Anthraquinones
Cytarabine
Antineoplastic Combined Chemotherapy Protocols
ATP-Binding Cassette Transporters
Drug Resistance, Multiple
Drug Resistance, Neoplasm
Prednisone
Vidarabine
Doxorubicin
Etoposide
Daunorubicin
Idarubicin
P-Glycoprotein
Amsacrine
Neoplasm Proteins
Remission Induction
Intercalating Agents
Taxoids
Estramustine
Topotecan
Cardiotoxins
Drug Evaluation
Cyclophosphamide
Leukemia, Myeloid
DNA Topoisomerases, Type II
Leukemia, Myeloid, Acute
Drug Administration Schedule
Atypical multidrug resistance: breast cancer resistance protein messenger RNA expression in mitoxantrone-selected cell lines. (1/750)
BACKGROUND: Human cancer cell lines grown in the presence of the cytotoxic agent mitoxantrone frequently develop resistance associated with a reduction in intracellular drug accumulation without increased expression of the known drug resistance transporters P-glycoprotein and multidrug resistance protein (also known as multidrug resistance-associated protein). Breast cancer resistance protein (BCRP) is a recently described adenosine triphosphate-binding cassette transporter associated with resistance to mitoxantrone and anthracyclines. This study was undertaken to test the prevalence of BCRP overexpression in cell lines selected for growth in the presence of mitoxantrone. METHODS: Total cellular RNA or poly A+ RNA and genomic DNA were isolated from parental and drug-selected cell lines. Expression of BCRP messenger RNA (mRNA) and amplification of the BCRP gene were analyzed by northern and Southern blot hybridization, respectively. RESULTS: A variety of drug-resistant human cancer cell lines derived by selection with mitoxantrone markedly overexpressed BCRP mRNA; these cell lines included sublines of human breast carcinoma (MCF-7), colon carcinoma (S1 and HT29), gastric carcinoma (EPG85-257), fibrosarcoma (EPF86-079), and myeloma (8226) origins. Analysis of genomic DNA from BCRP-overexpressing MCF-7/MX cells demonstrated that the BCRP gene was also amplified in these cells. CONCLUSIONS: Overexpression of BCRP mRNA is frequently observed in multidrug-resistant cell lines selected with mitoxantrone, suggesting that BCRP is likely to be a major cellular defense mechanism elicited in response to exposure to this drug. It is likely that BCRP is the putative "mitoxantrone transporter" hypothesized to be present in these cell lines. (+info)Multiple mechanisms confer drug resistance to mitoxantrone in the human 8226 myeloma cell line. (2/750)
Selection for in vitro drug resistance can result in a complex phenotype with more than one mechanism of resistance emerging concurrently or sequentially. We examined emerging mechanisms of drug resistance during selection with mitoxantrone in the human myeloma cell line 8226. A novel transport mechanism appeared early in the selection process that was associated with a 10-fold resistance to mitoxantrone in the 8226/MR4 cell line. The reduction in intracellular drug concentration was ATP-dependent and ouabain-insensitive. The 8226/MR4 cell line was 34-fold cross-resistant to the fluorescent aza-anthrapyrazole BBR 3390. The resistance to BBR 3390 coincided with a 50% reduction in intracellular drug concentration. Confocal microscopy using BBR 3390 revealed a 64% decrease in the nuclear:cytoplasmic ratio in the drug-resistant cell line. The reduction in intracellular drug concentration of both mitoxantrone and BBR 3390 was reversed by a novel chemosensitizing agent, fumitremorgin C. In contrast, fumitremorgin C had no effect on resistance to mitoxantrone or BBR 3390 in the P-glycoprotein-positive 8226/DOX6 cell line. Increasing the degree of resistance to mitoxantrone in the 8226 cell line from 10 to 37 times (8226/MR20) did not further reduce the intracellular drug concentration. However, the 8226/MR20 cell line exhibited 88 and 70% reductions in topoisomerase II beta and alpha expression, respectively, compared with the parental drug sensitive cell line. This decrease in topoisomerase expression and activity was not observed in the low-level drug-resistant, 8226/MR4 cell line. These data demonstrate that low-level mitoxantrone resistance is due to the presence of a novel, energy-dependent drug efflux pump similar to P-glycoprotein and multidrug resistance-associated protein. Reversal of resistance by blocking drug efflux with fumitremorgin C should allow for functional analysis of this novel transporter in cancer cell lines or clinical tumor samples. Increased resistance to mitoxantrone may result from reduced intracellular drug accumulation, altered nuclear/cytoplasmic drug distribution, and alterations in topoisomerase II activity. (+info)Dose-escalation study of docetaxel in combination with mitoxantrone as first-line treatment in patients with metastatic breast cancer. (3/750)
PURPOSE: To define the maximum-tolerated dose (MTD) and the dose-limiting toxicities (DLTs) of docetaxel in combination with mitoxantrone in patients with metastatic breast cancer (MBC). PATIENTS AND METHODS: Forty-one chemotherapy-naive patients with MBC (median age, 61 years) were enrolled. Thirty-eight (93%) had performance status (World Health Organization [WHO]) 0, 29 (71%) were postmenopausal, and 21 (51%) had estrogen receptor-negative tumors. Patients received escalated doses of docetaxel (75 to 100 mg/m2) on day 1 and mitoxantrone (8 to 22 mg/m2) on day 8. Treatment was repeated every 3 weeks. RESULTS: A total of 217 chemotherapy cycles were administered. Without recombinant human granulocyte colony-stimulating factor (rhG-CSF) support, the MTD1 occurred at the first dose level (docetaxel 75 mg/m2 and mitoxantrone 8 mg/m2); DLTs were febrile neutropenia, grade 4 neutropenia lasting more than 5 days, and grade 3 diarrhea. With prophylactic rhG-CSF, the MTD2 was docetaxel 100 mg/m2 and mitoxantrone 20 mg/m2; DLTs were febrile neutropenia and grade 4 neutropenia. Nine (22%) patients developed neutropenia after the first cycle of treatment. A total of 19 episodes of febrile neutropenia (9% of the cycles) occurred during the whole period of the study; there were no toxic deaths. At high docetaxel (100 mg/m2) and mitoxantrone (> 12 mg/m2) dose levels, a significant decrease of the absolute lymphocyte number was observed; immunophenotyping revealed that all lymphocyte subpopulations were reduced. Grades 2 and 3 neurosensory toxicity occurred in six patients (15%) and one patient (2%), respectively. No cardiac toxicity was observed. Nine complete responses (22%) and 23 partial responses (56%) were achieved (overall response rate, 78%; 95% confidence interval, 62.5% to 88.8%). The median duration of response was 12.5 months, and the median time to tumor progression was 14.5 months. CONCLUSION: The reported combination of docetaxel and mitoxantrone with G-CSF support is a safe, intensified, well-tolerated, and effective regimen as first-line treatment in patients with MBC. (+info)Autologous transplantation of chemotherapy-purged PBSC collections from high-risk leukemia patients: a pilot study. (4/750)
