Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.)
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.
An antimitotic agent with immunosuppressive properties.
Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
Forms to which substances are incorporated to improve the delivery and the effectiveness of drugs. Drug carriers are used in drug-delivery systems such as the controlled-release technology to prolong in vivo drug actions, decrease drug metabolism, and reduce drug toxicity. Carriers are also used in designs to increase the effectiveness of drug delivery to the target sites of pharmacological actions. Liposomes, albumin microspheres, soluble synthetic polymers, DNA complexes, protein-drug conjugates, and carrier erythrocytes among others have been employed as biodegradable drug carriers.
Artificial, single or multilaminar vesicles (made from lecithins or other lipids) that are used for the delivery of a variety of biological molecules or molecular complexes to cells, for example, drug delivery and gene transfer. They are also used to study membranes and membrane proteins.
A 170-kDa transmembrane glycoprotein from the superfamily of ATP-BINDING CASSETTE TRANSPORTERS. It serves as an ATP-dependent efflux pump for a variety of chemicals, including many ANTINEOPLASTIC AGENTS. Overexpression of this glycoprotein is associated with multidrug resistance (see DRUG RESISTANCE, MULTIPLE).
Simultaneous resistance to several structurally and functionally distinct drugs.
A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.
Tumors or cancer of the human BREAST.
A cell line derived from cultured tumor cells.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
Polymers of ETHYLENE OXIDE and water, and their ethers. They vary in consistency from liquid to solid depending on the molecular weight indicated by a number following the name. They are used as SURFACTANTS, dispersing agents, solvents, ointment and suppository bases, vehicles, and tablet excipients. Some specific groups are NONOXYNOLS, OCTOXYNOLS, and POLOXAMERS.
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
Antitumor alkaloid isolated from Vinca rosea. (Merck, 11th ed.)
An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
The relationship between the dose of an administered drug and the response of the organism to the drug.
An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.
Agents that have a damaging effect on the HEART. Such damage can occur from ALKYLATING AGENTS; FREE RADICALS; or metabolites from OXIDATIVE STRESS and in some cases is countered by CARDIOTONIC AGENTS. Induction of LONG QT SYNDROME or TORSADES DE POINTES has been the reason for viewing some drugs as cardiotoxins.
Monohydroxyethyl derivative of rutin. Peripheral circulation stimulant used in treatment of venous disorders.
The action of a drug in promoting or enhancing the effectiveness of another drug.
Positional isomer of CYCLOPHOSPHAMIDE which is active as an alkylating agent and an immunosuppressive agent.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
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.
A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.
Organic compounds that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.
A complex of related glycopeptide antibiotics from Streptomyces verticillus consisting of bleomycin A2 and B2. It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors.
Systems for the delivery of drugs to target sites of pharmacological actions. Technologies employed include those concerning drug preparation, route of administration, site targeting, metabolism, and toxicity.
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
An anthracenedione-derived antineoplastic agent.
An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.
Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.
A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
Pathological conditions involving the HEART including its structural and functional abnormalities.
A calcium channel blocker that is a class IV anti-arrhythmia agent.
The hollow, muscular organ that maintains the circulation of the blood.
A sarcoma originating in bone-forming cells, affecting the ends of long bones. It is the most common and most malignant of sarcomas of the bones, and occurs chiefly among 10- to 25-year-old youths. (From Stedman, 25th ed)
A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
A group of diterpenoid CYCLODECANES named for the taxanes that were discovered in the TAXUS tree. The action on MICROTUBULES has made some of them useful as ANTINEOPLASTIC AGENTS.
DNA TOPOISOMERASES that catalyze ATP-dependent breakage of both strands of DNA, passage of the unbroken strands through the breaks, and rejoining of the broken strands. These enzymes bring about relaxation of the supercoiled DNA and resolution of a knotted circular DNA duplex.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
Drug therapy given to augment or stimulate some other form of treatment such as surgery or radiation therapy. Adjuvant chemotherapy is commonly used in the therapy of cancer and can be administered before or after the primary treatment.
Polyacenes with four ortho-fused benzene rings in a straight linear arrangement. This group is best known for the subclass called TETRACYCLINES.
An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.
A compound that, on administration, must undergo chemical conversion by metabolic processes before becoming the pharmacologically active drug for which it is a prodrug.
Nanometer-sized, hollow, spherically-shaped objects that can be utilized to encapsulate small amounts of pharmaceuticals, enzymes, or other catalysts (Glossary of Biotechnology and Nanobiotechnology, 4th ed).
An anthracycline which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA.
The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods.
An anthracycline produced by Streptomyces galilaeus. It has potent antineoplastic activity.
Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.
In vivo methods of screening investigative anticancer drugs, biologic response modifiers or radiotherapies. Human tumor tissue or cells are transplanted into mice or rats followed by tumor treatment regimens. A variety of outcomes are monitored to assess antitumor effectiveness.
Tumors or cancer located in bone tissue or specific BONES.
Neoplasms of whatever cell type or origin, occurring in the extraskeletal connective tissue framework of the body including the organs of locomotion and their various component structures, such as nerves, blood vessels, lymphatics, etc.
Experimental transplantation of neoplasms in laboratory animals for research purposes.
Tumors or cancer of the LUNG.
Compounds that inhibit the activity of DNA TOPOISOMERASE II. Included in this category are a variety of ANTINEOPLASTIC AGENTS which target the eukaryotic form of topoisomerase II and ANTIBACTERIAL AGENTS which target the prokaryotic form of topoisomerase II.
Elements of limited time intervals, contributing to particular results or situations.
Therapeutic act or process that initiates a response to a complete or partial remission level.
Genes for MEMBRANE TRANSPORT PROTEINS that confer resistance to toxic compounds. Several superfamilies of these multidrug export proteins are known and found in both prokaryotes and eukaryotes.
A sequence-related subfamily of ATP-BINDING CASSETTE TRANSPORTERS that actively transport organic substrates. Although considered organic anion transporters, a subset of proteins in this family have also been shown to convey drug resistance to neutral organic drugs. Their cellular function may have clinical significance for CHEMOTHERAPY in that they transport a variety of ANTINEOPLASTIC AGENTS. Overexpression of proteins in this class by NEOPLASMS is considered a possible mechanism in the development of multidrug resistance (DRUG RESISTANCE, MULTIPLE). Although similar in function to P-GLYCOPROTEINS, the proteins in this class share little sequence homology to the p-glycoprotein family of proteins.
A decrease in the number of NEUTROPHILS found in the blood.
An antineoplastic agent. It has significant activity against melanomas. (from Martindale, The Extra Pharmacopoeia, 31st ed, p564)
A group of closely related cyclic undecapeptides from the fungi Trichoderma polysporum and Cylindocarpon lucidum. They have some antineoplastic and antifungal action and significant immunosuppressive effects. Cyclosporins have been proposed as adjuvants in tissue and organ transplantation to suppress graft rejection.
Any of a group of malignant tumors of lymphoid tissue that differ from HODGKIN DISEASE, being more heterogeneous with respect to malignant cell lineage, clinical course, prognosis, and therapy. The only common feature among these tumors is the absence of giant REED-STERNBERG CELLS, a characteristic of Hodgkin's disease.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
The concentration of a compound needed to reduce population growth of organisms, including eukaryotic cells, by 50% in vitro. Though often expressed to denote in vitro antibacterial activity, it is also used as a benchmark for cytotoxicity to eukaryotic cells in culture.
A biologic alkylating agent that exerts its cytotoxic effects by forming DNA ADDUCTS and DNA interstrand crosslinks, thereby inhibiting rapidly proliferating cells. The hydrochloride is an antineoplastic agent used to treat HODGKIN DISEASE and LYMPHOMA.
Malignant lymphoma composed of large B lymphoid cells whose nuclear size can exceed normal macrophage nuclei, or more than twice the size of a normal lymphocyte. The pattern is predominantly diffuse. Most of these lymphomas represent the malignant counterpart of B-lymphocytes at midstage in the process of differentiation.
Antibodies obtained from a single clone of cells grown in mice or rats.
A glycoprotein of MW 25 kDa containing internal disulfide bonds. It induces the survival, proliferation, and differentiation of neutrophilic granulocyte precursor cells and functionally activates mature blood neutrophils. Among the family of colony-stimulating factors, G-CSF is the most potent inducer of terminal differentiation to granulocytes and macrophages of leukemic myeloid cell lines.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.
Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.
A malignant disease characterized by progressive enlargement of the lymph nodes, spleen, and general lymphoid tissue. In the classical variant, giant usually multinucleate Hodgkin's and REED-STERNBERG CELLS are present; in the nodular lymphocyte predominant variant, lymphocytic and histiocytic cells are seen.
Each of the upper and lower folds of SKIN which cover the EYE when closed.
Nanometer-sized particles that are nanoscale in three dimensions. They include nanocrystaline materials; NANOCAPSULES; METAL NANOPARTICLES; DENDRIMERS, and QUANTUM DOTS. The uses of nanoparticles include DRUG DELIVERY SYSTEMS and cancer targeting and imaging.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)

Decreased expression of the pro-apoptotic protein Par-4 in renal cell carcinoma. (1/8107)

Par-4 is a widely expressed leucine zipper protein that confers sensitization to apoptosis induced by exogenous insults. Because the expression of genes that promote apoptosis may be down-regulated during tumorigenesis, we sought to examine the expression of Par-4 in human tumors. We present here evidence that Par-4 protein levels were severely decreased in human renal cell carcinoma specimens relative to normal tubular cells. Replenishment of Par-4 protein levels in renal cell carcinoma cell lines conferred sensitivity to apoptosis. Because apoptosis may serve as a defense mechanism against malignant transformation or progression, decreased expression of Par-4 may contribute to the pathophysiology of renal cell carcinoma.  (+info)

Tumour ablation and hepatic decompensation rates in multi-agent chemoembolization of hepatocellular carcinoma. (2/8107)

