An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
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)
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
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.
Therapeutic act or process that initiates a response to a complete or partial remission level.
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.
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 hemoflagellate parasite affecting domestic and wild animals, as well as humans and invertebrates. Though it induces an immune response, it is non-pathogenic in humans and other vertebrates. It is cross-reactive with TRYPANOSOMA CRUZI and can thus cause false positives for CHAGAS DISEASE.
Initial drug treatment designed to bring about REMISSION INDUCTION. It is typically a short-term and high-dose drug treatment that is followed by CONSOLIDATION CHEMOTHERAPY and then MAINTENANCE CHEMOTHERAPY.
An acute myeloid leukemia in which abnormal PROMYELOCYTES predominate. It is frequently associated with DISSEMINATED INTRAVASCULAR COAGULATION.
Chronic refractory anemia with granulocytopenia, and/or thrombocytopenia. Myeloblasts and progranulocytes constitute 5 to 40 percent of the nucleated marrow cells.
Dioxolanes are specific chemical compounds characterized by a saturated six-membered ring containing two oxygen atoms and two carbon atoms, often formed through the reaction between aldehydes or ketones and diols, and significant in pharmaceutical synthesis and organic chemistry.
An anthracenedione-derived antineoplastic agent.
Organic compounds that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.
Compounds that inhibit the activity of DNA TOPOISOMERASES.
Any process by which toxicity, metabolism, absorption, elimination, preferred route of administration, safe dosage range, etc., for a drug or group of drugs is determined through clinical assessment in humans or veterinary animals.
A connective tissue disorder characterized by widespread thickening of SKIN with a cobblestone-like appearance. It is caused by proliferation of FIBROBLASTS and deposition of MUCIN in the DERMIS in the absence of thyroid disease. Most scleromyxedema cases are associated with a MONOCLONAL GAMMOPATHY, immunoglobulin IgG-lambda.
A nucleoside antibiotic isolated from Streptomyces antibioticus. It has some antineoplastic properties and has broad spectrum activity against DNA viruses in cell cultures and significant antiviral activity against infections caused by a variety of viruses such as the herpes viruses, the VACCINIA VIRUS and varicella zoster virus.
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.
I'm sorry for any confusion, but "Rome" is not a medical term or concept, and it doesn't have a specific medical definition. It is the capital city of Italy, known for its rich history, culture, and influence on various aspects including medicine, particularly during the Roman Empire period. If you have any questions about medical topics or definitions, I would be happy to help!
A surgical procedure used in treatment of glaucoma in which an opening is created through which aqueous fluid may pass from the anterior chamber into a sac created beneath the conjunctiva, thus lowering the pressure within the eye. (Hoffman, Pocket Glossary of Ophthalmologic Terminology, 1989)
Layers of connective tissue of variable thickness. The superficial fascia is found immediately below the skin; the deep fascia invests MUSCLES, nerves, and other organs.
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)
A reaction that severs one of the covalent sugar-phosphate linkages between NUCLEOTIDES that compose the sugar phosphate backbone of DNA. It is catalyzed enzymatically, chemically or by radiation. Cleavage may be exonucleolytic - removing the end nucleotide, or endonucleolytic - splitting the strand in two.
A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.
Disease having a short and relatively severe course.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in leukemia.

Induction of MDR1 gene expression by anthracycline analogues in a human drug resistant leukaemia cell line. (1/261)

The effects of 4-demethoxydaunorubicin (idarubicin, IDA) and MX2, a new morpholino-anthracycline, on up-regulation of the MDR1 gene in the low-level multidrug resistant (MDR) cell line CEM/A7R were compared at similar concentrations (IC10, IC50 and IC90) over a short time exposure (4 and 24 h). The chemosensitivity of each drug was determined by a 3-day cell growth inhibition assay. Compared with epirubicin (EPI), IDA and MX2 were 17- and eightfold more effective in the CEM/A7R line respectively. No cross-resistance to 5-FU was seen in the CEM/A7R line. Verapamil (5 microM) and PSC 833 (1 microM), which dramatically reversed resistance to EPI in the CEM/A7R line, had no sensitizing effect on the resistance of this line to MX2, but slightly decreased resistance to IDA. The sensitivity to 5-FU was unchanged by these modulators. The induction of MDR1 mRNA expression by IDA, MX2 and 5-FU was analysed by Northern blotting and semiquantitatively assessed by scanning Northern blots on a phosphorimager. The relative level of MDR1 expression was expressed as a ratio of MDR1 mRNA to the internal RNA control glyceraldehyde-3-phosphate dehydrogenase (GAPDH). IDA, MX2 and 5-FU differentially up-regulated MDR1 mRNA in the CEM/A7R line in a dose-dependent manner. Both IDA and MX2 induced MDR1 expression within 4 h. 5-FU up-regulated MDR1 expression only when drug exposure was prolonged to 24 h. Based on MRK 16 binding, flow cytometric analysis of P-glycoprotein (Pgp) expression paralleled the increase in MDR1 mRNA levels. For the three anthracyclines, the increase in MDR1 expression was stable in cells grown in the absence of drug for more than 3 weeks after drug treatment. The induction of MDR1 expression by 5-FU was transient, associated with a rapid decrease in the increased Pgp levels which returned to baseline 72 h after the removal of 5-FU. This study demonstrates that MDR1 expression can be induced by analogues of anthracyclines not pumped by Pgp, and that this induction appears to be stable despite a 3-week drug-free period.  (+info)

Early detection by ultrasound scan of severe post-chemotherapy gut complications in patients with acute leukemia. (2/261)

BACKGROUND AND OBJECTIVE: Acute leukemia patients may develop life-threatening gut complications after intensive chemotherapy. We evaluated the role of abdominal and pelvic ultrasound (US) examination in early detection of these complications. DESIGN AND METHODS: A cohort of twenty adult acute leukemia patients undergoing intensive chemotherapy for remission induction entered the study. All chemotherapy regimens included cytarabine by continuous i.v. infusion for several days. RESULTS: Three patients had severe gut complications: 2 cases of enterocolitis and 1 case of gall bladder overdistension in the absence of calculi. In all cases the abnormality was documented by US examination: US scan showed thickening of the intestinal wall (two cases), and gall bladder overdistension with biliary sludge (one case). Immediate medical care included bowel rest, a broad-spectrum antibiotic, antimycotic treatment, and granulocyte colony-stimulating factor. All patients recovered from the complication. INTERPRETATION AND CONCLUSIONS: We believe that the favorable outcome obtained in our small series can be attributed to early diagnosis followed by appropriate treatment. Early recognition by US and immediate medical management can lead to complete recovery of severe intestinal complications in patients with acute leukemia undergoing intensive chemotherapy.  (+info)

Randomized phase II study of fludarabine + cytosine arabinoside + idarubicin +/- all-trans retinoic acid +/- granulocyte colony-stimulating factor in poor prognosis newly diagnosed acute myeloid leukemia and myelodysplastic syndrome. (3/261)