We have recently demonstrated that the combination of the alkylating agent nitrogen mustard (NM) and etoposide (VP-16) is capable of eliminating, ex vivo, leukemic cells contaminating PBSC collections and this is associated with a significant recovery of primitive and committed hematopoietic progenitor cells. Based on these data a pilot study on autologous transplantation of NM/VP-16 purged PBSC for high-risk leukemic patients was recently initiated. Twelve patients (seven females and five males) with a median age of 46 years (range 18-57) have been treated. Two patients had acute myeloblastic leukemia (AML) resistant to conventional induction treatment, four patients had secondary AML in I complete remission (CR), one patient was in II CR after failing a previous autologous BM transplantation, while two additional AML individuals were in I CR achieved after three or more cycles of induction treatment. Two patients with high-risk acute lymphoblastic leukemia (ALL) in I CR and one patient with mantle cell lymphoma and leukemic dissemination were also included. Eight patients showed karyotypic abnormalities associated with a poor clinical outcome. The mobilizing regimens included cytosine arabinoside and mitoxantrone with (n = 6) or without fludarabine (n = 3) followed by subcutaneous administration of G-CSF (5 microg/kg/day until the completion of PBSC collection) and G-CSF alone (n = 3) (15 microg/kg/day). A median of two aphereses (range 1-3) allowed the collection of 7.2 x 10(8) TNC/kg (range 3.4-11.5), 5 x 10(6) CD34+ cells/kg (range 2.1-15.3) and 9.2 x 10(4) CFU-GM/kg (0.3-236). PBSC were treated with a constant dose of 20 microg of VP-16/ml and a median individual-adjusted dose (survival < or = 5% of steady-state BM CFU-GM) of NM of 0.7 microg/ml (range 0.25-1.25). Eleven patients were reinfused after busulfan (16 mg/kg) and Cy (120 mg/kg) conditioning with a median residual dose of 0.3 x 10(4) CFU-GM/kg (0-11.5). The median time to neutrophil engraftment (>0.5 x 10(9)/l) for evaluable patients was 25 days (range 12-59); the median time to platelet transfusion independence (>20 and >50 x 10(9)/l) was 40 days (18-95) and 69 days (29-235), respectively. Hospital discharge occurred at a median of 25 days (18-58) after stem cell reinfusion. Four individuals are alive in CR (n = 3) or with residual nodal disease (n = 1 lymphoma patient) with a follow-up of 32, 26, 3 and 14 months, respectively. Seven patients died due to disease progression or relapse (n = 5) or extrahematological transplant toxicity (n = 2). Our data suggest that pharmacological purging of leukapheresis collections of leukemic patients at high-risk of relapse is feasible and ex vivo treated cells reconstitute autologous hematopoiesis. (+info)Follicular large cell lymphoma: an aggressive lymphoma that often presents with favorable prognostic features. (5/750)
It is debated whether follicular large cell lymphoma (FLCL) has a clinical behavior that is distinct from indolent follicular lymphomas, and whether there is a subset of patients who can be potentially cured. We report here our experience with 100 FLCL patients treated at our institution since 1984 with three successive programs. We evaluated the predictive value of pretreatment clinical features, including two risk models, the Tumor Score System and the International Prognostic Index (IPI). With a median follow-up of 67 months, the 5-year survival is 72% and the failure-free survival (FFS) is 67%, with a possible plateau in the FFS curve, particularly for patients with stage I-III disease. Features associated with shorter survival included age >/=60, elevated lactic dehydrogenase (LDH) or beta-2-microglobulin (beta2M), advanced stage, and bone marrow involvement. Stage III patients had significantly better survival than stage IV patients (P <.05). By the IPI and Tumor Score System, 80% of the patients were in the lower risk groups; both systems stratified patients into prognostic groups. Patients with FLCL have clinical features and response to treatment similar to that reported for diffuse large cell lymphoma. Prognostic risk systems for aggressive lymphomas are useful for FLCL. A meaningful fraction of patients may possibly be cured when treated as aggressive lymphomas. (+info)Early detection of anthracycline induced cardiotoxicity in asymptomatic patients with normal left ventricular systolic function: autonomic versus echocardiographic variables. (6/750)
