Italy where the compound was isolated, with the French word for ruby, rubis, describing the color. (wikipedia.org)
  • Small volumes of daunorubicin can be wrapped up in these minuscule pods, which can then be released into a leukemia cell-filled environment. (wikipedia.org)
  • Daunorubicin should only be administered in a rapid intravenous infusion. (wikipedia.org)
  • Daunorubicin is sometimes given together with certain other medicines. (mayoclinic.org)
  • Other medications may also interact with daunorubicin, so be sure to tell your doctor about all the medications you are taking, even those that do not appear on this list. (medlineplus.gov)
  • Daunorubicin and cytarabine lipid complex is different than other products containing these medications and should not be substituted for one another. (safemedication.com)
  • citation needed] In addition to its major use in treating AML, daunorubicin is also used to treat neuroblastoma. (wikipedia.org)
  • You or your partner should not become pregnant while you are receiving daunorubicin and cytarabine lipid complex. (safemedication.com)
  • If you become pregnant while receiving daunorubicin and cytarabine lipid complex, call your doctor. (safemedication.com)
  • Do not use Daunorubicin if you are pregnant or planning to become pregnant. (magicinepharma.com)
  • You should use birth control to prevent pregnancy in yourself or your partner during your treatment with daunorubicin and cytarabine lipid complex and for 6 months after your final dose. (safemedication.com)
  • Daunorubicin may cause serious or life-threatening heart problems at any time during your treatment or months to years after your treatment has ended. (medlineplus.gov)
  • Your doctor will order tests before and during your treatment to see if your heart is working well enough for you to safely receive daunorubicin. (medlineplus.gov)
  • When daunorubicin is used to treat AML, it is usually injected once a day on certain days of your treatment period. (medlineplus.gov)
  • You should not breastfeed during your treatment with daunorubicin and cytarabine lipid complex and for at least 2 weeks after your final dose. (safemedication.com)
  • By colorimetric MTT assay, it was found that contrast media (0-3500 μM) had no effect on both K562 and K562/adr cell viabilities, but in co-treatment with daunorubicin (DNR), diatrizoate decreased cell viability in K562/adr cells by decreasing IC so of DNR from 610.7 ±74.5 nM to 360±108.9 nM. (thescipub.com)
  • Before starting treatment with Daunorubicin, please inform your doctor about your previous medical history. (magicinepharma.com)
  • Daunorubicin (DAN) is mostly used in the treatment of leukaemia and some solid tumour such as glioma. (farmaciajournal.com)
  • The recommended initial intensive treatment for AML outside a clinical study is DA, i.e., daunorubicin, i.v. infusion 60 mg/m 2 /8h daily for 3 days in combination with cytarabine, i.v. infusion 1 g/m 2 /2h b.i.d daily for 5 days. (cancercentrum.se)
  • The combination of daunorubicin and PKC412 resulted in more synergistic and less antagonistic effects compared to combinations with ara-C, in both patient material and cell lines. (lu.se)
  • Your doctor will order certain tests to check your body's response to daunorubicin. (medlineplus.gov)
  • While you are receiving daunorubicin, your doctor may want you to drink extra fluids so that you will pass more urine. (mayoclinic.org)
  • if you are having surgery, including dental surgery, tell the doctor or dentist that you are receiving daunorubicin and cytarabine lipid complex. (safemedication.com)
  • Patients in the standard arm (surgery alone) will undergo large en- bloc curative intent surgery will be performed within 4 weeks following randomization. (who.int)
  • Daunorubicin was approved for medical use in the United States in 1979. (wikipedia.org)
  • Daunorubicin and cytarabine lipid complex slows or stops the growth of cancer cells in your body. (safemedication.com)
  • Previous research show that daunorubicin (DNR) works well in inhibiting PVR development [2] looked after has been proven to work for the treating experimental PVR [3-5]. (research-in-field.com)