Preclinical data suggest that retinoids, eg, all-trans retinoic acid (ATRA), lower concentrations of antiapoptotic proteins such as bcl-2, possibly thereby improving the outcome of anti-acute myeloid leukemia (AML) chemotherapy. Granulocyte colony-stimulating factor (G-CSF) has been considered to be potentially synergistic with ATRA in this regard. Accordingly, we randomized 215 patients with newly diagnosed AML (153 patients) or high-risk myelodysplastic syndrome (MDS) (refractory anemia with excess blasts [RAEB] or RAEB-t, 62 patients) to receive fludarabine + ara-C + idarubicin (FAI) alone, FAI + ATRA, FAI + G-CSF, or FAI + ATRA + G-CSF. Eligibility required one of the following: age over 71 years, a history of abnormal blood counts before M.D. Anderson (MDA) presentation, secondary AML/MDS, failure to respond to one prior course of chemotherapy given outside MDA, or abnormal renal or hepatic function. For the two treatment arms containing ATRA, ATRA was given 2 days (day-2) before beginning and continued for 3 days after completion of FAI. For the two treatment arms including G-CSF, G-CSF began on day-1 and continued until neutrophil recovery. Patients with white blood cell (WBC) counts >50,000/microL began ATRA on day 1 and G-CSF on day 2. Events (death, failure to achieve complete remission [CR], or relapse from CR) have occurred in 77% of the 215 patients. Reflecting the poor prognosis of the patients entered, the CR rate was only 51%, median event-free survival (EFS) time once in CR was 36 weeks, and median survival time was 28 weeks. A Cox regression analysis indicated that, after accounting for patient prognostic variables, none of the three adjuvant treatment combinations (FAI + ATRA, FAI + G, FAI + ATRA + G) affected survival, EFS, or EFS once in CR compared with FAI. Similarly, there were no significant effects of either ATRA ignoring G-CSF, or of G-CSF ignoring ATRA. As previously found, a diagnosis of RAEB or RAEB-t rather than AML was insignificant. There were no indications that the effect of ATRA differed according to cytogenetic group, diagnosis (AML or MDS), or treatment schedule. Logistic regression analysis indicated that, after accounting for prognosis, addition of G-CSF +/- ATRA to FAI improved CR rate versus either FAI or FAI + ATRA, but G-CSF had no effect on the other outcomes. We conclude that addition of ATRA +/- G-CSF to FAI had no effect on CR rate, survival, EFS, or EFS in CR in poor prognosis, newly diagnosed AML or high-risk MDS.  (+info)

Bacteremia caused by a novel isolate resembling leptotrichia species in a neutropenic patient. (4/261)

We report a case of Leptotrichia species bacteremia in a patient undergoing treatment for acute myelogenous leukemia. Like previously reported Leptotrichia species, this is a gram-variable, pleomorphic rod that is catalase negative and utilizes glucose and sucrose. However, it is more fastidious than previously reported isolates of Leptotrichia and may represent a novel species.  (+info)

Topoisomerase poisoning activity of novel disaccharide anthracyclines. (5/261)

Doxorubicin and idarubicin are very effective anticancer drugs in the treatment of human hematological malignancies and solid tumors. These agents are well known topoisomerase II poisons; however, some anthracycline analogs recently have been shown to poison topoisomerase I. In the present work, we assayed novel disaccharide analogs and the parent drug, idarubicin, for their poisoning effects of human topoisomerase I and topoisomerases IIalpha and IIbeta. Drugs were evaluated with a DNA cleavage assay in vitro and with a yeast system to test whether the agents were able to poison the enzymes in vivo. We have found that the test agents are potent poisons of both topoisomerases IIalpha and IIbeta. The axial orientation of the second sugar relative to the first one of the novel disaccharide analogs was shown to be required for poisoning activity and cytotoxicity. Interestingly, idarubicin and the new analogs stimulated topoisomerase I-mediated DNA cleavage at low levels in vitro. As expected, the cytotoxic level of the drug was highly affected by the content of topoisomerase II; nevertheless, the test agents had a yeast cell-killing activity that also was weakly dependent on cellular topoisomerase I content. The results are relevant for the full understanding of the molecular mechanism of topoisomerase poisoning by anticancer drugs, and they define structural determinants of anthracyclines that may help in the rational design of new compounds directed against topoisomerase I.  (+info)

Effect of the cytostatic agent idarubicin on fibroblasts of the human Tenon's capsule compared with mitomycin C. (6/261)

BACKGROUND/AIMS: To investigate the in vitro effect of a short time exposure to the anthracycline idarubicin on proliferation, protein synthesis, and motility of human Tenon's capsule fibroblasts in comparison with the antitumour antibiotic mitomycin C. METHODS: After determination of effective concentrations of idarubicin, fibroblasts of the human Tenon's capsule were exposed to idarubicin or mitomycin C at concentrations ranging from 0.1 microg/ml to 1 microg/ml or from 2.5 microg/ml to 250 microg/ml, respectively, for 0.5, 2, or 5 minutes and cultured for 60 days. Cell death by apoptosis caused by idarubicin treatment was confirmed by Hoechst 33258 staining. Further proliferation was explored by cell counting and by (3)H-thymidine uptake. Protein synthesis was measured by (3)H-proline uptake and motility was assessed by agarose droplet motility assay. RESULTS: Idarubicin is able to exert toxicity and to induce apoptosis during a short time exposure of 0.5 minutes at concentrations of 0.3-1 microg/ml resulting in a significant reduction in cell number compared with the control after 60 days. For mitomycin C, higher concentrations and longer expositions were necessary. Even after treatment with 1 microg/ml idarubicin or 250 microg/ml mitomycin C a few cells were able to incorporate (3)H-thymidine. (3)H-proline uptake up to 10 days after exposure to 0.3 microg/ml idarubicin was found not to be decreased. Cell motility was reduced after treatment with 1 microg/ml idarubicin for 5 minutes or with 250 microg/ml mitomycin C for 2 or 5 minutes. For low mitomycin C concentrations, an increase in motility was found during the first 10 days. CONCLUSION: Idarubicin reduces proliferation of human Tenons's capsule fibroblasts after incubation for 0.5 minutes at concentrations as low as 0.3-1 microg/ml. In comparison, mitomycin C requires longer exposure times and higher doses for equal results. Therefore, idarubicin may be useful in the prevention of glaucoma filtering surgery failure.  (+info)

Improvement of amyloid-related symptoms after autologous stem cell transplantation in a patient with hepatomegaly, macroglossia and purpura. (7/261)

AL amyloidosis was diagnosed in a 56-year-old woman with spontaneous purpura, macroglossia and hepatomegaly, a serum IgGk monoclonal gammopathy and a 25% plasma cell bone marrow infiltration. She was started on high-dose treatment consisting of four monthly cycles of VID chemotherapy, then underwent a stem cell collection after priming with cyclophosphamide + G-CSF. Myeloablative therapy was with melphalan and busulfan. Hematologic recovery was fast and uncomplicated. At follow-up 22 months from ASCT, the patient shows a complete remission of the clonal plasma cell disorder, normalization of liver size and alkaline phosphatase level and a significant improvement in the signs of vascular and soft tissue amyloid infiltration.  (+info)

Use of peripheral blood stem cells for autologous transplantation in acute myeloid leukemia patients allows faster engraftment and equivalent disease-free survival compared with bone marrow cells. (8/261)