Thirty-seven cirrhotic patients with 62 hepatocellular carcinoma (HCC) foci--most Child-Pugh class B or C and/or with large, inoperable tumours--underwent 148 sessions of transcatheter arterial chemoembolization (TACE) using lipiodol, doxorubicin and cisplatin. Treatment efficacy was assessed by serial hepatic arteriography in 34/37 (91.9%) patients and abdominal CT scanning in 3/37 (8.1%) patients. Child-Pugh status was determined prior to each treatment session. Varying degrees of control of tumour neovascularity occurred for a median 390 days (range 90 to > 1680 days) in 33/34 (97.1%) patients in whom progress hepatic arteriography was performed. Ablation of tumour neovascularity occurred in 6/6 (100%), 4/12 (33.3%) and 6/16 (37.5%) patients with HCC diameters < 4 cm, 4-7 cm and > 8 cm, respectively (p < 0.02). Significantly more sessions were required for ablation of larger tumours (p < 0.05). Recurrent HCC was detected in 50% of patients after a median 240 days (range 60-1120 days). Deterioration in Child-Pugh status followed a session of TACE on 19/148 (12.8%) occasions but resulted in unscheduled hospitalization on only 4/148 (2.7%) occasions, the highest incidence (8.3%) in Child-Pugh C patients. Actuarial survival was 27/36 (75.0%) at 6 months, 17/34 (50.0%) at 12 months, 14/34 (41.2%) at 18 months, 9/31 (29.0%) at 24 months and 4/27 (14.8%) at 36 months. Multi-agent TACE with lipiodol, doxorubicin and cisplatin provides a useful anti-tumour effect, even in cirrhotic patients with large HCCs. The incidence of clinically significant deterioration in hepatic function due to ischaemia of non-tumorous liver is acceptably low, even in Child-Pugh C patients.  (+info)

Inhibition of doxorubicin toxicity in cultured neonatal mouse cardiomyocytes with elevated metallothionein levels. (3/8107)

Controversial results have been reported regarding whether metallothionein (MT) functions in doxorubicin (DOX) detoxification in the heart. To determine unequivocally the role of MT in cardiac protection against the toxicity of DOX, ventricular cardiomyocytes isolated from 1- to 3-day neonatal transgenic mice with high levels of cardiac MT and from nontransgenic control animals were applied. On the 6th day of culturing, MT concentrations in the transgenic cardiomyocytes were about 2-fold higher than those in the nontransgenic cells. DOX was added directly into the cultures. Compared with nontransgenic controls, transgenic cardiomyocytes displayed a significant (p <.05) resistance to DOX cytotoxicity, as measured by morphological alterations, cell viability, and lactate dehydrogenase leakage from the cells. This cytoprotective effect of MT correlated with its inhibition of DOX-induced lipid peroxidation. These observations demonstrate unequivocally that elevation of MT concentrations in the cardiomyocytes of 2-fold higher than normal provides efficient protection against DOX toxicity.  (+info)

1,25-Dihydroxyvitamin D3 enhances the susceptibility of breast cancer cells to doxorubicin-induced oxidative damage. (4/8107)

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3), the hormonal form of vitamin D, has anticancer activity in vivo and in vitro. Doxorubicin exerts its cytotoxic effect on tumor cells mainly by two mechanisms: (a) generation of reactive oxygen species (ROS); and (b) inhibition of topoisomerase II. We studied the combined cytotoxic action of 1,25(OH)2D3 and doxorubicin on MCF-7 breast cancer cells. Pretreatement with 1,25(OH)2D3 resulted in enhanced cytotoxicity of doxorubicin. The average enhancing effect after a 72-h pretreatment with 1,25(OH)2D3 (10 nM) followed by a 24-h treatment with 1 microg/ml doxorubicin was 74+/-9% (mean +/- SE). Under these experimental conditions, 1,25(OH)2D3 on its own did not affect cell number or viability. 1,25(OH)2D3 also enhanced the cytotoxic activity of another ROS generating quinone, menadione, but did not affect cytotoxicity induced by the topoisomerase inhibitor etoposide. The antioxidant N-acetylcysteine slightly reduced the cytotoxic activity of doxorubicin but had a marked protective effect against the combined action of 1,25(OH)2D3 and doxorubicin. These results indicate that ROS are involved in the interaction between 1,25(OH)2D3 and doxorubicin. 1,25(OH)2D3 also increased doxorubicin cytotoxicity in primary cultures of rat cardiomyocytes. Treatment of MCF-7 cells with 1,25(OH)2D3 alone markedly reduced the activity, protein, and mRNA levels of the cytoplasmic antioxidant enzyme Cu/Zn superoxide dismutase, which indicated that the hormone inhibits its biosynthesis. This reduction in the antioxidant capacity of the cells could account for the synergistic interaction between 1,25(OH)2D3 and doxorubicin and may also suggest increased efficacy of 1,25(OH)2D3 or its analogues in combination with other ROS-generating anticancer therapeutic modalities.  (+info)

Cell adhesion mediated drug resistance (CAM-DR): role of integrins and resistance to apoptosis in human myeloma cell lines. (5/8107)

Integrin-mediated adhesion influences cell survival and may prevent programmed cell death. Little is known about how drug-sensitive tumor cell lines survive initial exposures to cytotoxic drugs and eventually select for drug-resistant populations. Factors that allow for cell survival following acute cytotoxic drug exposure may differ from drug resistance mechanisms selected for by chronic drug exposure. We show here that drug-sensitive 8226 human myeloma cells, demonstrated to express both VLA-4 (alpha4beta1) and VLA-5 (alpha5beta1) integrin fibronectin (FN) receptors, are relatively resistant to the apoptotic effects of doxorubicin and melphalan when pre-adhered to FN and compared with cells grown in suspension. This cell adhesion mediated drug resistance, or CAM-DR, was not due to reduced drug accumulation or upregulation of anti-apoptotic Bcl-2 family members. As determined by flow cytometry, myeloma cell lines selected for drug resistance, with either doxorubicin or melphalan, overexpress VLA-4. Functional assays revealed a significant increase in alpha4-mediated cell adhesion in both drug-resistant variants compared with the drug-sensitive parent line. When removed from selection pressure, drug-resistant cell lines reverted to a drug sensitive and alpha4-low phenotype. Whether VLA-4-mediated FN adhesion offers a survival advantage over VLA-5-mediated adhesion remains to be determined. In conclusion, we have demonstrated that FN-mediated adhesion confers a survival advantage for myeloma cells acutely exposed to cytotoxic drugs by inhibiting drug-induced apoptosis. This finding may explain how some cells survive initial drug exposure and eventually express classical mechanisms of drug resistance such as MDR1 overexpression.  (+info)

Combination of theanine with doxorubicin inhibits hepatic metastasis of M5076 ovarian sarcoma. (6/8107)

Theanine is a peculiar amino acid existing in green tea leaves, which was previously indicated to enhance the antitumor activity of doxorubicin. In the present study, the effect of combination of theanine with doxorubicin against hepatic metastasis of M5076 ovarian sarcoma was investigated. The primary tumor was significantly reduced by the combined treatment on M5076 transplanted (s.c.) mice. The liver weight of control mice increased to twice the normal level because of hepatic metastasis of M5076. In contrast, the injection of doxorubicin alone or theanine plus doxorubicin suppressed the increase in liver weight and inhibited hepatic metastasis. Moreover, the liver weights and metastasis scores demonstrated that theanine enhanced the inhibition of hepatic metastasis induced by doxorubicin. Furthermore, in vitro experiments indicated that theanine increased the intracellular concentration of doxorubicin remaining in M5076 cells. This action suggests that theanine leads the enhancement of the suppressive efficacy of doxorubicin on hepatic metastasis in vivo. Therefore, it was proved that theanine increased not only the antitumor activity on primary tumor but also the metastasis-suppressive efficacy of doxorubicin. The effect of theanine on the efficacy of antitumor agents is expected to be applicable in clinical cancer chemotherapy.  (+info)

Inhibition of p53 transcriptional activity by Bcl-2 requires its membrane-anchoring domain. (7/8107)

We show here that the anti-apoptosis protein Bcl-2 potently inhibits p53-dependent transcriptional activation of various p53-responsive promoters in reporter gene co-transfection assays in human embryonic kidney 293 and MCF7 cells, without affecting nuclear accumulation of p53 protein. In contrast, Bcl-2(Deltatransmembrane (TM)), which lacks a hydrophobic membrane-anchoring domain, had no effect on p53 activity. Similarly, in MCF7 cells stably expressing either Bcl-2 or Bcl-2(DeltaTM), nuclear levels of p53 protein were up-regulated upon treatment with the DNA-damaging agents doxorubicin and UV radiation, whereas p53-responsive promoter activity and expression of p21(CIP1/WAF1) were strongly reduced in MCF7-Bcl-2 cells but not in MCF7-Bcl-2(DeltaTM) or control MCF7 cells. The issue of membrane anchoring was further explored by testing the effects of Bcl-2 chimeric proteins that contained heterologous transmembrane domains from the mitochondrial protein ActA or the endoplasmic reticulum protein cytochrome b5. Both Bcl-2(ActA) and Bcl-2(Cytob5) suppressed p53-mediated transactivation of reporter gene plasmids with efficiencies comparable to wild-type Bcl-2. These results suggest that (a) Bcl-2 not only suppresses p53-mediated apoptosis but also interferes with the transcriptional activation of p53 target genes at least in some cell lines, and (b) membrane anchoring is required for this function of Bcl-2. We speculate that membrane-anchored Bcl-2 may sequester an unknown factor necessary for p53 transcriptional activity.  (+info)

MycN sensitizes neuroblastoma cells for drug-induced apoptosis. (8/8107)

Amplification of the MYCN gene is found in a large proportion of neuroblastoma and considered as an adverse prognostic factor. To investigate the effect of ectopic MycN expression on the susceptibility of neuroblastoma cells to cytotoxic drugs we used a human neuroblastoma cell line harboring tetracycline-controlled expression of MycN. Neither conditional expression of MycN alone nor low drug concentrations triggered apoptosis. However, when acting in concert, MycN and cytotoxic drugs efficiently induced cell death. Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. Loss of mitochondrial transmembrane potential and release of cytochrome c from mitochondria preceded activation of caspase-8 and caspase-3 and cleavage of PARP. CD95 expression was upregulated by treatment with cytotoxic drugs, while MycN cooperated with cytotoxic drugs to increase sensitivity to CD95-induced apoptosis and enhancing CD95-L expression. MycN overexpression and cytotoxic drugs also synergized to induce p53 and Bax protein expression, while Bcl-2 and Bcl-X(L) protein levels remained unchanged. Since amplification of MYCN is usually associated with a poor prognosis, these findings suggest that dysfunctions in apoptosis pathways may be a mechanism by which MycN-induced apoptosis of neuroblastoma cells is inhibited.  (+info)