OBJECTIVE: To investigate left ventricular dysfunction in patients who had been treated with anthracycline based chemotherapy. METHODS: Autonomic function was compared with left ventricular diastolic function in 20 asymptomatic women with normal systolic function (left ventricular ejection fraction (LVEF) > 0.50) treated for breast cancer with high dose anthracycline based chemotherapy, and 20 age matched healthy controls. Left ventricular diastolic function was assessed echocardiographically by measuring the early peak flow velocity to atrial peak flow velocity ratio, isovolumic relaxation time, and deceleration time. Heart rate variability analysis was assessed for time domain and frequency domain parameters. RESULTS: The mean (SD) age of the patients was 45 (7) years and the mean LVEF was 0.59 (0.06). The time interval after the end of chemotherapy was 29 (27) months. One or more diastolic variables were abnormal in 50% of the patients. Heart rate variability was abnormal in 85% of patients. Mean values of both time domain and frequency domain parameters were decreased (p < 0.05), in particular the parasympathetic indices. CONCLUSIONS: Autonomic impairment occurs in a large proportion of asymptomatic patients with normal systolic left ventricular function after high dose anthracycline based chemotherapy. In particular, heart rate variability analysis may be a sensitive tool to identify the first signs of cardiotoxicity in these patients. (+info)Time sequential chemotherapy for primary refractory or relapsed adult acute myeloid leukemia: results of the phase II Gemia protocol. (7/750)
BACKGROUND AND OBJECTIVE: High-dose cytarabine (HDAra-C), mitoxantrone and etoposide are the mainstay of several active regimens against relapsed or refractory acute myelogenous leukemia (AML). We designed a phase II study to assess the efficacy and side effects of a time sequential application of mitoxantrone plus intermediate-dose Ara-C followed by HDAra-C plus etoposide (GEMIA) in adult patients with refractory or relapsed AML. DESIGN AND METHODS: Patients with refractory or relapsed AML were eligible for GEMIA salvage therapy, which comprised mitoxantrone 12 mg/m2/day on days 1-3, Ara-C 500 mg/m2/day as a 24-hour continuous infusion on days 1-3, followed by HDAra-C 2 g/m2/12-hourly on days 6-8 and etoposide 100 mg/m2/12-hourly on days 6-8. Granulocyte colony-stimulating factor was started on day 14. In patients above the age of 55 the dose of Ara-C in the first sequence (days 1-3) was reduced to 250 mg/m2. RESULTS: Twenty patients were included, of whom 12 achieved complete remission after GEMIA (60%, 95% CI 40-80%), one was refractory and five died early from infection. Two additional patients achieved partial remission after GEMIA and complete remission after consolidation chemotherapy, for a final CR rate of 70% (95% CI 48-88%). Neutrophils recovered at a median of 27 days (range, 22-43) and platelets 46 days (range, 25-59) after the start of treatment. The median duration of remission was 133 days (range, 36-417+) whereas overall survival time lasted for a median of 153 days (range, 13-554+). Treatment-associated toxicity was comprised predominantly of infection, mucositis and diarrhea that reached World Health Organization grades III-V in 40%, 40% and 30% of patients, respectively. Despite the intention to rapidly proceed to a hematopoietic stem cell transplant in patients in remission, only five patients reached the transplant. INTERPRETATION AND CONCLUSIONS: The GEMIA time sequential chemotherapy regimen appears effective in obtaining remissions in refractory and relapsed adult AML. The high toxicity seen, however, suggests that its design is amenable to further improvements, especially in more elderly patients. Since remissions are short-lived, more innovative post-remission strategies are needed. (+info)Trisomy 21 associated transient neonatal myeloproliferation in the absence of Down's syndrome. (8/750)
Although usually associated with Down's syndrome, transient neonatal myeloproliferation (TMD) can occur in the absence of a constitutional trisomy 21. This report describes two such cases, both of whom had a trisomy 21 restricted to clonal cells. Unlike in previous such reported cases, spontaneous morphological, cytogenetic, and molecular remission in both cases was followed by re-emergence, in one case, of an evolved clone with a more malignant phenotype which required pharmacological intervention. Awareness that trisomy 21 bearing leukaemia in the neonatal period can be transient even in the absence of Down's syndrome is important to prevent unnecessary treatment. Equally, such cases require indefinite follow up as a proportion may have a recurrence which may require treatment. (+info)Mitoxantrone is a chemotherapy drug that is used to treat various types of cancer, including breast cancer, prostate cancer, and leukemia. It works by interfering with the growth and division of cancer cells, which can slow down or stop the growth of tumors. Mitoxantrone is usually given intravenously (through a vein) or by injection into a muscle. It can cause side effects such as hair loss, nausea, vomiting, and a low white blood cell count.
Anthraquinones are a group of naturally occurring organic compounds that are derived from the anthracene molecule. They are commonly found in plants, particularly in the roots, bark, and leaves of certain species. Anthraquinones have a variety of biological activities, including anti-inflammatory, anti-cancer, and anti-microbial properties. In the medical field, anthraquinones are used as ingredients in a number of medications and natural remedies. For example, some anthraquinones are used as laxatives to relieve constipation, while others are used to treat inflammatory bowel disease. Anthraquinones have also been studied for their potential use in treating cancer, particularly in the treatment of colon cancer and other types of gastrointestinal cancer.
Cytarabine, also known as cytosine arabinoside, is an antineoplastic medication used to treat various types of cancer, including acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), and non-Hodgkin's lymphoma. It works by inhibiting the growth and division of cancer cells, thereby slowing or stopping their growth and spread. Cytarabine is typically administered intravenously or intramuscularly, and its dosage and duration of treatment depend on the type and stage of cancer being treated, as well as the patient's overall health. Common side effects of cytarabine include nausea, vomiting, fatigue, fever, and low blood cell counts, which can increase the risk of infection and bleeding. It is important to note that cytarabine is a chemotherapy drug and can cause serious side effects, so it is typically administered under the supervision of a healthcare professional in a hospital or clinic setting.