We compared the feasibility and efficacy of autologous bone marrow (ABMT) and peripheral blood progenitor cell transplantation (PBSCT) performed after an identical induction/consolidation in adults with acute myeloid leukemia (AML). From January 1993 to June 1996 91 consecutive AML patients were enrolled in a program consisting of anthracycline-based induction and high-dose cytarabine consolidation (NOVIA). Until May 1994 ABMT was performed; from June 1994, if PBSC collection was adequate, PBSCT was performed. Out of 88 evaluable patients, 73 obtained a complete remission (CR) and 15 were resistant. Allogeneic bone marrow transplantation was performed in 16 patients. Forty-four (50%) were given autologous stem cell transplantation. ABMT was performed in 21 cases; twenty-nine patients were given G-CSF mobilization after NOVIA administration. An adequate number of PBSC was obtained in 23/29 (79%) cases, which were then re-infused. Median times to both neutrophil and platelet recovery from transplant were significantly shorter for the PBSC group (17 vs 36 days to 500 PMN/microl, P < 0.01; 20 vs 150 days to 20000 platelets/microl, P < 0.02; 37 vs 279 days to 50000 platelets/microl, P < 0.03), as were days of hospitalization after the reinfusion (18 vs 33, P < 0.03) and median days to transfusion independence. Toxicity was not significant in either group. After a minimum follow-up for live patients of 24 months (longer than the mean time for relapse observed for the PBSC series - 14 months) the percentage of relapses was similar: 11 of 21 (52.4%) and 12 of 23 (52.1%) in the ABMT and PBSC groups, respectively. Our results indicate that autologous PBSC transplantation, performed after an intensive chemotherapy regimen, is not inferior to ABMT in terms of disease-free survival and allows faster recovery times and reduced need for transfusion support.  (+info)

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.

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.

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.

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.

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.

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.

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.

Trypanosoma rangeli is a species of protozoan parasite that belongs to the family Trypanosomatidae. It is primarily found in various insects, particularly in triatomine bugs (also known as "kissing bugs"), which serve as its vectors. This parasite is closely related to another more well-known species called Trypanosoma cruzi, which causes Chagas disease in humans and other mammals.

Unlike T. cruzi, however, T. rangeli is not typically associated with causing severe or life-threatening diseases in humans. In fact, most human infections with T. rangeli are considered to be asymptomatic or mildly symptomatic. Some people may experience localized reactions, such as swelling and redness at the site of the insect bite, while a small number of cases might develop fever, headache, or muscle pain.

It is important to note that although T. rangeli infections are generally not harmful to humans, they can still have significant impacts on public health by complicating the diagnosis and treatment of Chagas disease, which can be caused by T. cruzi. The two species can co-infect both vectors and mammalian hosts, making it difficult to distinguish between them based on clinical symptoms or laboratory tests alone.

In summary, Trypanosoma rangeli is a protozoan parasite that primarily infects insects but can also be found in humans and other mammals. While it is not typically associated with severe disease in humans, its presence can complicate the diagnosis and management of Chagas disease caused by T. cruzi.

Induction chemotherapy is a type of cancer treatment that involves the use of cytotoxic drugs to reduce the size of tumors prior to administering other forms of therapy, such as radiation therapy or surgery. The goal of induction chemotherapy is to eliminate as many cancer cells as possible and shrink the tumor to improve the chances of a successful outcome with subsequent treatments.

This approach is often used in the treatment of certain types of cancer, including lymphoma, leukemia, and testicular cancer, among others. The specific drugs used and the duration of treatment may vary depending on the type and stage of cancer being treated.

It's important to note that induction chemotherapy is a complex medical procedure that should be administered under the close supervision of an experienced oncologist. Patients undergoing this treatment may experience side effects, such as nausea, vomiting, fatigue, and hair loss, among others. However, these side effects can often be managed with supportive care and medications.

Acute Promyelocytic Leukemia (APL) is a specific subtype of acute myeloid leukemia (AML), a cancer of the blood and bone marrow. It is characterized by the accumulation of abnormal promyelocytes, which are immature white blood cells, in the bone marrow and blood. These abnormal cells are produced due to a genetic mutation that involves the retinoic acid receptor alpha (RARA) gene on chromosome 17, often as a result of a translocation with the promyelocytic leukemia (PML) gene on chromosome 15 [t(15;17)]. This genetic alteration disrupts the normal differentiation and maturation process of the promyelocytes, leading to their uncontrolled proliferation and impaired function.

APL typically presents with symptoms related to decreased blood cell production, such as anemia (fatigue, weakness, shortness of breath), thrombocytopenia (easy bruising, bleeding, or petechiae), and neutropenia (increased susceptibility to infections). Additionally, APL is often associated with a high risk of disseminated intravascular coagulation (DIC), a serious complication characterized by abnormal blood clotting and bleeding.

The treatment for Acute Promyelocytic Leukemia typically involves a combination of chemotherapy and all-trans retinoic acid (ATRA) or arsenic trioxide (ATO) therapy, which target the specific genetic alteration in APL cells. This approach has significantly improved the prognosis for patients with this disease, with many achieving long-term remission and even cures.

Refractory anemia with excess blasts is a type of blood disorder that is characterized by the presence of increased numbers of immature blood cells, or "blasts," in the bone marrow and peripheral blood. This condition is considered a subtype of myelodysplastic syndrome (MDS), which is a group of disorders caused by abnormalities in the production of blood cells in the bone marrow.

In refractory anemia with excess blasts, the bone marrow fails to produce sufficient numbers of healthy red blood cells, white blood cells, and platelets. This results in anemia (low red blood cell count), neutropenia (low white blood cell count), and thrombocytopenia (low platelet count). Additionally, there is an increased number of blasts in the bone marrow and peripheral blood, which can indicate the development of acute myeloid leukemia (AML), a more aggressive form of blood cancer.

Refractory anemia with excess blasts is considered "refractory" because it does not respond well to treatment, including chemotherapy and stem cell transplantation. The prognosis for this condition varies depending on the severity of the disease and other individual factors, but it is generally poor, with many patients progressing to AML within a few years.

Dioxolanes are a class of organic compounds that contain a five-membered ring consisting of two carbon atoms, one oxygen atom, and two adjacent oxygen or sulfur atoms. The general structure of dioxolane is C2O2S2 or C2O3. These compounds are often used in the synthesis of pharmaceuticals, agrochemicals, and other organic compounds due to their high reactivity and ability to act as protecting groups for carbonyl functionalities. Dioxolanes can also be found naturally in some foods and plants.

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.

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.

Topoisomerase inhibitors are a class of anticancer drugs that work by interfering with the function of topoisomerases, which are enzymes responsible for relaxing supercoiled DNA during processes such as replication and transcription. Topoisomerase I inhibitors selectively bind to and stabilize the cleavage complex formed between topoisomerase I and DNA, preventing the relegation of the broken DNA strand and resulting in DNA damage and cell death. Examples include irinotecan and topotecan. Topoisomerase II inhibitors, on the other hand, bind to and stabilize the cleavage complex formed between topoisomerase II and DNA, leading to double-stranded DNA breaks and cell death. Examples include doxorubicin, etoposide, and mitoxantrone. These drugs are used in the treatment of various types of cancer.