PRIMARY OBJECTIVES:. I. To determine the maximum tolerated dose of intraperitoneal (IP) paclitaxel when given concurrently with fixed dose intravenous (IV) doxorubicin (doxorubicin hydrochloride) and IV cisplatin.. II. To determine the maximum tolerated dose of IP paclitaxel when given concurrently with fixed dose IV doxorubicin hydrochloride and IP cisplatin.. III. To determine the feasibility of an IV/IP based doxorubicin hydrochloride, paclitaxel, and cisplatin chemotherapy regimen in patients with advanced endometrial cancer.. OUTLINE: This is a dose-escalation study of paclitaxel.. Patients receive doxorubicin hydrochloride IV over 30 minutes followed by cisplatin IV over 1 hour on day 1, paclitaxel IV over 3 hours on day 2, and filgrastim subcutaneously (SC) on days 3-12 or pegfilgrastim SC on day 3. Treatment repeats every 21 days for up to 2 courses in the absence of disease progression or unacceptable toxicity.. Patients then receive doxorubicin hydrochloride IV and cisplatin IV or IP ...
Doxorubicin (5 mg kg-1) was administered intravenously to C57 mice bearing subcutaneous B16F10 melanomas, distributing into the tumour with an area under the concentration-time curve (0-48 h; AUC) of 8.7 micrograms h g-1. Injection of doxorubicin-N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer conjugate, containing 5 mg of doxorubicin equivalent per kg, mediated an AUC for free doxorubicin (i.e. doxorubicin released from the conjugate) of 15.2 micrograms h g-1 and for total doxorubicin (i.e. free plus conjugated) of 149.1 micrograms h g-1. An increased dose of doxorubicin-HPMA copolymer conjugate (18 mg of doxorubicin equivalent per kg) produced AUC values of 40.1 micrograms h g-1 and 671.7 micrograms h g-1 for free and total doxorubicin respectively. Hence administration of doxorubicin-HPMA copolymer conjugate achieved rises of 1.7- to 4.6-fold in tumour AUC (free doxorubicin) and 17.19 to 77.0-fold in tumour AUC (total doxorubicin). HPMA copolymers bearing fluorescein isothiocyanate accumulated in
Pharmacokinetic studies conducted in patients with various types of tumors have shown that doxorubicin follows multiphasic disposition after intravenous injection. The distribution half-life is approximately 5 minutes, while the terminal half-life is 20 to 48 hours. In four patients, doxorubicin demonstrated dose-independent pharmacokinetics across a dose range of 30 to 70 mg/m2 .. Distribution Steady-state distribution volume ranges from 809 to 1214 L/m2. Binding of doxorubicin and its major metabolite, doxorubicinol, to plasma proteins is about 75% and is independent of plasma concentration of doxorubicin up to 1.1 mcg/mL. Doxorubicin was measured in the milk of one lactating patient after therapy with 70 mg/m2 of doxorubicin given as a 15 minute intravenous infusion. The peak milk concentration at 24 hours after treatment was 4.4 fold greater than the corresponding plasma concentration. Doxorubicin was detectable in the milk up to 72 hours.. Doxorubicin does not cross the blood brain ...
We investigated in vivo the chemotherapeutic anthracycline agents doxorubicin and its ability to activate mitochondrial-mediated, receptor-mediated and endoplasmic/sarcoplasmic reticulum-mediated apoptosis transduction pathways in cardiac tissue from male and female rats. We administered a single low dose of doxorubicin (10 mg/kg of body weight, i.p.) and then isolated mitochondrial and cytosolic proteins one and four days later from the heart. Caspase-3 protein content and caspase-3 activity were significantly increased after day four of doxorubicin treatment in both male and female rats. However, while males had DNA fragmentation at day one but not day four following doxorubicin administration, females showed no significant increase in DNA fragmentation at either time. Caspase-12, localized in the SR, is considered a central caspase, and its activation by cleavage via calpain indicates activation of the SR-mediated pathway of apoptosis. Cleaved caspase-12 content and calpain activity significantly
TY - JOUR. T1 - Complement activation following first exposure to pegylated liposomal doxorubicin (Doxil®). T2 - Possible role in hypersensitivity reactions. AU - Chanan-Khan, Asher. AU - Szebeni, J.. AU - Savay, S.. AU - Liebes, L.. AU - Rafique, N. M.. AU - Alving, C. R.. AU - Muggia, F. M.. PY - 2003/9/1. Y1 - 2003/9/1. N2 - Background: Pegylated liposomal doxorubicin (Doxil®) has been reported to cause immediate hypersensitivity reactions (HSRs) that cannot be explained as IgE-mediated (type I) allergy. Previous in vitro and animal studies indicated that activation of the complement (C) system might play a causal role in the process, a proposal that has not been tested in humans to date. Patients and methods: Patients with solid tumors (n = 29) treated for the first time with Doxil were evaluated for HSRs and concurrent C activation. HSRs were classified from mild to severe, while C activation was estimated by serial measurement of plasma C terminal complex (SC5b-9) levels. Increases in ...
Pegylated liposomal doxorubicin (PLD) is the first antineoplastic drug derived from the new technology of liposome formulation to be introduced in clinical practice. The low myocardium uptake of this formulation accounts for its reduced cardiac toxicity, confirmed both in preclinical models and in humans. Preclinical data have shown activity in NSCLC xenografts. This Phase II study is to explore the efficacy and toxicity of Pegylated liposomal doxorubicin and Carboplatin in patients with previously untreated non-small cell lung cancer (NSCLC) not amenable to radiotherapy or surgical treatment ...
The efficacy of liposomal doxorubicin for treating Kaposis sarcoma (KS) in patients infected with human immunodeficiency virus (HIV) was studied. Eight men with HIV infection and KS were to be given liposomal doxorubicin 20 mg/sq m i.v. monthly for six months and 10 mg/sq m i.v. monthly thereafter, depending on the response. They were assessed for the onset, extent, and duration of clinical response; relapse; adverse effects; development of new opportunistic infections; quality of life; and survival. Five patients had a clinical complete response (i.e., complete resolution of the manifestations of KS, as determined by physical examination but not confirmed by biopsy) and three patients had a partial response to the induction regimen of liposomal doxorubicin. Relapse occurred in all patients in whom therapy was stopped; reinstatement of therapy elicited a partial response. Neutropenia occurred in two patients; filgrastim therapy enabled the liposomal doxorubicin therapy to continue uninterrupted.
Doxorubicin is a commonly used antineoplastic agent in the treatment of many types of cancer. Little is known about the interactions of doxorubicin with cardiac biomolecules. Serious cardiotoxicity including dilated cardiomyopathy often resulting in a fatal congestive heart failure may occur as a consequence of chemotherapy with doxorubicin. The purpose of this study was to determine the effect of exposure to doxorubicin on the changes in major amino acids in tissue of cardiac muscle (proline, taurine, glutamic acid, arginine, aspartic acid, leucine, glycine, valine, alanine, isoleucine, threonine, lysine and serine). An in vitro interaction study was performed as a comparison of amino acid profiles in heart tissue before and after application of doxorubicin. We found that doxorubicin directly influences myocardial amino acid representation even at low concentrations. In addition, we performed an interaction study that resulted in the determination of breaking points for each of analyzed amino acids.
Verapamil reversed resistance to doxorubicin in a human multiple myeloma cell line selected for multiple drug resistance. The drug-resistant cell line 8226/DOX40 is known to have reduced intracellular drug accumulation associated with the overexpression of P-glycoprotein when compared to the sensitive parent cell line 8226/S. Verapamil alone was minimally cytotoxic in both cell lines, but reversed doxorubicin resistance in a dose-related manner in 8226/DOX40. A similar dose-response relationship was observed for verapamil in increasing net intracellular doxorubicin accumulation. This increased net accumulation was secondary to block of enhanced doxorubicin efflux by verapamil from resistant cells. In contrast, verapamil did not alter initial doxorubicin accumulation over the first 60 s when incubated with resistant cells. Addition of verapamil to the 8226/DOX40 cells enhanced the formation of doxorubicin-induced DNA single strand breaks, double strand breaks, and DNA-protein cross-links. ...
Objective: The present study was designed to investigate the cardioprotective potential of Galangin on Doxorubicin induced cardiotoxicity in rats.. Methods: Albino rats used in this experiment were pretreated with vehicle, Galangin (100 & 200µg/kg) and Vit-C (20 mg/kg) for 28 days. On 25th day, a single dose of Doxorubicin (10 mg/kg, i. p) was administered to groups. After 72 h of Doxorubicin administration, ECG, serum and tissues biomarkers were evaluated. Histopathological examination of the heart was performed.. Results: Doxorubicin treated rats exhibited abnormal ECG pattern followed by significant increase in CK-MB, LDH, SGOT, SGPT and LPO level and decrease in GSH, CAT, TT when compared to control rats. Pretreatment with different doses of Galangin and Vit-C significantly reduced the serum biomarkers and increased the tissue antioxidant level when compared to Doxorubicin alone treated groups. Moreover, pretreatment also improved Doxorubicin induced changes in ECG pattern and ...
China Doxorubicin Hydrochloride a Synthesis of Antitumor Antibiotics, Find details about China Undecylenate, Testosterone Enanthate from Doxorubicin Hydrochloride a Synthesis of Antitumor Antibiotics - Wuhan Lianshangwang Technology Co., Ltd.
BACKGROUND: We aimed to define the maximum tolerated dose (MTD) and characterize the toxicity of the combination of pegylated liposomal doxorubicin (PLD; Caelyx trade mark ) and weekly paclitaxel (wPTX), and to investigate pharmacokinetics of PLD in this combination. METHODS: A phase I study was performed with an initial dose of 50 mg/m(2) wPTX and 30 mg/m(2) PLD. The paclitaxel dose was escalated in increments of 10 mg/m(2) and PLD in increments of 5 mg/m(2) until the MTD was reached. The pharmacokinetics of PLD were studied at the highest achieved dose levels. RESULTS: Forty-four cancer patients were enrolled. The MTD was 30/90 and 35/80 mg/m(2) for PLD/wPTX. Dose-limiting toxicities included treatment delay for neutropenia grade 3, febrile neutropenia, palmar-plantar erythrodysesthesia and deep venous thrombosis. Toxicity below the MTD was mild: skin toxicity grade 1-2 developed at high cumulative doses and vascular thrombotic events occurred in two patients with predisposing factors. No ...