ATP-binding cassette (ABC) transporters are a large family of membrane proteins that use the energy from ATP hydrolysis to transport a wide variety of molecules across cell membranes. These transporters are found in all kingdoms of life, from bacteria to humans, and play important roles in many physiological processes, including drug metabolism, detoxification, and the transport of nutrients and waste products across cell membranes. In the medical field, ABC transporters are of particular interest because they can also transport drugs and other xenobiotics (foreign substances) across cell membranes, which can affect the efficacy and toxicity of these compounds. For example, some ABC transporters can pump drugs out of cells, making them less effective, while others can transport toxins into cells, increasing their toxicity. As a result, ABC transporters are an important factor to consider in the development of new drugs and the optimization of drug therapy. ABC transporters are also involved in a number of diseases, including cancer, cystic fibrosis, and certain neurological disorders. In these conditions, the activity of ABC transporters is often altered, leading to the accumulation of toxins or the loss of important molecules, which can contribute to the development and progression of the disease. As a result, ABC transporters are an important target for the development of new therapies for these conditions.
Prednisone is a synthetic corticosteroid medication that is used to treat a variety of medical conditions, including allergies, autoimmune disorders, inflammatory diseases, and certain types of cancer. It works by reducing inflammation and suppressing the immune system, which can help to reduce symptoms and slow the progression of the disease. Prednisone is available in both oral and injectable forms, and it is typically prescribed in doses that are gradually increased or decreased over time, depending on the patient's response to the medication and the specific condition being treated. While prednisone can be effective in treating a wide range of medical conditions, it can also have side effects, including weight gain, mood changes, and increased risk of infections. Therefore, it is important for patients to work closely with their healthcare provider to monitor their response to the medication and adjust the dosage as needed.
Vidarabine, also known as vidarabine phosphate or ara-A, is an antiviral medication used to treat herpes simplex virus (HSV) infections, including genital herpes and herpes encephalitis. It works by inhibiting the replication of the virus, thereby reducing the severity and duration of symptoms. Vidarabine is typically administered intravenously, either as a single dose or as a series of doses over several days. It is not effective against all types of viruses, and its use is limited to treating HSV infections. Common side effects of vidarabine include nausea, vomiting, headache, and fever. More serious side effects are rare, but may include allergic reactions, liver damage, and bone marrow suppression. Vidarabine is a prescription medication and should only be used under the guidance of a healthcare professional.
Doxorubicin is an anthracycline chemotherapy drug that is used to treat a variety of cancers, including breast cancer, ovarian cancer, and leukemia. It works by interfering with the production of DNA and RNA, which are essential for the growth and division of cancer cells. Doxorubicin is usually administered intravenously, and its side effects can include nausea, vomiting, hair loss, and damage to the heart and kidneys. It is a powerful drug that can be effective against many types of cancer, but it can also have serious side effects, so it is typically used in combination with other treatments or in low doses.
Etoposide is a chemotherapy drug that is used to treat various types of cancer, including small cell lung cancer, ovarian cancer, testicular cancer, and some types of leukemia. It works by interfering with the process of cell division, which is necessary for cancer cells to grow and multiply. Etoposide is usually given intravenously or orally, and its side effects can include nausea, vomiting, hair loss, and an increased risk of infection.
Daunorubicin is an anthracycline chemotherapy drug that is used to treat various types of cancer, including acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), and some types of solid tumors such as breast cancer, ovarian cancer, and sarcomas. It works by interfering with the ability of cancer cells to divide and grow, ultimately leading to their death. Daunorubicin is usually administered intravenously, and its side effects can include nausea, vomiting, hair loss, low white blood cell count, and damage to the heart muscle.
Idarubicin is a chemotherapy drug that is used to treat certain types of cancer, including acute myeloid leukemia (AML), non-Hodgkin's lymphoma (NHL), and breast cancer. It works by interfering with the growth and division of cancer cells, which can slow or stop the growth of tumors. Idarubicin is usually administered intravenously, and the dosage and duration of treatment will depend on the type and stage of cancer being treated, as well as the patient's overall health. Side effects of idarubicin may include nausea, vomiting, hair loss, low blood cell counts, and an increased risk of infection.
P-Glycoprotein (P-gp) is a membrane protein that is primarily found in the cells of the liver, kidneys, and intestines. It is also expressed in the blood-brain barrier and other tissues. P-gp is responsible for the transport of a wide range of molecules across cell membranes, including many drugs and toxins. One of the main functions of P-gp is to act as a barrier to protect cells from potentially harmful substances. It does this by actively pumping certain molecules out of cells, effectively removing them from the body. This can be beneficial in preventing the accumulation of toxins and drugs in the body, but it can also make it more difficult for certain drugs to enter cells and be effective. P-gp is also involved in the metabolism of certain drugs, which can affect their effectiveness and toxicity. For example, P-gp can pump certain drugs out of cells before they have a chance to be fully metabolized, which can reduce their effectiveness. On the other hand, P-gp can also pump out metabolites of certain drugs, which can increase their toxicity. In the medical field, P-gp is an important factor to consider when developing new drugs. Drugs that are substrates of P-gp may have reduced effectiveness or increased toxicity if they are administered to patients who are also taking other drugs that are substrates of P-gp. Therefore, it is important to understand how P-gp affects the metabolism and transport of drugs in order to optimize their use in patients.
Amsacrine is a chemotherapy drug that is used to treat certain types of cancer, including leukemia, lymphoma, and sarcoma. It works by interfering with the ability of cancer cells to divide and grow. Amsacrine is usually given intravenously (into a vein) or orally (by mouth). It can cause side effects such as nausea, vomiting, diarrhea, and low blood cell counts.
Neoplasm proteins are proteins that are produced by cancer cells. These proteins are often abnormal and can contribute to the growth and spread of cancer. They can be detected in the blood or other body fluids, and their presence can be used as a diagnostic tool for cancer. Some neoplasm proteins are also being studied as potential targets for cancer treatment.
Razoxane, also known as hydroxyurea, is a medication used to treat certain types of cancer, including leukemia and lymphoma. It works by slowing the growth of cancer cells and preventing them from dividing and multiplying. Razoxane is usually given in combination with other chemotherapy drugs and is typically administered intravenously or orally. It can also be used to prevent or reduce the risk of blood clots in people who have had a heart attack or stroke.