"Drug evaluation" is a medical term that refers to the systematic process of assessing the pharmacological, therapeutic, and safety profile of a drug or medication. This process typically involves several stages, including preclinical testing in the laboratory, clinical trials in human subjects, and post-marketing surveillance.

The goal of drug evaluation is to determine the efficacy, safety, and optimal dosage range of a drug, as well as any potential interactions with other medications or medical conditions. The evaluation process also includes an assessment of the drug's pharmacokinetics, or how it is absorbed, distributed, metabolized, and eliminated by the body.

The findings from drug evaluations are used to inform regulatory decisions about whether a drug should be approved for use in clinical practice, as well as to provide guidance to healthcare providers about how to use the drug safely and effectively.

Scleromyxedema is a rare, progressive skin disorder characterized by the thickening and hardening of the skin due to excessive deposits of proteins called mucin and abnormal fibrous tissue in the dermis. It is also associated with monoclonal gammopathy, which means there is an overproduction of a specific type of antibody in the blood. The condition can affect various organs and systems in the body, potentially leading to systemic involvement.

The primary clinical features of scleromyxedema include:
- Widespread symmetric papules (small bumps) and plaques (thickened patches) on the skin
- Progressive thickening and hardening of the skin, particularly on the face, neck, hands, and feet
- Fine, waxy, "paradoxical" wrinkling of the skin when stretched or manipulated
- Occasionally, involvement of mucous membranes (e.g., mouth, eyes)

Scleromyxedema is differentiated from another similar condition called lichen myxedematosus by its association with monoclonal gammopathy and systemic symptoms. The exact cause of scleromyxedema remains unclear, but it is believed to involve abnormal immune system activity.

Treatment for scleromyxedema can be challenging due to the rarity and complexity of the condition. Various therapies have been used with varying degrees of success, including intravenous immunoglobulin (IVIG), glucocorticoids, chemotherapy agents, and biologics. The prognosis for scleromyxedema is variable, with some patients experiencing significant improvement or stabilization, while others may have progressive disease that can lead to severe complications and even death.

Vidarabine is an antiviral medication used to treat herpes simplex infections, particularly severe cases such as herpes encephalitis (inflammation of the brain caused by the herpes simplex virus). It works by interfering with the DNA replication of the virus.

In medical terms, vidarabine is a nucleoside analogue that is phosphorylated intracellularly to the active form, vidarabine triphosphate. This compound inhibits viral DNA polymerase and incorporates into viral DNA, causing termination of viral DNA synthesis.

Vidarabine was previously used as an injectable medication but has largely been replaced by more modern antiviral drugs such as acyclovir due to its greater efficacy and lower toxicity.

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.

I'm sorry for any confusion, but "Rome" is not a medical term. It is the capital city of Italy and has great historical and cultural significance. If you have any medical questions or terms you would like defined, I would be happy to help!

Filtering surgery is a type of ophthalmic procedure, specifically a glaucoma surgery, that involves creating a new pathway for the aqueous humor (the clear fluid inside the eye) to drain from the anterior chamber to the exterior through a synthetic implant. This surgery is aimed at reducing intraocular pressure (IOP) in patients with open-angle or closed-angle glaucoma who have not responded well to medication or laser treatments. The most common type of filtering surgery is trabeculectomy.

In a trabeculectomy, a small opening is made in the sclera (the white part of the eye), and a thin piece of the sclera along with the underlying trabecular meshwork is removed to create a filtering bleb. This bleb is a raised area on the surface of the eye that allows the aqueous humor to drain out, forming a fluid-filled space under the conjunctiva. The fluid then gradually reabsorbs into the bloodstream, lowering the IOP and relieving pressure on the optic nerve, which can help prevent further vision loss due to glaucoma.

It is important to note that filtering surgery carries risks such as infection, bleeding, cataract formation, and potential loss of vision. Proper postoperative care and follow-up with an ophthalmologist are crucial for successful outcomes.

A fascia is a band or sheet of connective tissue, primarily collagen, that covers, connects, and separates muscles, organs, and other structures in the body. It provides support and stability, allows for smooth movement between structures, and has the ability to transmit forces throughout the body. Fascia is found throughout the body, and there are several layers of it, including superficial fascia, deep fascia, and visceral fascia. Injury, inflammation, or strain to the fascia can cause pain and restriction of movement.

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.

DNA cleavage is the breaking of the phosphodiester bonds in the DNA molecule, resulting in the separation of the two strands of the double helix. This process can occur through chemical or enzymatic reactions and can result in various types of damage to the DNA molecule, including single-strand breaks, double-strand breaks, and base modifications.

Enzymatic DNA cleavage is typically carried out by endonucleases, which are enzymes that cut DNA molecules at specific sequences or structures. There are two main types of endonucleases: restriction endonucleases and repair endonucleases. Restriction endonucleases recognize and cleave specific DNA sequences, often used in molecular biology techniques such as genetic engineering and cloning. Repair endonucleases, on the other hand, are involved in DNA repair processes and recognize and cleave damaged or abnormal DNA structures.

Chemical DNA cleavage can occur through various mechanisms, including oxidation, alkylation, or hydrolysis of the phosphodiester bonds. Chemical agents such as hydrogen peroxide, formaldehyde, or hydrazine can induce chemical DNA cleavage and are often used in laboratory settings for various purposes, such as DNA fragmentation or labeling.

Overall, DNA cleavage is an essential process in many biological functions, including DNA replication, repair, and recombination. However, excessive or improper DNA cleavage can lead to genomic instability, mutations, and cell death.

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.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

Chronic myelogenous leukemia (CML), BCR-ABL positive is a specific subtype of leukemia that originates in the bone marrow and involves the excessive production of mature granulocytes, a type of white blood cell. It is characterized by the presence of the Philadelphia chromosome, which is formed by a genetic translocation between chromosomes 9 and 22, resulting in the formation of the BCR-ABL fusion gene. This gene encodes for an abnormal protein with increased tyrosine kinase activity, leading to uncontrolled cell growth and division. The presence of this genetic abnormality is used to confirm the diagnosis and guide treatment decisions.

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.

Gene expression regulation in leukemia refers to the processes that control the production or activation of specific proteins encoded by genes in leukemic cells. These regulatory mechanisms include various molecular interactions that can either promote or inhibit gene transcription and translation. In leukemia, abnormal gene expression regulation can lead to uncontrolled proliferation, differentiation arrest, and accumulation of malignant white blood cells (leukemia cells) in the bone marrow and peripheral blood.

Dysregulated gene expression in leukemia may involve genetic alterations such as mutations, chromosomal translocations, or epigenetic changes that affect DNA methylation patterns and histone modifications. These changes can result in the overexpression of oncogenes (genes with cancer-promoting functions) or underexpression of tumor suppressor genes (genes that prevent uncontrolled cell growth).

Understanding gene expression regulation in leukemia is crucial for developing targeted therapies and improving diagnostic, prognostic, and treatment strategies.