Dose limiting toxicities of therapy are myelosuppression and cardiotoxicity. Other reactions reported are:. Cardiotoxicity - (See WARNINGS.). Cutaneous- Reversible complete alopecia occurs in most cases. Hyperpigmentation of nailbeds and dermal creases, primarily in pediatric patients, and onycholysis have been reported in a few cases. Radiation recall reaction has occurred with doxorubicin administration. Rash, itching, or photosensitivity may occur.. Gastrointestinal-Acute nausea and vomiting occurs frequently and may be severe. This may be alleviated by antiemetic therapy. Mucositis (stomatitis and esophagitis) may occur within 5 to 10 of beginning therapy, and most patients recover from this adverse event within another 5 to 10 days. The effect may be severe leading to ulceration and represents a site of origin for severe infections. The dosage regimen consisting of administration of doxorubicin on three successive days results in greater incidence and severity of mucositis. Ulceration and ...
Preclinical studies have reported that a single treadmill session performed 24h prior to doxorubicin provides cardio-protection. We aimed to characterize the acute change in cardiac function following an initial doxorubicin treatment in humans and determine whether an exercise session performed 24h prior to treatment changes this response. Breast cancer patients were randomized to either 30min of vigorous-intensity exercise 24h prior to the first doxorubicin treatment (n=13), or no vigorous exercise for 72h prior to treatment (control, n=11). Echocardiographically-derived left ventricular volumes, longitudinal strain, twist, E/A ratio, and circulating NT-proBNP, a marker of later cardiotoxicity, were measured before and 24-48h after the treatment. Following treatment in the control group, NT-proBNP, end-diastolic and stroke volumes, cardiac output, E/A ratio, strain, diastolic strain rate, twist, and untwist velocity significantly increased (all p≤0.01). Whereas systemic vascular resistance ...
Doxorubicin is an antineoplastic in the anthracycline class. General properties of drugs in this class include: interaction with DNA in a variety of different ways including intercalation (squeezing between the base pairs), DNA strand breakage and inhibition with the enzyme topoisomerase II. Most of these compounds have been isolated from natural sources and antibiotics. However, they lack the specificity of the antimicrobial antibiotics and thus produce significant toxicity. The anthracyclines are among the most important antitumor drugs available. Doxorubicin is widely used for the treatment of several solid tumors while daunorubicin and idarubicin are used exclusively for the treatment of leukemia. Doxorubicin may also inhibit polymerase activity, affect regulation of gene expression, and produce free radical damage to DNA. Doxorubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. The anthracyclines are cell cycle-nonspecific ...
Various researches about doxorubicin work mechanism have done. Anthracyclin antibiotic like doxorubicin has cytotoxic action mechanism through four mechanism, that are: (1) Inhibition of topoisomerase II. (2) Intercalation of DNA so that cause DNA and RNA synthesis inhibition. (3) Cell membrane binding which cause ion flow and transport. (4) Formation of semiquinon free radicals and oxygen free radicals through iron dependent processes and reductive process that is mediated enzyme. This free radicals mechanism has known responsible in cardiotoxicity cause antracyclin antibiotic (Bruton et al, 2005). Doxorubicin can intercalation with DNA, it will directly affect transcription and replication. Doxorubicin can form complex tripartite with topoisomerase II and DNA. Topoisomerase II is an enzyme dependent ATP that work to bind DNA and cause double-stand break in the tip 3phosphate so that allowing strand exchange and streamlining the supercoiled DNA. The streamlining of this strand is followed by ...
TY - JOUR. T1 - Doxorubicin Blocks Cardiomyocyte Autophagic Flux by Inhibiting Lysosome Acidification. AU - Li, Dan L.. AU - Wang, Zhao. AU - Ding, Guanqiao. AU - Tan, Wei. AU - Luo, Xiang. AU - Criollo, Alfredo. AU - Xie, Min. AU - Jiang, Nan. AU - May, Herman. AU - Kyrychenko, Viktoriia. AU - Schneider, Jay W. AU - Gillette, Thomas G.. AU - Hill, Joseph A. PY - 2016/4/26. Y1 - 2016/4/26. N2 - Background - The clinical use of doxorubicin is limited by cardiotoxicity. Histopathological changes include interstitial myocardial fibrosis and the appearance of vacuolated cardiomyocytes. Whereas dysregulation of autophagy in the myocardium has been implicated in a variety of cardiovascular diseases, the role of autophagy in doxorubicin cardiomyopathy remains poorly defined. Methods and Results - Most models of doxorubicin cardiotoxicity involve intraperitoneal injection of high-dose drug, which elicits lethargy, anorexia, weight loss, and peritoneal fibrosis, all of which confound the interpretation ...
Shop Daunorubicin/doxorubicin resistance ATP-binding protein ELISA Kit, Recombinant Protein and Daunorubicin/doxorubicin resistance ATP-binding protein Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
In the present study, we explored sexual dimorphism of doxorubicin cardiotoxicity and energetic and signaling pathways that could be involved in these differences. Two clinically relevant cumulative doses of doxorubicin, either 14 mg/kg after 7 injections or 8 mg/kg after 4 injections were administrated to investigate sex differences in the cardiotoxicity of doxorubicin. Doxorubicin treatment resulted in sex differences characterized in males by (1) important weight loss and decrease in survival rate, (2) strong alterations of myocardial function, (3) decrease in energy signaling pathways, (4) downregulation of mitochondrial biogenesis, (5) decrease in cardiolipin content, (6) decrease in mitochondrial DNA content, and (7) and alteration of mitochondrial respiration. No sex differences were found for the oxidative stress response or for death markers, whereas mitochondrial dysfunction and mitochondrial protein expression were associated with early cardiotoxicity in males.. Several clinical ...
A new chemotherapeutic approach using doxorubicin simultaneously with geopropolis favoring monocyte functions.. Lucas Pires Garcia Oliveira, Fernanda Lopes Conte, Eliza de Oliveira Cardoso, Bruno José Conti, Karina Basso Santiago, Marjorie de Assis Golim, Geórgiada Silva Feltran, Willian Fernando Zambuzzi, José Maurício Sforcin. Abstract. Aims. Chemotherapy has been widely used to treat cancer although it may affect non-target cells involved in the immune response. This work aimed at elucidating whether the chemotherapeutic agent doxorubicin in combination with geopropolis produced by Melipona fasciculata Smith could affect nontumor immune cells, evaluating their immunomodulatory effects on human monocytes.. Main methods. Cell viability, expression of cell markers (HLA-DR, TLR-2, TLR-4, C80 and CD40), cytokine production (TNF-α, IL-1β, IL-6 and IL-10), intracellular pathways (NF-κB and autophagy), the microbicidal activity of monocytes and hydrogen peroxide (H2O2) production were ...
Cardiomyopathy. Doxorubicin hydrochloride can result in myocardial damage, including acute left ventricular failure. The risk of cardiomyopathy is generally proportional to the cumulative exposure. Include prior doses of other anthracyclines or anthracenediones in calculations of total cumulative dosage for doxorubicin hydrochloride. Cardiomyopathy may develop during treatment or up to several years after completion of treatment and can include decrease in LVEF and signs and symptoms of congestive heart failure (CHF). The probability of developing cardiomyopathy is estimated to be 1 to 2% at a total cumulative dose of 300 mg/m2 of doxorubicin hydrochloride, 3 to 5% at a dose of 400 mg/m2, 5 to 8% at a dose of 450 mg/m2, and 6 to 20% at a dose of 500 mg/m2, when doxorubicin hydrochloride is administered every 3 weeks. There is an additive or potentially synergistic increase in the risk of cardiomyopathy in patients who have received radiotherapy to the mediastinum or concomitant therapy with ...
This randomized phase III trial studies how well doxorubicin hydrochloride and cyclophosphamide followed by paclitaxel with or without carboplatin work in
The optimal cardiac toxicity prevention strategy for doxorubicin would include an agent that improves the efficacy of the doxorubicin-based cancer therapy and prevents cardiac toxicity. In our experiments, pretreatment with GGA blocked doxorubicin cardiac toxicity by maintaining systolic function and decreasing cell death in the heart. Most remarkably, GGA also contributed to doxorubicins chemotherapy efficacy in MDA-MB-231 xenografts in parallel with protecting the heart. GGAs antineoplastic effect is likely due to its inhibition of RHO family proteins in both the heart and cancer cells, and we selected MDA-MB-231 for these experiments because of the endogenous high RHO activity in these cells. Because GGA has been used in Japan since 1984 to prevent stomach ulcers and has a long history of safety and lack of adverse effects, we suggest that this novel approach to prevention of doxorubicin toxicity should be further investigated.. By comparison, dexrazoxane, an iron chelator used to reduce ...
Clinical resistance to chemotherapeutic agents is one of the major hindrances in the treatment of human cancers. Erythroblastosis virus E26 oncogene homolog 1 (ETS1) is involved in the drug resistance of various cancer cells, and is overexpressed in drug-resistant human breast cancer cell lines. In this study, we investigated the effects of ETS1 on adriamycin resistance in MCF-7/ADR cells. siRNAs against ETS1 or negative control siRNAs was transfected to MCF-7/ADR breast cancer cells. Reverse transcription-PCR and Western blotting were used to determine the mRNA and protein expression of ETS1 and MDR1. The cytotoxicity of adriamycin was assessed using the MTT assay. Drug efflux was investigated by flow cytometry using the Rhodamine 123 intracellular accumulation assay. ETS1 mRNA and protein was significantly overexpressed in MCF-7/ADR cells, compared to MCF-7 cells. ETS1 siRNA successfully silenced ETS1 mRNA and protein expression. Silencing of ETS1 also significantly reduced the mRNA and protein
A total of 10 patients with histologically proved carcinoma in situ of the bladder had remission of tumor after topical chemotherapy with doxorubicin hydrochloride for 24 months. Of the 10 patients 3 suffered new areas of carcinoma in situ 9 to 12 months after termination of intravesical chemotherapy. Furthermore, 1 of these 3 patients had a distal ureteral tumor. Fibrosis of the submucosal tissue was observed in every patient but a decrease in bladder capacity was observed in only 1 with prior radiotherapy. ...