Taxoids are a class of natural compounds found in certain plants, particularly in the yew tree family. They are a type of chemotherapy drug that are used to treat various types of cancer, including ovarian, breast, and lung cancer. Taxoids work by interfering with the ability of cancer cells to divide and grow, ultimately leading to their death. The most well-known taxoid is paclitaxel, which is used in the treatment of ovarian and breast cancer. Other taxoids include docetaxel and nab-paclitaxel.
Estramustine is a medication that is used to treat prostate cancer. It is a combination of two hormones, estradiol and mustine, which work together to slow the growth of cancer cells and shrink tumors. Estramustine is usually given as a capsule or a liquid to be taken by mouth. It can also be given as an injection into a muscle or a vein. Estramustine is often used in combination with other treatments, such as surgery, radiation therapy, or chemotherapy, to help manage prostate cancer. It can cause side effects such as nausea, vomiting, diarrhea, and hot flashes.
Topotecan is a chemotherapy drug that is used to treat certain types of cancer, including ovarian cancer, small cell lung cancer, and cervical cancer. It works by interfering with the ability of cancer cells to divide and grow. Topotecan is usually given intravenously (through a vein) or orally (by mouth). It can cause side effects such as nausea, vomiting, hair loss, and low blood cell counts.
Cyclophosphamide is an immunosuppressive drug that is commonly used to treat various types of cancer, including lymphoma, leukemia, and multiple myeloma. It works by inhibiting the growth and division of cells, including cancer cells, and by suppressing the immune system. Cyclophosphamide is usually administered intravenously or orally, and its dosage and duration of treatment depend on the type and stage of cancer being treated, as well as the patient's overall health. Side effects of cyclophosphamide can include nausea, vomiting, hair loss, fatigue, and an increased risk of infection. It can also cause damage to the kidneys, bladder, and reproductive organs, and may increase the risk of developing certain types of cancer later in life.
Leukemia, Myeloid is a type of cancer that affects the myeloid cells in the bone marrow. Myeloid cells are a type of white blood cell that helps fight infections and diseases in the body. In leukemia, myeloid cells grow and divide uncontrollably, leading to an overproduction of these cells in the bone marrow and bloodstream. There are several subtypes of myeloid leukemia, including acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). AML is a rapidly progressing cancer that usually affects older adults, while CML is a slower-growing cancer that is more common in middle-aged and older adults. Symptoms of myeloid leukemia may include fatigue, weakness, fever, night sweats, weight loss, and easy bruising or bleeding. Treatment for myeloid leukemia typically involves chemotherapy, radiation therapy, targeted therapy, and bone marrow transplantation. The prognosis for myeloid leukemia depends on the subtype, age of the patient, and the stage of the disease at diagnosis.
Prostatic neoplasms refer to tumors that develop in the prostate gland, which is a small gland located in the male reproductive system. These tumors can be either benign (non-cancerous) or malignant (cancerous). Benign prostatic neoplasms, also known as benign prostatic hyperplasia (BPH), are the most common type of prostatic neoplasm and are typically associated with an increase in the size of the prostate gland. Malignant prostatic neoplasms, on the other hand, are more serious and can spread to other parts of the body if left untreated. The most common type of prostate cancer is adenocarcinoma, which starts in the glandular cells of the prostate. Other types of prostatic neoplasms include sarcomas, which are rare and start in the connective tissue of the prostate, and carcinoid tumors, which are rare and start in the neuroendocrine cells of the prostate.
DNA topoisomerases, type II, are a class of enzymes that play a crucial role in regulating DNA topology during various cellular processes, such as DNA replication, transcription, and recombination. These enzymes are responsible for relaxing or tightening the supercoiled structure of DNA, which is essential for maintaining the proper function of the genome. Type II topoisomerases are divided into two subclasses: type IIA and type IIB. Type IIA topoisomerases, also known as topoisomerase II, are involved in DNA replication and transcription, and are often targeted by anti-cancer drugs. Type IIB topoisomerases, on the other hand, are involved in DNA repair and recombination. Type II topoisomerases work by creating temporary breaks in the DNA double helix, allowing the DNA strands to pass through each other and relieve tension. Once the topoisomerase has completed its task, it seals the DNA break, restoring the original topology of the DNA. In the medical field, type II topoisomerases are often targeted by drugs, such as etoposide and doxorubicin, which are used to treat various types of cancer. These drugs work by inhibiting the activity of type II topoisomerases, leading to the accumulation of DNA damage and ultimately causing cell death. However, the use of these drugs can also lead to side effects, such as nausea, vomiting, and hair loss.
Acute Myeloid Leukemia (AML) is a type of cancer that affects the bone marrow and blood cells. It is characterized by the rapid growth of abnormal white blood cells, called myeloid cells, in the bone marrow. These abnormal cells do not function properly and can crowd out healthy blood cells, leading to a variety of symptoms such as fatigue, weakness, and frequent infections. AML can occur in people of all ages, but it is most common in adults over the age of 60. Treatment for AML typically involves chemotherapy, radiation therapy, and/or stem cell transplantation.
Mitoxantrone
Drug discovery
Multiple sclerosis
Management of multiple sclerosis
Chemotherapy
Anthracycline
Marburg acute multiple sclerosis
Management of prostate cancer
Docetaxel
Multiple sclerosis drug pipeline
Neuromyelitis optica spectrum disorder
Neutrophilic eccrine hidradenitis
Anti-AQP4 disease
Balo concentric sclerosis
Losoxantrone
List of RNAs
Cabazitaxel
Inflammatory demyelinating diseases of the central nervous system
Ester H. Segal
Interferon beta-1a
Metronomic therapy
Multiple sclerosis research
Topoisomerase
Interferon beta-1b
FCM (chemotherapy)
Anthraquinones
ATP-binding cassette transporter
Mantle cell lymphoma
Ultrasound-triggered drug delivery using stimuli-responsive hydrogels
Blood-spinal cord barrier
Mitoxantrone Injection: MedlinePlus Drug Information
Prostate Cancer Medication: Antineoplastics, GnRH Agonist, Antineoplastics, Antiandrogen, Antineoplastics, GnRH Antagonist,...