"Idarubicin Side Effects: Common, Severe, Long Term". Drugs.com. Retrieved 2019-06-21. Idarubicin bound to proteins in the PDB v ... Idarubicin /ˌaɪdəˈruːbɪsɪn/ or 4-demethoxydaunorubicin is an anthracycline antileukemic drug. It inserts itself into DNA and ... nausea and vomiting are common among patients treated with idarubicin. Miller JP, Stoodley RJ (2013). "Studies directed towards ...
Daunorubicin Idarubicin Doxorubicin Grethe, Guenter; Mitt, Toomas; Williams, Thomas H; Uskokovic, Milan R (1983). "Synthesis of ...
Doxorubicin Idarubicin "Daunorubicin (Cerubidine) Use During Pregnancy". Drugs.com. 19 September 2019. Retrieved 15 August 2020 ... epirubicin and idarubicin. Similar to doxorubicin, daunorubicin interacts with DNA by intercalation and inhibition of ...
Derivatives of these compounds include epirubicin and idarubicin. Other clinically used drugs in the anthracycline group are ... idarubicin, and liposomal doxorubicin). The cause of this is most likely due to the production of free radicals in the cell and ...
Idarubicin is a fat soluble variant of daunorubicin and is orally bioavailable. Several groups of researchers focused on ... Only epirubicin and idarubicin have been adopted for worldwide use. Epirubicin has similar activity to doxorubicin, however has ... Other novel anthracycline analogues such as epirubicin and idarubicin also provide options to reduce adverse cardiac events; ... Clinically the most important anthracyclines are doxorubicin, daunorubicin, epirubicin and idarubicin. The anthracyclines are ...
Anthracyclines (Aclarubicin · Daunorubicin · Doxorubicin · Epirubicin · Idarubicin · Amrubicin · Pirarubicin · Valrubicin · ...
It consists of chemotherapy, frequently consisting of cytarabine, daunorubicin, and idarubicin. It can also involve bone marrow ...
Daunorubicin is the precursor to idarubicin (Idamycin), epirubicin (Ellence), and zorubicin.[citation needed] Streptomyces is ...
It has given encouraging results in a phase II trial for myelodysplastic syndromes in combination with idarubicin and ... June 2012). "Phase II trial of vorinostat with idarubicin and cytarabine for patients with newly diagnosed acute myelogenous ... Langholtz J, Haehle M (11 January 2012). "Zolinza, Idarubicin, Cytarabine Combination Yields High Response Rates In MDS ...
"Lestaurtinib, Cytarabine, and Idarubicin in Treating Younger Patients With Relapsed or Refractory Acute Myeloid Leukemia". ...
"Development of Idarubicin and Doxorubicin Solid Lipid Nanoparticles to Overcome Pgp-Mediated Multiple Drug Resistance in ...
... idarubicin or mitoxantrone)-based chemotherapy. Both chemotherapies result in a clinical remission in approximately 90% of ...
... idarubicin, etc.). The only FDA approved treatment for vasopressor extravasation is phentolamine Pain management and local ... Amsacrine Cisplatin Dactinomycin Daunorubicin Docetaxel Doxorubicin Epirubicin Idarubicin Mechlorethamine Mitomycin C ...
In the FLAG-IDA regimen (also called FLAG-Ida, IDA-FLAG, or Ida-FLAG), idarubicin-an anthracycline antibiotic that is able to ... Mitoxantrone is a synthetic anthracycline analogue (an anthracenedione) that, like idarubicin, can intercalate DNA and prevent ...
Idarubicin (a daunorubicin derivative) Idarubicin is able to pass through cell membranes easier than daunorubicin and ... It is hypothesized that doxorubicin, which possesses a hydroxyl group and a methoxy group not present in idarubicin, can form ... "Interactions of anticancer drugs doxorubicin and idarubicin with lipid monolayers: New insight into the composition, structure ...
Chemotherapy with combination of cytosine arabinoside and either idarubicin, daunomycin, or mitoxantrone as for acute myeloid ...
October 2007). "Adding lomustine to idarubicin and cytarabine for induction chemotherapy in older patients with acute myeloid ...
... leukemia are usually given induction chemotherapy with cytarabine and an anthracycline such as daunorubicin or idarubicin. This ...
... leukemia patients developing retinoic acid syndrome during induction treatment with all-trans retinoic acid and idarubicin". ...
Cytarabine plus idarubicin or daunorubicin as induction and consolidation therapy for previously untreated adult patients with ... Attempts were made to prolong the course (cytarabine for 10 days instead of 7, or daunorubicin/idarubicin for 4-5 days instead ... can be substituted for doxorubicin or idarubicin or mitoxantrone). There were attempts to intensify the "7+3" regimen in order ...
Gabapentin Galzin Haloperidol Haloperidol Decanoate Hydroxychloroquine Hydroxyzine Hydrochloride Ibuprofen Max Idarubicin HCl ...
Idarubicin and Cytarabine in Patients (Pts) with Relapsed or Refractory (R/R) Acute Myeloid Leukemia (AML) and High-Risk ...
... idarubicin MeSH D09.408.051.059.200.650 - nogalamycin MeSH D09.408.051.059.200.650.500 - menogaril MeSH D09.408.051.059.650 - ...
L01DB01 Doxorubicin L01DB02 Daunorubicin L01DB03 Epirubicin L01DB04 Aclarubicin L01DB05 Zorubicin L01DB06 Idarubicin L01DB07 ...
... idarubicin (INN) idaverine (INN) idazoxan (INN) idebenone (INN) idenast (INN) Idkit:HP (Exalenz Bioscience) idoxifene (INN) ...
Examples of anthracyclines include: Daunorubicin Doxorubicin (Adriamycin®) Epirubicin Idarubicin Anti-tumor antibiotics that ...
... idarubicin - IDEC-Y2B8 monoclonal antibody - idiopathic - idiopathic myelofibrosis - idoxifene - idoxuridine - ifosfamide - ...
7) and the related derivatives daunorubicin, epirubicin, and idarubicin are anthracyclines obtained from the bacterium ...
... with Idarubicin and cytarabine Ia (genus), of vespertilionid bats Phase Ia of a clinical trial Immunoassay, biochemical test to ...
Cyclophosphamide Cytosine arabinoside Dasatinib Daunorubicin Decitabine Etoposide Fludarabine Gemtuzumab ozogamicin Idarubicin ...
"Idarubicin Side Effects: Common, Severe, Long Term". Drugs.com. Retrieved 2019-06-21. Idarubicin bound to proteins in the PDB v ... Idarubicin /ˌaɪdəˈruːbɪsɪn/ or 4-demethoxydaunorubicin is an anthracycline antileukemic drug. It inserts itself into DNA and ... nausea and vomiting are common among patients treated with idarubicin. Miller JP, Stoodley RJ (2013). "Studies directed towards ...
Idarubicin: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Before receiving idarubicin,. *tell your doctor and pharmacist if you are allergic to idarubicin, any other medications, or any ... If you become pregnant while receiving idarubicin, call your doctor. Idarubicin may harm the fetus. ... Idarubicin can cause a severe decrease in the number of blood cells in your bone marrow. This may cause certain symptoms and ...