RATIONALE: Drugs used in chemotherapy, such as gemcitabine hydrochloride, docetaxel, and doxorubicin hydrochloride, work in different ways to stop the g
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Patient information for DOXORUBICIN HYDROCHLORIDE 2 MG/ML SOLUTION FOR INFUSION Including dosage instructions and possible side effects.
From March 1996 to March 1998, 106 patients with untreated metastatic breast cancer (MBC) were treated with docetaxel (Taxotere) (100 mg/m²) and doxorubicin (75 mg/m²) on an alternating cycle-by-cycle (doxorubicin, docetaxel, doxorubicin, etc) or sequential (four cycles of docetaxel, then four cycles of doxorubicin) basis, every 3 weeks, for a maximum of eight cycles. 1
Background. Prognosis of acute lymphoblastic leukemia in elderly is poor. The GRAALL-SA1 phase II trial randomly compared the efficacy and toxicity of pegylated liposomal doxorubicin versus continuous-infusion doxorubicin in patients ≥55 years with Philadelphia chromosome-negative ALL. Design and Methods. Sixty patients received either continuous infusion-Doxorubicin (12 mg/m²/d) and continuous infusion-vincristine (0.4 mg/day) on day1-4 or liposomal-Doxorubicin (40 mg/m2;) and standard vincristine (2 mg) on day1, accompanied by dexamethasone, followed at day 28 by a second cycle, reinforced by cyclophosphamide. Endpoints were safety, outcome and prognostic factors. Results. Myelosupression was reduced in the Peg-Dox arm with shorter severe neutropenia (P=0.05), shorter severe thrombocytopenia (P=0.03), and less erythrocytes transfusions (P=0.04). Grade 3/4 infections and gram-negative bacteremia were reduced in the Peg-Dox arm (P=0.04 and 0.02, respectively). There was a trend toward less ...
Anthracyclines such as, doxorubicin (DOX) are an effective class of antineoplastic agents. Despite its efficacy in the treatment of a variety of cancers including breast cancer, the clinical use of DOX is limited by cardiac side effects. While it has been shown that DOX alters myocardial fatty acid metabolism, it is poorly understood whether variations in myocardial triacylglycerol (TG) metabolism contribute to DOX-induced cardiotoxicity. Since TG catabolism in the heart is primarily controlled by adipose triglyceride lipase (ATGL), this study examined the influence of DOX on cardiac ATGL expression and TG levels as well as the consequence of forced-expression of ATGL in the setting of DOX-induced cardiotoxicity. To do this, wild type (WT) mice and mice with cardiomyocyte-specific ATGL over-expression (MHC-ATGL) received weekly intraperitoneal injections of saline or DOX (8mg/kg) for four weeks. Heart rate, heart weight to tibia length ratio and DOX-induced body weight loss were comparable ...
|strong|Resveratrol enhances the sensitivity of doxorubicin-mediated cell proliferation invasion and migration in human breast cancer cell lines.|/stron ...
Purpose Anthracyclines (including doxorubicin) are still the backbone of commonly used breast cancer chemotherapy regimens. Despite increasing use of doxorubicin and cyclophosphamide (AC) combinations...
This phase IIb trial investigated the efficacy and tolerability of adding vintafolide [EC 145] to pegylated doxorubicin liposomal in patients with
Doxorubicin - Get up-to-date information on Doxorubicin side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about Doxorubicin
Detection of dose response in chronic doxorubicin-mediated cell death with cardiac technetium 99m annexin V single-photon emission computed tomography. Mol Imaging. 2008 May-Jun; 7(3):132-8 ...
There are direct and indirect indications that PEGylated liposomal doxorubicin (Doxil), a widely used anticancer nanomedicine, has a subclinical immune suppressive effect. As an example of a seemingly bad pharmacological property turning out to be not-so-ugly, but actually beneficial, the authors highlight the potential benefits of Doxils immune suppressive effect. ... read more These include (1) the decreased uptake of the drug by the MPS which may entail enhanced tumor uptake, and, hence, improved therapeutic efficacy; (2) the use of slow infusion protocols in reducing the risk of hypersensitivity (infusion) reactions; and (3), possible protection against hypersensitivity reactions to co-administered reactogenic drugs. To consider immune suppression as useful represents a paradigm shifts in nanotoxicology and anticancer chemotherapy. show less ...
Symptoms of Male reproductive toxicity - Doxorubicin hydrochloride including 1 medical symptoms and signs of Male reproductive toxicity - Doxorubicin hydrochloride, alternative diagnoses, misdiagnosis, and correct diagnosis for Male reproductive toxicity - Doxorubicin hydrochloride signs or Male reproductive toxicity - Doxorubicin hydrochloride symptoms.
Evidence-based recommendations on topotecan, pegylated liposomal doxorubicin hydrochloride (Caelyx; PLDH), paclitaxel, trabectedin (Yondelis) and gemcitabine
Cardiomyopathy is a clinical problem that occurs in the hearts of type 2 diabetic patients as well as cancer patients undergoing doxorubicin chemotherapy. The number of diabetic cancer patients is increasing but surprisingly the cardiac damaging effects of doxorubicin, a commonly used chemotherapeutic drug, on diabetic hearts have not been well-examined. As the signaling mechanisms of the doxorubicin-induced cardiomyopathy in type 2 diabetic heart are largely unknown, this study examined the molecular signaling pathways that are responsible for the doxorubicin-induced cardiotoxicity in type 2 diabetic hearts. Male 14- to 18-week-old db/db mice were used as the type 2 diabetic model, and age-matched non-diabetic db/+ mice served as controls. The db/+ non-diabetic and db/db diabetic mice were randomly assigned to the following groups: db/+CON, db/+DOX-5d, db/+DOX-7d, db/dbCON, db/dbDOX-5d, and db/dbDOX-7d. Mice assigned to doxorubicin (DOX) group were exposed to an intraperitoneal (i.p.) injection of DOX
PURPOSE: This randomized multicenter study was designed to compare the activity of a high-dose doxorubicin-containing chemotherapy regimen with a conventional standard-dose regimen in adult patients with advanced soft tissue sarcomas (ASTS). PATIENTS AND METHODS: Between 1992 and 1995, 314 patients were randomized to receive a standard-dose regimen (arm A), containing doxorubicin (50 mg/m(2) on day 1) and ifosfamide (5 g/m(2) on day 1), or an intensified regimen (arm B), combining doxorubicin (75 mg/m(2) on day 1), the same ifosfamide dose, and recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF; sargramostim, 250 microgram/m(2) on days 3 to 16); all courses were repeated every 3 weeks. RESULTS: The median age of the 294 eligible patients was 50 years. They received a median of five chemotherapy cycles. The median dose and relative doxorubicin dose-intensity achieved were 245 mg and 97% in arm A and 360 mg and 99% in arm B, respectively. Thirty-eight percent and 23% of ...
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A phase III trial (TH CR-406/SARC021) has shown no survival benefit of adding evofosfamide to doxorubicin in the first-line treatment of locally advanced unresectable or metastatic soft-tissue sarcoma. Trial results were reported in The Lancet Oncology by Tap et al. Evofosfamide is a hypoxia-activated prodrug of bromo-isophosphoramide mustard.. Study Details. In the open-label trial, 640 patients from 81 sites in 13 countries were randomized between September 2011 and January 2014 to receive evofosfamide plus doxorubicin (n = 317) or doxorubicin alone (n = 323). Doxorubicin was given at 75 mg/m² via bolus injection over 5 to 20 minutes or continuous infusion for 6 to 96 hours on day 1 of every 21-day cycle for up to 6 cycles. Evofosfamide was given at 300 mg/m² intravenously for 30 to 60 minutes on days 1 and 8 of every 21-day cycle for up to 6 cycles. After 6 cycles, patients in the doxorubicin group were followed, and patients with stable or responsive disease in the combination group were ...
Results Doxorubicin decreased calpain activities in cultured neonatal mouse cardiomyocytes and in vivomouse hearts, which correlated with down-regulation of calpain-1 and calpain-2 proteins. Over-expression of calpastatin or treatment with pharmacological calpain inhibitors aggravated apoptosis in neonatal and adult cardiomyocytes caused by doxorubicin. On the while, over-expression of calpain-2 but not calpain-1 decreased doxorubicin-induced apoptosis in cardiomyocytes. The pro-apoptotic effects of calpain inhibition were concerned with down-regulation of AKT protein and mRNA expression, and a concomitant reduction in GSK-3 beta phosphorylation (Ser9) in doxorubicin-treated cardiomyocytes. Inhibiting AKT further increased doxorubicin-induced cardiac injuries, suggesting the effects of calpain inhibition may be mediated through inactivating the AKT signalling. In an in vivomodel of doxorubicin-induced cardiotoxicity, overexpression of calpastatin aggravated myocardial dysfunction in transgenic ...
New approaches to the chemotherapy of glioblastoma [Elektronische Ressource] : investigations on doxorubicin nanoparticles, inhibition of PDGF receptors and kinesin Eg5, with emphasis on confocal laser-scanning microscopy / vorgelegt von Dietmar Gross : New Approaches to the Chemotherapy of Glioblastoma: investigations on doxorubicin nanoparticles, inhibition of PDGF receptors and kinesin Eg5, with emphasis on confocal laser-scanning microscopy Dissertation zur Erlangung des Doktorgrades der Naturwissenschaften (Dr. rer. nat.) der Naturwissenschaftlichen Fakultät IV - Chemie und Pharmazie - der Universität Regensburg
Title:Comparison of Physicochemical Properties of Generic Doxorubicin HCl Liposome Injection with the Reference Listed Drug. VOLUME: 18 ISSUE: 4. Author(s):Kuntal Maiti *, Subhas Bhowmick, Pankaj Jain, Murlidhar Zope, Keyur Doshi and Thennati Rajamannar. Affiliation:Sun Pharma Advanced Research Company Ltd., Mumbai, Sun Pharmaceutical Industries Ltd. Mumbai, Sun Pharma Advanced Research Company Ltd., Mumbai, Sun Pharma Advanced Research Company Ltd., Mumbai, Sun Pharma Advanced Research Company Ltd., Mumbai, Sun Pharmaceutical Industries Ltd. Mumbai. Keywords:Doxorubicin hydrochloride, liposome, sterically stable, generic, physicochemical equivalence, cancer.. Abstract:Background: Liposomal doxorubicin is widely used for treating ovarian cancer and Kaposis sarcoma. Encapsulation of doxorubicin in highly complex polyethylene glycol-coated (stealth) liposomes prolongs residence time and avoids the systemic toxicity associated with administration of the free drug. Small variations in ...