Table 1 - Disseminated Infections with Talaromyces marneffei in Non-AIDS Patients Given Monoclonal Antibodies against CD20 and...
Provenge (sipuleucel-T) dosing, indications, interactions, adverse effects, and more
NIOSHTIC-2 Search Results - Full View
Acute Lymphoblastic Leukemia Medication: Corticosteroids, Antineoplastics, Tyrosine Kinase Inhibitors, Bispecific T-Cell...
National Ambulatory Medical Care Survey, 1994
Multiple Sclerosis (MS) - Neurologic Disorders - MSD Manual Professional Edition
Prostate Cancer Guidelines: Prostate Cancer Screening, Multiparametric Magnetic Resonance Imaging, Management of Clinically...
ICTRP Search Portal
Pesquisa | Prevenção e Controle de Câncer
SAS VALUE LABELS FOR 2007 NHHCS PUBLIC USE FILE
DeCS 2017 - July 04, 2017 version
DeCS 2020 - June 23, 2020 version
DeCS 2019 - June 12, 2019 version
DeCS 2018 - July 31, 2018 version
Should All Patients With MS Receive Aggressive Treatment?
Cardiac Monitoring for Patients on Mitoxantrone
MitoXANTRONE Injection, USP
MedlinePlus - Search Results for: MITOXANTRONE
Mitoxantrone - PubMed
Mitoxantrone - PubMed
mitoxantrone) dosing, indications, interactions, adverse effects, and more
Non-Hodgkin Lymphoma (NHL) Medication: Cytotoxic agents, Antineoplastic Agents, Histone Deacetylase Inhibitors, Antineoplastics...
mitoxantrone) dosing, indications, interactions, adverse effects, and more
Chemotherapy for Childhood Leukemia | American Cancer Society
Effect of GenX on P-Glycoprotein, Breast Cancer Resistance Protein, and Multidrug Resistance-Associated Protein 2 at the Blood...
Discontinuation of Disease Modifying Therapies (DMTs) in Multiple Sclerosis (MS): Extension of the DISCOMS Study | National...
Biomarkers Search
CellMiner - Drug Status List | Genomics and Pharmacology Facility
Publications - Yihong Ye, Ph.D. - NIDDK
NIH Clinical Center Search the Studies: Study Number, Study Title
Doxorubicin: MedlinePlus Drug Information
Van Nevel, Paul 2001 - Office of NIH History and Stetten Museum
Multiple Sclerosis (MS) - Neurologic Disorders - MSD Manual Professional Edition
Code System Concept
Human Genome Epidemiology Literature Finder|Home|PHGKB
165Amount of mitoxantrone2
- The risk of heart damage may depend on the total amount of mitoxantrone given to a person over a lifetime, so your doctor will probably limit the total number of doses you receive if you are using this medication for MS. If you experience any of the following symptoms, call your doctor immediately: difficulty breathing, chest pain, swelling of the legs or ankles, or irregular or fast heartbeat. (medlineplus.gov)
- Because of the risk of heart injury there is a lifetime limit on the amount of mitoxantrone a person may receive. (abilitymagazine.com)
Doxorubicin3
- Tell your doctor and pharmacist if you are taking or have ever received certain cancer chemotherapy medications such as daunorubicin (Cerubidine), doxorubicin (Doxil), epirubicin (Ellence), or idarubicin (Idamycin), or if you have ever been treated with mitoxantrone in the past. (medlineplus.gov)
- Mitoxantrone has activity similar to that of doxorubicin, is less cardiotoxic, and is widely used to treat prostate cancer. (elsevierpure.com)
- Caution with doxorubicin is advised, because during the second cycle, the maximum accumulative dose is achieved and the substitute of doxorubicin with actinomycin-D or mitoxantrone is recommended. (vin.com)
Novantrone1
- The most prominent of these drugs is Novantrone (mitoxantrone), which is given intravenously once every three months. (abilitymagazine.com)
Given intravenously1
- Mitoxantrone injection comes as a liquid to be given intravenously (into a vein) by a doctor or nurse in a hospital or clinic. (medlineplus.gov)
Intravenously1
- After enrollment onto a multicenter local consortium study, subjects were treated with mitoxantrone at a dose of 12 mg/m 2 intravenously every 3 weeks plus continuous oral ketoconazole at a dose of 400 mg 3 times daily and ascorbic acid at a dose of 250 mg. (elsevierpure.com)
Chemotherapy2
- Mitoxantrone should be given only under the supervision of a doctor with experience in the use of chemotherapy medications. (medlineplus.gov)
- Mitoxantrone may increase your risk for developing leukemia (cancer of the white blood cells), especially when it is given in high doses or together with certain other chemotherapy medications. (medlineplus.gov)
Leukemia6
- Mitoxantrone injection is also used with other medications to treat certain types of leukemia. (medlineplus.gov)
- When mitoxantrone injection is used to treat leukemia, you will continue to receive this medication based on your condition and how you respond to the treatment. (medlineplus.gov)
- Mitoxantrone is a member of the antibiotics/antineoplastics drug class and is commonly used for Acute Nonlymphocytic Leukemia, Mantle Cell Lymphoma, Multiple Sclerosis, and others. (drugs.com)
- Those studies showed that acute leukemia occurred in .07 percent to .25 percent of MS patients taking mitoxantrone. (scienceblog.com)
- The potential risk of leukemia should be carefully considered against the potential benefits of mitoxantrone treatment on every single patient. (scienceblog.com)
- It is vital that all MS patients treated with mitoxantrone undergo prolonged and careful hematological follow-up to check for acute leukemia," Martinelli said. (scienceblog.com)
Dose2
- and problems with vision, speech, and bladder control), your doctor will also perform certain tests before each dose of mitoxantrone injection and yearly after you have completed your treatment. (medlineplus.gov)
- They also had a greater cumulative dose of mitoxantrone. (scienceblog.com)
Injection6
- Mitoxantrone injection may cause damage to your heart at any time during your treatment or months to years after your treatment has ended. (medlineplus.gov)