... idarubicin hydrochloride) is a cancer medication used to treat acute myeloid leukemia (AML), a type of blood cancer in adults. ... Generic drug: idarubicin hydrochloride. Brand name: Idamycin PFS. What is Idamycin PFS (idarubicin hydrochloride), and how does ... If idarubicin is to be used during pregnancy, or if the patient becomes pregnant during therapy, the patient should be apprised ... Idamycin PFS Injection (idarubicin hydrochloride) is a cancer (antineoplastic) medication used to treat a type of blood cancer ...
IDARUBICIN HYDROCHLORIDE (UNII: 5VV3MDU5IE) (IDARUBICIN - UNII:ZRP63D75JW) IDARUBICIN HYDROCHLORIDE. 1 mg in 1 mL. ... IDARUBICIN HYDROCHLORIDE (UNII: 5VV3MDU5IE) (IDARUBICIN - UNII:ZRP63D75JW) IDARUBICIN HYDROCHLORIDE. 1 mg in 1 mL. ... IDARUBICIN HYDROCHLORIDE (UNII: 5VV3MDU5IE) (IDARUBICIN - UNII:ZRP63D75JW) IDARUBICIN HYDROCHLORIDE. 1 mg in 1 mL. ... Idarubicin is a potent bone marrow suppressant. Idarubicin should not be given to patients with pre-existing bone marrow ...
This patient-friendly article is about chemotherapy drug, Idarubicin (Zavedos) which is a cytotoxic anthracycline antibiotic ...
Provides a summary of interactions with vitamins, herbs, and food
Top of the pageIdarubicinDrug InformationCommon brand names:Idamycin PFSSummary of Interactions with Vitamins, Herbs, & FoodsWhat Are Nutrient Interactions Types of interactions:BeneficialAdverseCheckReplenish Depleted Nutrients The chemotherapy drug cisplatin may cause excessive loss of magnesium and potassium in the urine. Preliminary reports suggest that both potassium and
Sirolimus, Idarubicin, and Cytarabine in Treating Patients With Newly Diagnosed Acute Myeloid Leukemia. May 27, 2020. ... Idarubicin, and Cytarabine in Treating Patients With Newly Diagnosed Acute Myeloid Leukemia Lithium Carbonate and Tretinoin in ...
Idarubicin. This is my archive. A patients perspective …. Nickys story. My drive for supporting blood cancer started in ...
... a global supplier of Idarubicin (CAS No.: 58957-92-9) offers for your requirements of RND / Development quantities or ... Idarubicin (CAS No.: 58957-92-9). Manus Aktteva Biopharma LLP is an ISO 9001:2015 Certified Global Supplier based in India for ... The list of intermediates for Idarubicin (CAS No.: 58957-92-9) will be updated soon.. If you can not locate your required ... Are you looking for Idarubicin (CAS No.: 58957-92-9) with documentation like USDMF, EDMF, CEP / COS, PMDA - JAPAN, DMF - CANADA ...
Idarubicin (Idamycin PFS). Idarubicin can treat AML in adults, and researchers are studying its use for other types of cancer. ... Idarubicin hydrochloride. (2021).. https://pubchem.ncbi.nlm.nih.gov/compound/636362. *. Kim, H., et al. (2019). Risk factor ... Idarubicin 10 mg/10 ml solution for injection. (2021).. https://www.medicines.org.uk/emc/product/775/smpc. ...
Find information on Idarubicin (Idamycin PFS) in Daviss Drug Guide including dosage, side effects, interactions, nursing ... "IDArubicin." Daviss Drug Guide, 18th ed., F.A. Davis Company, 2023. Emergency Central, emergency.unboundmedicine.com/emergency ... Davis-Drug-Guide/51396/all/IDArubicin. Vallerand AHA, Sanoski CAC, Quiring CC. IDArubicin. Daviss Drug Guide. F.A. Davis ... Vallerand, A. H., Sanoski, C. A., & Quiring, C. (2023). IDArubicin. In Daviss Drug Guide (18th ed.). F.A. Davis Company. https ...
Idarubicin Hydrochloride published on 01 Jan 2023 by ASHP. ... Idarubicin Hydrochloride AHFS 10:00 in ASHP® Injectable Drug ...
Idarubicin. Most other Common Side Effects: Infection, nausea, vomiting, hair loss, abdominal cramps, diarrhea, mental illness ...
Idarubicin monotherapy in multiply pretreated leukemia patients: Response in relation to P-glycoprotein expression. in: Annals ... Idarubicin monotherapy in multiply pretreated leukemia patients: Response in relation to P-glycoprotein expression. Annals of ... Fractionated idarubicin (12 mg/m2/week) was given to 36 acute myelogenous leukemia (AML) patients, 12 acute lymphoblastic ... With regard to idarubicin monotherapy, overall response was 33/56 (59%) patients, and 23/33 (70%) responding patients showed a ...
Acyclovir reference guide for safe and effective use from the American Society of Health-System Pharmacists (AHFS DI).
Detailed drug Information for Bacillus of calmette and guerin vaccine, live (Intradermal). Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Cytarabine (ara-C) with idarubicin. *Cytarabine with topotecan. *Cytarabine with fludarabine. Sometimes, topotecan is given by ...
Conclusion: The ZHER2-affibody conjugate of idarubicin has a more specific cytotoxic effect compared with idarubicin alone ... Idarubicin is an effective anti-neoplastic drug but specific delivery of it to the targeted cells is still a great challenge. ... Results: Idarubicin showed a potent and dose-dependent cytotoxic effect against all treated cell lines while the SK-OV-3 cells ... The constructed Idarubicin-ZHER2 affibody conjugate decreased the viability of SK-OV-3 cells at its optimal concentration, more ...
A single high dose of idarubicin combined with high-dose ARA-C for treatment of first relapse in childhood high-risk acute ... The treatment plan included the combination of a single high-dose idarubicin and high-dose cytarabine as induction therapy ... The treatment plan included the combination of a single high-dose idarubicin and high-dose cytarabine as induction therapy ...
... idarubicin are superior to regimens containing idarubicin + ara-C(IA) without either fludarabine or topotecan for treatment of ... idarubicin are superior to regimens containing idarubicin + ara-C(IA) without either fludarabine or topotecan for treatment of ... idarubicin are superior to regimens containing idarubicin + ara-C(IA) without either fludarabine or topotecan for treatment of ... idarubicin are superior to regimens containing idarubicin + ara-C(IA) without either fludarabine or topotecan for treatment of ...
Idarubicin (); Magrolimab (); Venetoclax (); Zevados (Idarubicin); acetaminophen (); azacitidine (5-azacitidine); daunorubicin ...
The effects of idarubicin versus other anthracyclines for induction therapy of patients with newly diagnosed leukaemia: ... The effects of idarubicin versus other anthracyclines for induction therapy of patients with newly diagnosed leukaemia: ... "The Effects of Idarubicin Versus Other Anthracyclines for Induction Therapy of Patients With Newly Diagnosed Leukaemia: ... The effects of idarubicin versus other anthracyclines for induction therapy of patients with newly diagnosed leukaemia: ...
Teva Pharmaceuticals has initiated a voluntary nationwide recall of lot 31329657B of IDArubicin Hydrochloride Injection USP 5 ... Teva Issues Voluntary Nationwide Recall of One Lot of IDArubicin Hydrochloride Injection USP 5 mg/5 mL Due to the Presence of ... Teva Pharmaceuticals has initiated a voluntary nationwide recall of lot 31329657B of IDArubicin Hydrochloride Injection USP 5 ... 00Teva Issues Voluntary Nationwide Recall of One Lot of IDArubicin Hydrochloride Injection USP 5 mg/5 mL Due to the Presence of ...