Аннотация: In isotonic medium, daunorubicin in the concentration range of 0.5-5.0 mg/ml of cells and doxorubicin in the concentration range of 0.2-1.0 mg/ml of cells caused hemoglobin (Hb) and K+ to efflux from red blood cells (RBC), to increase RBC size and to lower their deformability. Hb and K+ efflux rates were proportional to the antibiotic concentrations and remained stable for a few hours. Hb efflux did not change significantly in the 4-21 degrees C range (exempt at an experimental concentration of daunorubicin of 5.0 mg/ml of cells) but soared sharply at 37 degrees C. At the daunorubicin and doxorubicin concentration of 0.2 mg/ml of cells, Hb and K+ efflux virtually did not differ from control values. At the antibiotic concentration of 1.0 mg/ml of cells, 37 degrees C, Hb efflux rate was 0.34-5.6%, while that of K+(-) 1.0-8.2%, per hour, of possible maximum value. For the daunorubicin level of 5.0 mg/ml of cells, the respective values were 10 and 17%. At the daunorubicin ...
Doxorubicin-mediated radiosensitivity in multicellular spheroids from a lung cancer cell line is enhanced by composite micelle encapsulation Wen-Hong Xu,1 Min Han,2 Qi Dong,3 Zhi-Xuan Fu,3 Yuan-Yuan Diao,2 Hai Liu,3 Jing Xu,3 Hong-Liang Jiang,4 Su-Zhan Zhang,3 Shu Zheng,3 Jian-Qing Gao,2 Qi-Chun Wei11Department of Radiation Oncology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, 2Institute of Pharmaceutics, College of Pharmaceutical Sciences, 3Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), The Second Affiliated Hospital, School of Medicine, 4Department of Polymer Science and Engineering, Zhejiang University, Hangzhou, Zhejiang, ChinaBackground: The purpose of this study is to evaluate the efficacy of composite doxorubicin-loaded micelles for enhancing doxorubicin radiosensitivity in multicellular spheroids from a non-small cell lung cancer cell line.Methods: A novel composite doxorubicin-loaded micelle consisting
Cardiotoxicity with rituximab, cyclophosphamide, non-pegylated liposomal doxorubicin, vincristine and prednisolone compared to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone in frontline treatment of patients with diffuse large B-cell lymphoma: A randomised phase-III study from the Austrian Cancer Drug Therapy Working Group [Arbeitsgemeinschaft Medikamentöse Tumortherapie AGMT](NHL-14 ...
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Background: Progressive apoptosis following the primary injury has been implicated in the progression to end-stage heart failure. Survivin, a member of the inhibitor of apoptosis protein, is one of the most potent suppressor of apoptosis. We hypothesized that preventing apoptosis by survivin gene therapy may prevent deterioration in left ventricular (LV) systolic dysfunction in a doxorubicin-induced cardiomyopathy model in rats.. Methods and Results: A reproducible model of doxorubicin (dox)-induced cardiomyopathy was established in male Fisher rats by 6 equal doses (2.5 mg/kg bw) of i.p. injection every other day for 2 weeks. Echocardiographic assessment was performed at week 0, 3, and 6. A subset of animals (DOX+SURV, n=8) was treated with the survivin gene using the ultrasound targeted microbubble destruction (UTMD) technique at week 3. Control animals (DOX, n=12) did not receive any treatment at week 3. At week 0 (pre-dox), LV% fractional shortening (FS) was comparable in DOX+SURV and DOX ...
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Life Sci 2019 Dec 18;239:117070. Epub 2019 Nov 18.. Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA; Kosair Charities Pediatric Heart Research Program, Cardiovascular Innovation Institute, University of Louisville School of Medicine, Louisville, KY 40202, USA. Electronic address: Doxorubicin (DOX) induced cardiotoxicity is a life-threatening side effect of chemotherapy and decreased cardiac function can present years after treatment. Despite the investigation of a broad range of pharmacologic interventions, to date the only drug shown to reduce DOX-related cardiotoxicity in preclinical studies and limited clinical trials is the iron chelating agent, dexrazoxane (DRZ), although the mechanisms responsible for DRZ mediated protection from DOX related cardiotoxicity remain unclear. Engineered cardiac tissues (ECTs) can be used for tissue repair strategies and as in vitro surrogate models to test cardiac toxicities and preventative countermeasures. Read ...
The advantages of cytotoxic drugs such as anthracyclines can be limited by the harmful damage that they inflicted on the human body. One of the main side effects of administering such powerful chemotherapeutic drugs is their negative impact on the cardiovascular system. These adverse side effects can significantly limit the usefulness of freely administered drugs such as doxorubicin. Lower doses must be given for the safety and well being of the patients while ultimately reducing the potency of the drug itself. Immunoliposomes can allow for the targeted delivery of anthracyclines such as doxorubicin. Specific targeting greatly decreases the detrimental side effects to sensitive tissues outside the targeted site while simultaneously acquiescing a larger dosage of drug at the tumor site without larger doses actually being administered. Immunoliposomes contain reactive lipids on their outer surface that allow for the conjugation of different molecules such as antibodies, peptides, or proteins. The ...
PURPOSE: To estimate the cost effectiveness of TAC (docetaxel, doxorubicin, and cyclophosphamide) compared with FAC (fluorouracil, doxorubicin, and cyclophosphamide) when administered as adjuvant therapy to women with node-positive early breast cancer in the United Kingdom (UK), both with and without primary prophylaxis with granulocyte colony-stimulating factor (G-CSF). METHODS: A standard health economic Markov model estimated the cost and outcome for node-positive early breast cancer patients, from initiation of adjuvant chemotherapy to death.
The protein p53 plays a crucial role in the regulation of cellular responses to diverse stresses. Thus, a major priority in cell biology is to define the mechanisms that regulate p53 activity in response to stresses or maintain it at basal levels under normal conditions. Moreover, further investigation is required to establish whether RNA participates in regulating p53s interaction with other proteins. Here, by conducting systematic experiments, we discovered a p53 interactor-hnRNPC-that directly binds to p53, destabilizes it, and prevents its activation under normal conditions. Upon doxorubicin treatment, the lncRNA SNHG1 is retained in the nucleus through its binding with nucleolin and it competes with p53 for hnRNPC binding, which upregulates p53 levels and promotes p53‐dependent apoptosis by impairing hnRNPC regulation of p53 activity. Our results indicate that a balance between lncRNA SNHG1 and hnRNPC regulates p53 activity and p53‐dependent apoptosis upon doxorubicin treatment, and ...
QUÉBEC CITY, Feb. 4, 2014 /PRNewswire/ - Aeterna Zentaris Inc. (NASDAQ: AEZS) (TSX: AEZ) (the Company) today announced that an article on Phase 2 results for zoptarelin doxorubicin (AEZS-108) in endometrial cancer has been published in the February issue of the International Journal of Gynecological Cancer. Zoptarelin doxorubicin, is the Companys cytotoxic peptide conjugate which specifically targets luteinizing hormone-releasing hormone (LHRH) receptors. The article, Efficacy and Safety of AEZS-108 (LHRH Agonist Linked to Doxorubicin) in Women With Advanced or Recurrent Endometrial Cancer Expressing LHRH Receptors: A Multicenter Phase 2 Trial (AGO-GYN5), Emons G., Gorchev G., Harter P., Wimberger P., Stähle A., Hanker L., Hilpert F., Beckmann M.W., Dall P., Gründker C., Sindermann H., Sehouli J., outlines results of this study which had been previously presented at the European Society of Gynaecological Oncologys (ESGO) annual meeting in September 2011. The article is currently ...
Doxorubicin is an anthracycline antitumor antibiotic that inhibits DNA topoisomerase II by inducing double-stranded DNA breaks.{22647} By intercalating within DN...
Modern medicine had achieved the pinnacle of human. HBV reactivation has been noted in Breast Cancer patients following Cytoxan and Adriamycin chemotherapy,.. followed by doxorubicin (7.2 %) and vincristine. chemotherapy is to bring the disease into remission). Cyclophosphamide Daunorubicin Prednisone.Inicio » Arranca el US Open. â I went to have my pre-chemotherapy blood check this week. org/index.php/cytoxan-adriamycin-taxol.pdf gesture deliberate.. . ineligible for standard high-dose chemotherapy with. to vincristine plus doxorubicin plus. SE, Szubert AJ, et al. Cyclophosphamide,.Facial ,, Facial Mask Beauty Treatment. Facial Mask Beauty Treatment ¿Por qué pagar por la máscara cuándo usted puede usar ingredientes básicos encontrados ...
The anthracycline doxorubicin (DOX) is an exceptionally good antineoplastic agent, but its use is limited by formation of metabolites which induce acute and chronic cardiac toxicities. Whereas the acute toxicity is mild, the chronic toxicity can produce a life-threatening cardiomyopathy. Studies in laboratory animals are of limited value in predicting the structure and reactivity of toxic metabolites in humans; therefore, we used an ethically acceptable system which is suitable for exploring DOX metabolism in human myocardium. The system involves cytosolic fractions from myocardial samples obtained during aorto-coronary bypass grafting. After reconstitution with NADPH and DOX, these fractions generate the alcohol metabolite doxorubicinol (DOXol) as well as DOX deoxyaglycone and DOXol hydroxyaglycone, reflecting reduction of the side chain carbonyl group, reductase-type deglycosidation of the anthracycline, and hydrolase-type deglycosidation followed by carbonyl reduction, respectively. The ...
Understanding the survival mechanism of metastatic cancer cells in circulation will provide new perspectives on metastasis prevention and also shed new light on metastasis-derived drug resistance. In this study, we made it feasible to detect apoptosis of circulating tumor cells (CTCs) in real-time by integrating a fluorescence resonance energy transfer (FRET)-based caspase sensor into one in vitro microfluidic circulatory system, and two in vivo models: zebrafish circulation and mouse lung metastatic model. Our study demonstrated that fluid shear stresses triggered apoptosis of breast cancer cells in circulation by elevating the mitochondrial production of the primary free radical, superoxide anion. Cancer cells with high levels of manganese superoxide dismutase (MnSOD) exhibited stronger resistance to shear forceinduced apoptosis and formed more lung metastases in mice. These metastasized cells further displayed higher resistance to chemotherapeutic agent doxorubicin, which also generates ...