- Talk to your doctor about the risks of using mitoxantrone injection. (medlineplus.gov)
- Mitoxantrone injection is also used together with steroid medications to relieve pain in people with advanced prostate cancer who did not respond to other medications. (medlineplus.gov)
- Mitoxantrone injection is in a class of medications called anthracenediones. (medlineplus.gov)
- When mitoxantrone injection is used to treat MS, it is usually given once every 3 months for about 2 to 3 years (for a total of 8 to 12 doses). (medlineplus.gov)
- When mitoxantrone injection is used to treat prostate cancer, it is usually given once every 21 days. (medlineplus.gov)
Prostate cancer4
- The current study sought to evaluate the toxicity and activity of mitoxantrone plus ketoconazole in a cohort of patients with hormone-refractory prostate cancer. (elsevierpure.com)
- Mitoxantrone plus ketoconazole is well tolerated, is active in hormone-refractory prostate cancer, and should be studied further. (elsevierpure.com)
- Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. (sfu.ca)
- Prednisone plus cabazitaxel or mitoxantrone for metastatic castration resistant prostate cancer progressing after docetaxel treatment: A randomised open-label trial. (sfu.ca)
Treatment3
- Your doctor will examine you and perform certain tests to check how well your heart is working before beginning treatment with mitoxantrone and if you show any signs of heart problems. (medlineplus.gov)
- Mitoxantrone is an immunosuppressant drug approved by the FDA for treatment of several forms of advancing MS. It is one of only two drugs that has been shown to benefit people with secondary progressive MS who are having attacks. (scienceblog.com)
- The study participants all had at least one cycle of mitoxantrone treatment and were observed for at least one year. (scienceblog.com)
Patients1
- Determine the clinical effectiveness of bevacizumab, cytarabine, and mitoxantrone in patients with poor-risk hematologic malignancies. (knowcancer.com)
Form1
- Mitoxantrone offers may take the form of printable coupons, rebates, savings or copay cards, trial offers, or free samples. (drugs.com)
Cyclophosphamide1
- 14. Intravenous mitoxantrone and cyclophosphamide as second-line therapy in multiple sclerosis: an open-label comparative study of efficacy and safety. (nih.gov)
Hydrochloride2
- The concentrate is a sterile, nonpyrogenic, dark blue aqueous solution containing mitoxantrone hydrochloride equivalent to 2 mg/mL mitoxantrone free base, with the following inactive ingredients: sodium chloride (0.800% w/v), sodium acetate (0.005% w/v), acetic acid (0.046% w/v), and water for injection. (nih.gov)
- The chemotherapy agents included cabazitaxel, docetaxel, mitoxantrone hydrochloride, and estramustine, and were used as monotherapy or as combination therapy. (ahdbonline.com)
Cumulative mitoxantrone dose2
- Patients should not receive a cumulative mitoxantrone dose greater than 140 mg/m 2 . (medscape.com)
- Cardiotoxicity risk increases with cumulative mitoxantrone dose and may occur whether or not cardiac risk factors are present. (nih.gov)
Dose of mitoxantrone1
- and problems with vision, speech, and bladder control), your doctor will also perform certain tests before each dose of mitoxantrone injection and yearly after you have completed your treatment. (medlineplus.gov)
Risks of mitoxantrone1
- The possible danger of cardiac effects in patients previously treated with daunorubicin or doxorubicin should be considered when weighing the benefits and risks of mitoxantrone. (medscape.com)
Multiple sclerosis11
- 3. Revision of the risk of secondary leukaemia after mitoxantrone in multiple sclerosis populations is required. (nih.gov)
- 6. [Mitoxantrone-related acute leukemia by multiple sclerosis. (nih.gov)
- 7. Therapy-related acute leukemia in two patients with multiple sclerosis treated with Mitoxantrone. (nih.gov)
- 11. Long-term risk of leukaemia or cardiomyopathy after mitoxantrone therapy for multiple sclerosis. (nih.gov)
- 13. Acute promyelocytic leukemia after mitoxantrone therapy for multiple sclerosis. (nih.gov)
- 16. Management of worsening multiple sclerosis with mitoxantrone: a review. (nih.gov)
- 17. Mitoxantrone in the treatment of multiple sclerosis. (nih.gov)
- 18. Therapeutic role of mitoxantrone in multiple sclerosis. (nih.gov)
- 19. The current role of mitoxantrone in the treatment of multiple sclerosis. (nih.gov)
- 20. Acute myeloid leukaemia induced by mitoxantrone in a multiple sclerosis patient. (nih.gov)
- Early data show that the Cunningham group's system can identify medications including morphine, methadone, phenobarbital, the sedative promethazine, and mitoxantrone, which is used to treat multiple sclerosis. (innovationtoronto.com)
Injection13
- Mitoxantrone Injection, USP (concentrate) should be administered under the supervision of a physician experienced in the use of cytotoxic chemotherapy agents. (nih.gov)
- Mitoxantrone Injection, USP (concentrate) should be given slowly into a freely flowing intravenous infusion. (nih.gov)
- Mitoxantrone Injection, USP (concentrate) is a synthetic antineoplastic anthracenedione for intravenous use. (nih.gov)
- Mitoxantrone injection may cause damage to your heart at any time during your treatment or months to years after your treatment has ended. (medlineplus.gov)
- Talk to your doctor about the risks of using mitoxantrone injection. (medlineplus.gov)
- Mitoxantrone injection is also used together with steroid medications to relieve pain in people with advanced prostate cancer who did not respond to other medications. (medlineplus.gov)
- Mitoxantrone injection is also used with other medications to treat certain types of leukemia. (medlineplus.gov)
- Mitoxantrone injection is in a class of medications called anthracenediones. (medlineplus.gov)