7 + 3 regimen (cytarabine 100 or 200 mg/m 2/day IV on Days 1-7 plus daunorubicin 60 mg/m 2/day IV or idarubicin 12 mg/m 2/day ... Idarubicin 12 mg/m 2/day for 3d or daunorubicin 60-90 mg/m 2/day for 3d ... Cytarabine 2-3 g/m 2 q12h for 3d plus idarubicin 12 mg/m 2/day for 3d for one cycle or ... A phase I/II study of intensive dose escalation of cytarabine in combination with idarubicin and etoposide in induction and ...
Idarubicin Hydrochloride. Idarubicin Hydrochloride. 1.0 mg/mL. Chemotherapy Antitumor Antibiotic Anthracycline. Intravenous. ... Idarubicin Hydrochloride. Idarubicin Hydrochloride. 1.0 mg/mL. Chemotherapy Antitumor Antibiotic Anthracycline. Intravenous. ... Idarubicin Hydrochloride. Idarubicin Hydrochloride. 1.0 mg/mL. Chemotherapy Antitumor Antibiotic Anthracycline. Intravenous. ... Idarubicin Hydrochloride. Idarubicin Hydrochloride. 1.0 mg/mL. Chemotherapy Antitumor Antibiotic Anthracycline. Intravenous. ...
Idarubicin. Date of publication: 01/12/2014. *Imipenem/cilastatin. Date of publication: 06/01/2016 ...
Fleischhack G, Hasan C, Graf N, Mann G, Bode U.. IDA-FLAG (idarubicin, fludarabine, cytarabine, G-CSF), an effective remission- ... Karol SE, Alexander TB, Budhraja A. Venetoclax in combination with cytarabine with or without idarubicin in children with ... A phase 2 study of bortezomib combined with either idarubicin/cytarabine or cytarabine/etoposide in children with relapsed, ... AML: acute myeloid leukemia; FLAG: fludarabine/cytarabine + granulocyte colony-stimulating factor; ida: idarubicin; FLT3i: FLT3 ...
  • Idarubicin hydrochloride is a DNA-intercalating analog of daunorubicin which has an inhibitory effect on nucleic acid synthesis and interacts with the enzyme topoisomerase II. (nih.gov)
  • This phase III trial comparing idarubicin with high-dose daunorubicin as part of induction therapy in AML did not find significant differences in complete remission rates, relapse, or survival. (ascopost.com)
  • A significant interaction between the treatment arm and the FLT3-ITD mutation was found, and high-dose daunorubicin was more effective than idarubicin in patients with FLT3-ITD mutation. (ascopost.com)
  • 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)
  • Pharmacokinetic studies have been performed in adult leukemia patients with normal renal and hepatic function following intravenous administration of 10 to 12 mg/m 2 of idarubicin daily for 3 to 4 days as a single agent or combined with cytarabine. (nih.gov)
  • The elimination rate of idarubicin from plasma is slow with an estimated mean terminal half-life of 22 hours (range, 4 to 48 hours) when used as a single agent and 20 hours (range, 7 to 38 hours) when used in combination with cytarabine. (nih.gov)
  • Sirolimus, Idarubicin, and Cytarabine. (checkorphan.org)
  • The treatment plan included the combination of a single high-dose idarubicin and high-dose cytarabine as induction therapy followed by an intensive consolidation and stem cell transplant (SCT). (unipv.it)
  • What is Idamycin PFS (idarubicin hydrochloride), and how does it work? (medicinenet.com)
  • Idamycin PFS Injection (idarubicin hydrochloride) is a cancer (antineoplastic) medication used to treat a type of blood cancer ( acute myeloid leukemia -AML) in adults. (medicinenet.com)
  • 1. Idarubicin Hydrochloride Injection should be given slowly into a freely flowing intravenous infusion. (nih.gov)
  • 2. As is the case with other anthracyclines the use of idarubicin Hydrochloride can cause myocardial toxicity leading to congestive heart failure. (nih.gov)
  • 3. As is usual with antileukemic agents, severe myelosuppression occurs when idarubicin hydrochloride is used at effective therapeutic doses. (nih.gov)
  • 4. It is recommended that idarubicin hydrochloride be administered only under the supervision of a physician who is experienced in leukemia chemotherapy and in facilities with laboratory and supportive resources adequate to monitor drug tolerance and protect and maintain a patient compromised by drug toxicity. (nih.gov)
  • Idarubicin Hydrochloride Injection, USP contains idarubicin hydrochloride and is a sterile, semi-synthetic, preservative-free solution (PFS) antineoplastic anthracycline for intravenous use. (nih.gov)
  • Idarubicin Hydrochloride Injection, USP is a sterile, red-orange, isotonic parenteral preservative-free solution, available in 5 mL (5 mg), 10 mL (10 mg) and 20 mL (20 mg) single-use-only vials. (nih.gov)
  • Each mL contains idarubicin hydrochloride 1 mg and the following inactive ingredients: glycerin 25 mg and water for injection q.s. (nih.gov)
  • Teva Pharmaceuticals has initiated a voluntary nationwide recall of lot 31329657B of IDArubicin Hydrochloride Injection USP 5 mg/5 mL vial, to the user level in the United States. (clgtrial.com)
  • LifePearl™ microspheres are compatible with doxorubicin, epirubicin idarubicin and irinotecan. (terumo-europe.com)
  • Idarubicin /ˌaɪdəˈruːbɪsɪn/ or 4-demethoxydaunorubicin is an anthracycline antileukemic drug. (wikipedia.org)
  • Idarubicin is an anthracycline antineoplastic agent. (medscape.com)
  • Idarubicin is in a class of medications called anthracyclines. (medlineplus.gov)
  • Fractionated idarubicin (12 mg/m 2 /week) was given to 36 acute myelogenous leukemia (AML) patients, 12 acute lymphoblastic leukemia (ALL) patients, and eight chronic myelogenous leukemia (CML) patients in blast crisis. (uni-luebeck.de)
  • It has been unclear whether regimens containing topotecan + ara-C (TA) or fludarabine + ara-C (FA) ± idarubicin are superior to regimens containing idarubicin + ara-C(IA) without either fludarabine or topotecan for treatment of newly diagnosed acute myeloid leukemia (AML), refractory anemia with excess blasts in transformation (RAEB-t), or RAEB. (elsevierpure.com)
  • tell your doctor and pharmacist if you are allergic to idarubicin, any other medications, or any of the ingredients in idarubicin injection. (medlineplus.gov)
  • You should not become pregnant or breast-feed while you are receiving idarubicin injection. (medlineplus.gov)
  • Studies of cellular (nucleated blood and bone marrow cells) drug concentrations in leukemia patients have shown that peak cellular idarubicin concentrations are reached a few minutes after injection. (nih.gov)
  • Idarubicin should be given only under the supervision of a doctor with experience in the use of chemotherapy medications. (medlineplus.gov)
  • Idarubicin comes as a solution (liquid) to be injected intravenously (into a vein) over 10 to 15 minutes by a doctor or nurse in a medical facility along with other chemotherapy medications. (medlineplus.gov)
  • In the current study, we assessed the cytotoxic effects of idarubicin-Z HER2 affibody conjugate on the positive-HER2 cancer cell lines. (iranpath.org)