Fig. 1. Lack of p53 induction in cells lacking PARP-1 in response to doxorubicin treatment. Normal and PARP-1 −/− MEFs, the human breast carcinoma MCF-7, and human osteosarcoma Saos-2 cells were treated with 0.2 μg/ml (0.35 μm) doxorubicin for indicated times. B, PARP KO cells were also treated with increasing doxorubicin concentrations for 24 h. Total cell lysates (20 μg protein/lane) were separated on 10% SDS gels and transferred onto the PVDF membrane. Immunoblotting was performed with anti-p53 PAb421 antibody and subsequently with anti-PARP-1 C-2-10 and antiactin antibody. Saos-2 cells were used as the p53-negative control.. ...
Doxorubicin is an anticancer agent that is commonly used to treat a number of tumors and is associated with acute and chronic changes of the cardiovascular system. Ellagic acid has strong free radical scavenging capacity, neuroprotective and hepatoprotective effects, and is known to protect against changes occurring due to diabetes, cardiovascular diseases, and cancer. Twenty-four Wistar rats were divided in four groups: control group received saline, doxorubicin group received doxorubicin in a single dose of 20 mg/kg, ellagic acid group received ellagic acid in a dose of 4 mg/kg, and doxorubicin + ellagic acid group received doxorubicin and ellagic acid in same doses as in previous groups ...
This phase I dose-finding study examined the effects of the combination of doxorubicin and docetaxel (Taxotere) in 42 women with metastatic breast cancer. The combination was studied at six different dosing levels. The maximum tolerated doses were defined as doxorubicin, 50 mg/m², and docetaxel, 85 mg/m², with sepsis as the dose-limiting toxicity. 1
Onxeo S.A. (Euronext Paris, NASDAQ Copenhagen: ONXEO), an innovative company specializing in the development of orphan oncology drugs, today announced that the phase I/II clinical trial of belinostat in combination with doxorubicin (PXD101-CLN-14) in patients with soft tissue sarcoma (STS) was accepted for presentation in the Poster Discussion Session at the 2015 Annual Meeting of the American Society of Clinical Oncology (ASCO), taking place in Chicago, USA from May 29 to June 2, 2015.. The PXD101-CLN-14 study was an open-label, multicenter, dose-escalation phase I/II to evaluate the safety and efficacy of the combination of belinostat with doxorubicin in patients with advanced solid tumors (the phase I part of the study) and STS (the phase II part of the study).. The trial demonstrated that belinostat in combination with doxorubicin has an acceptable safety profile, allowing the combination of belinostat at the dose of 1000 mg/m2 on days 1-5 with 75 mg/m2 doxorubicin on day 5 in a three-week ...
Introduction: Protection of the heart from chemotherapeutic (Doxorubicin, DOX) drug-induced toxicity is a desirable goal, to limit side effects of cancer treatments. DOX toxicity has been linked to the activation (phosphorylation) of the AMP-activated kinase, AMPK. The 18 kDa low molecular weight isoform of fibroblast growth factor 2 (Lo-FGF-2) is a known cardioprotective and cytoprotective agent. In this study we have tested the ability of Lo-FGF-2 to protect from DOX-induced damage in rat cardiomyocytes in vitro, and in transgenic mouse models in vivo, in relation to AMPK activation.. Methods: Rat neonatal cardiomyocytes in culture were exposed to DOX (0.5 μM) in the presence or absence of pre-treatment Lo-FGF-2 (10 ng/ml). Compound C was used to block phosphorylation (activity) of AMPK. Levels of cell viability/death (using Calcein-AM/Propidium iodide assay), phospho -and total AMPK, and apoptotic markers such as active caspase 3 were analyzed. In addition, transgenic mice expressing only ...
A pH and redox dual-sensitive biodegradable polysaccharide, succinic acid-decorated dextran-g-phenylalanine ethyl ester-g-cysteine ethyl ester (Dex-SA-l-Phe-l-Cys), was synthesized to load doxorubicin hydrochloride (DOX·HCl). The DOX-loaded nanoparticles, which were prepared in aqueous solution and free of o
Doxorubicin (DOX) is a potent and widely used anthracycline antibiotic for the treatment of several malignancies. Unfortunately, the clinical utility of DOX is often restricted due to the elicitation of organ toxicity. Particularly, the increased risk for the development of dilated cardiomyopathy by DOX among the cancer survivors warrants major attention from the physicians as well as researchers to develop adjuvant agents to neutralize the noxious effects of DOX on the healthy myocardium. Despite these pitfalls, the use of traditional cytotoxic drugs continues to be the mainstay treatment for several types of cancer. Recently, phytochemicals have gained attention for their anticancer, chemopreventive, and cardioprotective activities. The ideal cardioprotective agents should not compromise the clinical efficacy of DOX and should be devoid of cumulative or irreversible toxicity on the naïve tissues. Furthermore, adjuvants possessing synergistic anticancer activity and quelling of chemoresistance
Media related to Doxorubicin at Wikimedia Commons "Doxorubicin". Drug Information Portal. U.S. National Library of Medicine. " ... Doxorubicin was originally made from the bacterium Streptomyces peucetius. In the EU doxorubicin pegylated liposomal (as Caelyx ... Mohan P, Rapoport N (2010). "Doxorubicin as a Molecular Nanotheranostic Agent: Effect of Doxorubicin Encapsulation in Micelles ... Substitution would be desirable because liposome-encapsulated doxorubicin is less cardiotoxic than unencapsulated doxorubicin. ...
... (developmental code names AEZS-108, AN-152) consists of doxorubicin linked to a small peptide agonist to ... June 2014). "Efficacy and safety of AEZS-108 (INN: zoptarelin doxorubicin acetate) an LHRH agonist linked to doxorubicin in ... Zoptarelin doxorubicin was invented by Andrew V. Schally while at the Tulane University School of Medicine, New Orleans and ... "Zoptarelin doxorubicin". Adis Insight. Springer Nature Switzerland AG. Emons G, Gorchev G, Sehouli J, Wimberger P, Stähle A, ...
... (BMS-182248/SGN-15; also known as cBR96-Dox) is an antibody-drug conjugate or (ADC) directed ... The payload is the chemotherapy drug doxorubicin which is connected with a hydrazone linker to cysteine residues of the Lewis-Y ... even in doxorubicin-resistant tumors. Hofland P (2013). "Harnessing The Power of Three: Advancing Antibody-drug Conjugates from ... "Antitumor activity of carcinoma-reactive BR96-doxorubicin conjugate against human carcinomas in athymic mice and rats and ...
Doxorubicin is synthesized by a specialized polyketide synthase. The initial event in DXR synthesis is the selection of the ... Doxorubicin (DXR) is a 14-hydroxylated version of daunorubicin, the immediate precursor of DXR in its biosynthetic pathway. ... Gandlur SM, Wei L, Levine J, Russell J, Kaur P (2004). "Membrane topology of the DrrB protein of the doxorubicin transporter of ... 1999). "Doxorubicin Overproduction in Streptomyces peucetius: Cloning and Characterization of the dnrU Ketoreductase and dnrV ...
"Doxorubicin - an overview , ScienceDirect Topics". Retrieved 2020-04-08. "Pralatrexate". ... Doxorubicin): blocks the enzyme that promotes growth and cell division Oncovin (Vincristine): used to inhibit the growth of ...
ISBN 978-0-412-26730-7. Arcamone, Federico (1981). Doxorubicin: Anticancer Antibiotics. Academic Press. ISBN 978-0-12-059280-7 ...
Doxorubicin Khosla, C.; Gokhale, R. S.; Jacobsen, J. R.; Cane, D. E. (1999). "Tolerance and Specificity of Polyketide Synthases ...
DOXORUBICIN Anticancer Antibiotics. Oxford: Elsevier Science. ISBN 0-323-13973-6. Type strain of Streptomyces capoamus at ...
etoposide and doxorubicin. In high doses it was found to be strongly toxic to normal cells. This effect may be responsible for ...
ISBN 978-81-88237-58-6. {{cite book}}: ,first1= has generic name (help) Federico, Arcamone (1981). DOXORUBICIN Anticancer ...
Alternatives such as doxorubicin are today more widely available and prescribed, due to more mild side effects along with ... Doxorubicin Azithromycin Kitamura, Tsuyoshi; Yoshihiro Sato; Miwako Mori (2004). "Synthetic study of (+)-anthramycin using ring ...
Doxorubicin (trade name Adriamycin; also known as hydroxydaunorubicin), the most widely used agent in HCC, has shown a 4% to ... Studies have shown that the overall response (OR) rate, but not overall survival (OS), doubles when doxorubicin was given in ...
Doxorubicin Mimosine "Vinblastine Sulfate". The American Society of Health-System Pharmacists. Archived from the original on ...
January 1999). "Phase I clinical and pharmacokinetic study of PK1 [N-(2-hydroxypropyl)methacrylamide copolymer doxorubicin]: ... HPMA copolymer-doxorubicin conjugate). The HPMA copolymers are also used as a scaffold for iBodies, polymer-based antibody ...
... doxorubicin, plus dacarbazine or cisplatin; cyclophosphamide, doxorubicin, plus dacarbazine; high dose methotrexate; or ... doxorubicin alone or combined with ifosfamide, olaratumab, trabectedin, gemcitabine, or docetaxel; cyclophosphamide, ...
Only the latter differs substantially compared to doxorubicin, as the terminal elimination half-life of doxorubicin is ... creating the doxorubicin and doxorubicinol aglycones and 7-deoxy-doxorubicin and 7-deoxy-doxorubicinol aglycones, respectively ... at 2.2% overall with a cumulative doxorubicin dose-dependent incidence of CHF of 3%, 7%, and 18% at 400, 550, and 700 mg/m2, ... Area under the plasma concentration versus time curve values (adjusted for dose) are 1.3 to 1.7 times higher for doxorubicin ...
Daunorubicin Idarubicin Doxorubicin Grethe, Guenter; Mitt, Toomas; Williams, Thomas H; Uskokovic, Milan R (1983). "Synthesis of ...
July 2004). "The effect of dexrazoxane on myocardial injury in doxorubicin-treated children with acute lymphoblastic leukemia ... 300 mg/m2 doxorubicin or > 540 mg/m2 epirubicin and general approval for use for cardioprotection. That showed a possibly ... such as daunorubicin or doxorubicin or other chemotherapeutic agents. However, in July 2011 the European Medicines Agency (EMA ... "Effects of dexrazoxane and amifostine on evolution of Doxorubicin cardiomyopathy in vivo". Experimental Biology and Medicine. ...
Doxorubicin is loaded into the liposomes just before administration to patients with a maximum single dose of 75 mg/m2 every 3 ... Doxorubicin was isolated from a mutated variant of S. peucetius (var. caesius). It differs from daunorubicin only by the ... Radiolabelled doxorubicin has been utilised as a breast cancer lesion imaging agent in a pilot study. This radiochemical, 99mTc ... Doxil has lower maximum tolerable dose (MTD) at 50 mg/m2 every 4 weeks compared to free doxorubicin at 60 mg/m2 every 3 weeks. ...
Doxorubicin is used in some cases. Chemotherapy in relatively healthy ferrets is tolerated very well, but possible side effects ... The most common treatment is a combination of cyclophosphamide, vincristine, prednisone, L-asparaginase, and doxorubicin. Other ...