- Mitoxantrone injection comes as a liquid to be given intravenously (into a vein) by a doctor or nurse in a hospital or clinic. (medlineplus.gov)
- When mitoxantrone injection is used to treat MS, it is usually given once every 3 months for about 2 to 3 years (for a total of 8 to 12 doses). (medlineplus.gov)
- When mitoxantrone injection is used to treat prostate cancer, it is usually given once every 21 days. (medlineplus.gov)
- When mitoxantrone injection is used to treat leukemia, you will continue to receive this medication based on your condition and how you respond to the treatment. (medlineplus.gov)
- The most often prescribed steroid is Methylprednisolone, while other treatments include Natalizumab, Interferon beta-1b and Mitoxantrone, all through injection of the MS patient. (medicalmarijuana411.com)
Cardiotoxicity4
- Given the potential severity of cardiotoxicity and evidence suggesting poor adherence to the recommendations for monitoring cardiac function, the FDA is currently working with the manufacturers of mitoxantrone to remind healthcare professionals of the importance of adhering to the recommendations for patients with MS who are treated with mitoxantrone. (medscape.com)
- Patients should undergo yearly quantitative LVEF evaluations after stopping mitoxantrone to monitor for late-occurring cardiotoxicity, using the same methodology that was used for assessments that were done during treatment. (medscape.com)
- MS patients should undergo yearly quantitative LVEF evaluation after stopping mitoxantrone to monitor for late occurring cardiotoxicity. (nih.gov)
- Mitoxantrone risk for cardiotoxicity has been significantly underestimated. (nih.gov)
Doses6
- Additional doses of mitoxantrone should not be administered to patients who have experienced either a drop in LVEF to below the lower limit of normal or a clinically significant reduction in LVEF during mitoxantrone therapy. (medscape.com)
- The risk of heart damage may depend on the total amount of mitoxantrone given to a person over a lifetime, so your doctor will probably limit the total number of doses you receive if you are using this medication for MS. If you experience any of the following symptoms, call your doctor immediately: difficulty breathing, chest pain, swelling of the legs or ankles, or irregular or fast heartbeat. (medlineplus.gov)
- Mitoxantrone may increase your risk for developing leukemia (cancer of the white blood cells), especially when it is given in high doses or together with certain other chemotherapy medications. (medlineplus.gov)
- The usual doses used in solid tumors and in lymphomas are mitoxantrone 12-14 mg/m2 iv q3-4wk and in leukemias is mitoxantrone 12 mg/m2/d X 5 d iv for initial induction. (nih.gov)
- Cabazitaxel 20 and 25 mg/m 2 were each evaluated in combination with escalating doses of mitoxantrone (starting dose 4 mg/m 2 ), given with prednisone 5 mg twice daily. (elsevierpure.com)
- The median radiographic progression-free survival was 14.5 months (95% CI: 8.0-not reached (NR)), and median overall survival was 23.3 months (95% CI: 14.3-NR). Conclusions The approved single-agent doses of mitoxantrone and cabazitaxel were safely combined. (elsevierpure.com)
Doxorubicin2
- Tell your doctor and pharmacist if you are taking or have ever received certain cancer chemotherapy medications such as daunorubicin (Cerubidine), doxorubicin (Doxil), epirubicin (Ellence), or idarubicin (Idamycin), or if you have ever been treated with mitoxantrone in the past. (medlineplus.gov)
- Mitoxantrone is an anthraquinone antineoplastic agent with structural similarities to doxorubicin. (nih.gov)
Mechanism of Act1
- Mitoxantrone has antitumor activity in mCRPC and nonoverlapping mechanism of action and toxicity profile. (elsevierpure.com)
Metastatic1
- Mitoxantrone has significant activity in the treatment of metastatic breast cancer, acute leukemias, and non-Hodgkin's lymphoma. (nih.gov)
Cabazitaxel2
- Objective To establish the maximally tolerated dose of the combination of cabazitaxel, mitoxantrone, and prednisone. (elsevierpure.com)
- The maximally tolerated dose was cabazitaxel 20 mg/m 2 plus mitoxantrone 12 mg/m 2 . (elsevierpure.com)
Leukemia2
Medications1
- Mitoxantrone should be given only under the supervision of a doctor with experience in the use of chemotherapy medications. (medlineplus.gov)
Phase2
Increases1
- lasmiditan increases levels of mitoxantrone by Other (see comment). (medscape.com)
Occur1
- Congestive heart failure (CHF), potentially fatal, may occur either during therapy with mitoxantrone or months to years after termination of therapy. (nih.gov)
Inhibit2
Infection1
- In order to monitor the occurrence of bone marrow suppression, primarily neutropenia, which may be severe and result in infection, it is recommended that frequent peripheral blood cell counts be performed on all patients receiving mitoxantrone. (nih.gov)
Perform1
- Your doctor will examine you and perform certain tests to check how well your heart is working before beginning treatment with mitoxantrone and if you show any signs of heart problems. (medlineplus.gov)
Clinical1
- Mitoxantrone: a new anticancer drug with significant clinical activity. (nih.gov)
Cardiac1
- Assess signs and symptoms of cardiac disease with a history, physical examination, and ECG before initiating therapy with mitoxantrone. (medscape.com)
Therapy2
Increase2
- darolutamide will increase the level or effect of mitoxantrone by Other (see comment). (medscape.com)
- mitoxantrone will increase the level or effect of lonafarnib by affecting hepatic/intestinal enzyme CYP3A4 metabolism. (medscape.com)
Effects2
- mitoxantrone decreases effects of adenovirus types 4 and 7 live, oral by pharmacodynamic antagonism. (medscape.com)
- mitoxantrone decreases effects of influenza virus vaccine quadrivalent, adjuvanted by pharmacodynamic antagonism. (medscape.com)