  • The cytotoxic effects of constructed idarubicin-Z HER2 affibody conjugate on the SK-BR-3, SK-OV-3, and MCF-7 cells with various levels of HER2 expression were evaluated by MTT assay after 48 hours of incubation time. (iranpath.org)
  • Idarubicin showed a potent and dose-dependent cytotoxic effect against all treated cell lines while the SK-OV-3 cells were significantly more sensitive. (iranpath.org)
  • The Z HER2 -affibody conjugate of idarubicin has a more specific cytotoxic effect compared with idarubicin alone against HER2-overexpressing ovarian cancerous cells. (iranpath.org)
  • Idarubicin has a potent and dose-dependent cytotoxic effect against breast and ovarian cancerous cells. (iranpath.org)
  • The Z HER2 -affibody conjugate of idarubicin has a more potent cytotoxic effect than idarubicin alone against HER2-overexpressing malignant cells. (iranpath.org)
  • The aim of the study was to test whether fractionated (weekly) idarubicin administration to multiply pretreated leukemia patients is effective and tolerable for outpatient treatment, and whether idarubicin alone can overcome P-glycoprotein (P-gp)-related resistance. (uni-luebeck.de)
  • This study demonstrates that P-gp-related resistance can be overcome in multiply pretreated leukemia patients with idarubicin alone, and that the protocol used here is tolerable for outpatient treatment. (uni-luebeck.de)
  • Diarrhea, stomach cramps, nausea and vomiting are common among patients treated with idarubicin. (wikipedia.org)
  • All idarubicin-responding patients with high P-gp expression before treatment showed a clear reduction of P-gp-positive blasts. (uni-luebeck.de)
  • It appears the Z HER2 -affibody conjugate of idarubicin has great potential to be implicated as an innovative anti-cancer agent in future clinical trials in patients with HER2-overexpressing ovarian cancer. (iranpath.org)
  • Idarubicin can cause a severe decrease in the number of blood cells in your bone marrow. (medlineplus.gov)
  • If idarubicin is to be used during pregnancy , or if the patient becomes pregnant during therapy, the patient should be apprised of the potential hazard to the fetus. (medicinenet.com)
  • Idarubicin 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 idarubicin. (medlineplus.gov)
  • It is important for you to tell your doctor how you are feeling during your treatment with idarubicin. (medlineplus.gov)
  • Idarubicin is an effective anti-neoplastic drug but specific delivery of it to the targeted cells is still a great challenge. (iranpath.org)
  • Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from idarubicin, mothers should discontinue nursing prior to taking this drug. (medicinenet.com)
  • Emergency Central , emergency.unboundmedicine.com/emergency/view/Davis-Drug-Guide/51396/all/IDArubicin. (unboundmedicine.com)
  • Idarubicin can treat AML in adults, and researchers are studying its use for other types of cancer. (medicalnewstoday.com)
  • The list of intermediates for Idarubicin (CAS No.: 58957-92-9) will be updated soon. (manusaktteva.com)
  • If you can not locate your required intermediate for Idarubicin (CAS No.: 58957-92-9) on this page, you may send us a sourcing request for the specific Idarubicin (CAS No.: 58957-92-9) intermediate you are looking for along with its Cas No., and the Intermediate name and we shall come back to you promptly with more details. (manusaktteva.com)
  • Concentrations of idarubicin and idarubicinol in nucleated blood and bone marrow cells are more than a hundred times the plasma concentrations. (nih.gov)
  • 1. Idarubicin Hydrochloride Injection should be given slowly into a freely flowing intravenous infusion. (nih.gov)
  • Idarubicin Hydrochloride Injection, USP contains idarubicin hydrochloride and is a sterile, semi-synthetic, preservative-free solution (PFS) antineoplastic anthracycline for intravenous use. (nih.gov)
  • Idarubicin Hydrochloride Injection, USP is a sterile, red-orange, isotonic parenteral preservative-free solution, available in 5 mL (5 mg), 10 mL (10 mg) and 20 mL (20 mg) single-use-only vials. (nih.gov)
  • found that IIVP (ifosfamide, idarubicin, and etoposide) was a salvage regimen with acceptable toxicity and highly effective for patients with R/R NHL 17 . (nature.com)
  • Due to the shortage of carmustine, bendamustine and nimustine in China, we aimed to examine conditioning with idarubicin and to compare the efficacy and toxicity between BEAC and idarubicin-substituted BEAC (IEAC). (nature.com)
  • cyclophosphamide increases toxicity of idarubicin by Other (see comment). (medscape.com)
  • paclitaxel increases toxicity of idarubicin by Other (see comment). (medscape.com)
  • palifermin increases toxicity of idarubicin by Other (see comment). (medscape.com)
  • Shortly before the all-trans retinoic acid (ATRA) era, the GIMEMA cooperative group initiated a randomized study comparing idarubicin (IDA) alone with IDA plus arabinosylcytosine (Ara-C) as induction treatment in patients with newly diagnosed hypergranular acute promyelocytic leukemia (APL). (nih.gov)
  • Determine the complete remission (CR) rate in patients with acute promyelocytic leukemia treated with induction comprising tretinoin (ATRA) and idarubicin (IDA). (knowcancer.com)
  • Induction: Patients receive oral tretinoin (ATRA) twice daily beginning on day 1 and continuing for 30-90 days and idarubicin (IDA) IV over 15 minutes on days 2, 4, and 8. (knowcancer.com)
  • However, idarubicin, which was a widely used anthracycline drug for NHL patients, was rarely reported to be added in conditioning regimen. (nature.com)
  • Consolidation therapy: Beginning 30-60 days after the start of induction therapy , patients receive oral pravastatin once daily on days 1-6 and idarubicin IV over 10-15 minutes and cytarabine IV continuously on days 4 and 5. (survivornet.com)
  • 2. Lipiodol trans-arterial chemoembolization of hepatocellular carcinoma with idarubicin: first experience. (nih.gov)
  • 5. Idarubicin-loaded Beads for Chemoembolization of Hepatocellular Carcinoma: The IDASPHERE II Single-Arm Phase II Trial. (nih.gov)
  • Due to the shortage of carmustine, we switched to idarubicin-substituted BEAC (IEAC) conditioning regimen. (nature.com)
  • In conclusion, IEAC regimen was well tolerated and replacement with idarubicin could be an alternative when carmustine was not available. (nature.com)
  • Idarubicin /ˌaɪdəˈruːbɪsɪn/ or 4-demethoxydaunorubicin is an anthracycline antileukemic drug. (wikipedia.org)
  • idarubicin decreases effects of adenovirus types 4 and 7 live, oral by pharmacodynamic antagonism. (medscape.com)
  • Idarubicin has already been shown to be an important antileukaemic agent in Phase II-III studies. (nih.gov)
  • Idarubicin 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 idarubicin. (medlineplus.gov)