FAC (or CAF): 5-fluorouracil, doxorubicin, cyclophosphamide. AC (or CA): Adriamycin (doxorubicin) and cyclophosphamide. AC- ... AT: Adriamycin (doxorubicin) and Taxotere (docetaxel). Since chemotherapy affects the production of white blood cells, a ... Taxol: AC followed by paclitaxel (Taxol). TAC: Taxotere (docetaxel), Adriamycin (doxorubicin), and cyclophosphamide. FEC: 5- ...
Currently, there are four main anthracyclines in medical use: Doxorubicin Daunorubicin (doxorubicin precursor) Epirubicin (a ... Some poisons, such as doxorubicin, have been proposed to intercalate in the strand break between the base pairs that flank the ... The first anthracycline (doxorubicin) was isolated from the bacteria Streptomyces peucetius in the 1960s. Anthracyclines are ... It is hypothesized that doxorubicin, which possesses a hydroxyl group and a methoxy group not present in idarubicin, can form ...
Aihara Y, Kurabayashi M, Tanaka T, Takeda SI, Tomaru K, Sekiguchi KI, Ohyama Y, Nagai R (Aug 2000). "Doxorubicin represses CARP ... In cardiomyocytes treated with doxorubicin, a model of anthracycline-induced cardiomyopathy, CARP mRNA and protein levels were ... "A novel cardiac-restricted target for doxorubicin. CARP, a nuclear modulator of gene expression in cardiac progenitor cells and ... and whose mRNA levels are exquisitely sensitive to Doxorubicin, mediated through a hydrogen peroxide/ERK/p38MAP kinase- ...
"Flavaglines Alleviate Doxorubicin Cardiotoxicity: Implication of Hsp27". PLoS ONE. 6 (10): e25302. Bibcode:2011PLoSO...625302B ...
"Role of RLIP76 in lung cancer doxorubicin resistance: I. The ATPase activity of RLIP76 correlates with doxorubicin and 4- ... Doxorubicin transport in lung cancer by RLIP76". Int. J. Oncol. 22 (4): 713-20. doi:10.3892/ijo.22.4.713. PMID 12632060. ... Awasthi S, Singhal SS, Singhal J, Yang Y, Zimniak P, Awasthi YC (2003). "Role of RLIP76 in lung cancer doxorubicin resistance: ... Awasthi S, Singhal SS, Singhal J, Cheng J, Zimniak P, Awasthi YC (2003). "Role of RLIP76 in lung cancer doxorubicin resistance ...
Doxorubicin has shown some promise in treatment. Most mammary tumors in rats are benign fibroadenomas, which are also the most ... "Retrospective Evaluation of Adjunctive Doxorubicin for the Treatment of Feline Mammary Gland Adenocarcinoma: 67 Cases". J Am ...
It was also shown that FL3 may enhance the efficacy of one of the most widely used anticancer agents, doxorubicin, and ... "Flavaglines Alleviate Doxorubicin Cardiotoxicity: Implication of Hsp27". PLoS ONE. 6 (10): e25302. Bibcode:2011PLoSO...625302B ...
Similar to doxorubicin, daunorubicin interacts with DNA by intercalation and inhibition of macromolecular biosynthesis. This ... Fornari FA, Randolph JK, Yalowich JC, Ritke MK, Gewirtz DA (April 1994). "Interference by doxorubicin with DNA unwinding in MCF ... Doxorubicin Idarubicin "Daunorubicin (Cerubidine) Use During Pregnancy". 19 September 2019. Retrieved 15 August 2020 ... Weiss RB (December 1992). "The anthracyclines: will we ever find a better doxorubicin?". Seminars in Oncology. 19 (6): 670-86. ...
In addition to a DNA repair response, exposure of spermatogonia to doxorubicin can also induce programmed cell death (apoptosis ... Anticancer drugs such as doxorubicin and vincristine can adversely affect male fertility by damaging the DNA of proliferative ... Habas K, Anderson D, Brinkworth MH (2017). "Germ cell responses to doxorubicin exposure in vitro" (PDF). Toxicol. Lett. 265: 70 ... Experimental exposure of rat undifferentiated spermatogonia to doxorubicin and vincristine indicated that these cells are able ...
For example, doxorubicin is consistently /ˌdɒksoʊˈruːbɪsɪn/ in English. Trade names almost always have one accepted ... "doxorubicin (Adriamycin)"). This pattern is important for the scientific literature, where conflict of interest is disclosed or ...
Doxorubicin: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Before receiving doxorubicin injection,. *tell your doctor and pharmacist if you are allergic to doxorubicin, daunorubicin ( ... Doxorubicin comes as a solution (liquid) or as a powder to be mixed with liquid to be injected intravenously (into a vein) by a ... Doxorubicin may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away: *nausea ...
A new review looks at the potential role of endothelial-to-mesenchymal transition in the development of doxorubicin-induced ... Table 1. Summary of drugs that alleviate doxorubicin-induced cardiotoxicity Classification of drugs. Drug names. Study object. ... As one of the most popular chemotherapy drugs, doxorubicin plays a substantial role in the treatment of tumors. Unfortunately, ... In recent years, endothelial damage caused by EndMT has gradually been discovered to be involved in doxorubicin-induced ...
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Adriamycin is the common name for the drug doxorubicin hydrochloride that is thought to bind DNA and inhibit nucleic acid ... Adriamycin (Doxorubicin). Adriamycin is the common name for the drug doxorubicin hydrochloride that is thought to bind DNA and ...
Doxorubicin liposome is an intravenous chemotherapy used to treat ovarian cancer, AIDS-related Kaposis sarcoma, and multiple ... Doxil (Doxorubicin Liposomal) - Intravenous Generic Name: doxorubicin liposome (dox-oh-ROO-bi-sin hye-droe-KLOR-ide LYE-poh- ... If doxorubicin liposome accidentally leaks out of the vein where it is injected, it may damage the skin and cause scars. ... Doxil (doxorubicin liposome) infusion is an intravenous (IV) chemotherapy medication used to treat different types of cancer, ...
CanMED: NDC. The Cancer Medications Enquiry Database (CanMED) is a two-part resource for cancer drug treatment related studies.
Transport of Liposome Encapsulated Drugs in Voxelized Computational Model of Human Brain Tumors 215 215 Transactions on NanoBioscience (TNB) Transactions on NanoBioscience (TNB) // ...
Free doxorubicin and untargeted doxorubicin-loaded exosomes showed insignificant effects, whereas targeted doxorubicin-loaded ... Selective delivery of doxorubicin to tumor tissues was analyzed by measuring the auto-fluorescence of doxorubicin by in vivo ... The results of MTT assay showed that cytotoxicity of targeted doxorubicin-loaded exosomes was higher than free doxorubicin at ... Doxorubicin was encapsulated into exosomes by electroporation. Flow cytometry was used to assess the attachment of exosomes to ...
DOXORUBICIN, 2MG/ML, INJECTABLE. Common uses. This medication is typically used for the treatment of breast cancer. ...
In these cells, doxorubicin (DOX) caused rapid apoptsis, whereas GA-induced heat-shock protein-70 (Hsp70) (a potent inhibitor ... In these cells, doxorubicin (DOX) caused rapid apoptsis, whereas GA-induced heat-shock protein-70 (Hsp70) (a potent inhibitor ... Hsp70 regulates the doxorubicin-mediated heart failure in Hsp70-transgenic mice *Katerina Naka K ... Demidenko, Z., Vivo, C., Halicka, H. et al. Pharmacological induction of Hsp70 protects apoptosis-prone cells from doxorubicin ...
PLD is a unique doxorubicin formulation in which a polyethylene glycol layer surrounds a doxorubicin-containing liposome. The ... Pegylated Liposomal Doxorubicin Plus Bortezomib Yields Improved Time-to-Progression vs. Bortezomib Alone in Patients With ... Pegylated Liposomal Doxorubicin in Combination With Bortezomib May Provide Therapeutic Advantage for High-Risk Multiple Myeloma ... Also, the size of the doxorubicin-containing vesicles allows leakage of the drug through the abnormally permeable tumor vessels ...
Receive NAPRA updates of interest directly to your inbox: general NAPRA news, NDS updates and/or updates on practice resources.. ...
Doxorubicin. Liposomal doxorubicin. Bleomycin. Vincristine. Antibiotics, Antineoplastic. Antineoplastic Agents. Topoisomerase ... Drug Information available for: Vincristine sulfate Bleomycin sulfate Bleomycin Doxorubicin Doxorubicin hydrochloride ... Drug: Doxorubicin hydrochloride (liposomal) Drug: Bleomycin sulfate Drug: Vincristine sulfate Phase 3 ... To determine the efficacy of Stealth liposomal doxorubicin hydrochloride (DOX-SL) in the treatment of moderate to severe AIDS- ...
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... nanodisks for the targeted delivery of doxorubicin (DOX) to liver cancer cells. LAP nanodisks were firstly modified with 3- ... Targeted doxorubicin delivery to hepatocarcinoma cells by lactobionic acid-modified laponite nanodisks G. Chen, D. Li, J. Li, X ... Targeted doxorubicin delivery to hepatocarcinoma cells by lactobionic acid-modified laponite nanodisks† ... nanodisks for the targeted delivery of doxorubicin (DOX) to liver cancer cells. LAP nanodisks were firstly modified with 3- ...
China Doxorubicin Hydrochloride Suppliers ,offers quality China Doxorubicin Hydrochloride. ... Doxorubicin, HCl;(8s-cis)-10-((3-amino-2,3,6-trideoxy-alpha-l-lyxo-hexopyranosyl)oxy)-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-( ...
Cardiac expression of human type 2 iodothyronine deiodinase increases glucose metabolism and protects against doxorubicin- ... Cardiac expression of human type 2 iodothyronine deiodinase increases glucose metabolism and protects against doxorubicin- ... Cardiac expression of human type 2 iodothyronine deiodinase increases glucose metabolism and protects against doxorubicin- ...
PSN-A augments doxorubicin toxicity in prostate cancer cells. Doxorubicin is one of the most important chemotherapeutic drugs ... Doxorubicin enhances curcumins cytotoxicity in human prostate cancer cells in vitro by enhancing its cellular uptake. Int J ... Since doxorubicin is being used clinically in the treatment of prostate cancer, we tested the efficacy of doxorubicin in ... PSN-A augments doxorubicin toxicity in prostate cancer cells. (A) LNCaP and DU145 cells were treated with PSN-A (25nM) and ...
Alone or in Combination With Pegylated Liposomal Doxorubicin Versus Pegylated Liposomal Doxorubicin Alone in Patients With ... Alone or in Combination With Pegylated Liposomal Doxorubicin Versus Pegylated Liposomal Doxorubicin Alone in Patients With ...
Learn how doctors are using this medication to increase life expectancy, and find out if doxorubicin is right for your ... Doxorubicin is a chemotherapy drug for mesothelioma patients. ... What is Doxorubicin?. Doxorubicin-also known by its brand names ... Doxorubicin in Clinical Trials. In a recent study carried out in Belgium, researchers combined doxorubicin and valproate, a ... Intraoperative doxorubicin helps shrink mesothelioma tumors while doctors perform surgery.. Discover How You Can Beat The Odds ...
... compared to methotrexate/vinblastine/doxorubicin/cisplatin (MVAC) for locally advanced or metastatic transitional cell ... Doxorubicin, Plus Cisplatin in Patients with Bladder Cancer December 12, 2018 PURPOSE: To compare long-term survival in ... or methotrexate/vinblastine/doxorubicin/cisplatin (MVAC).. PATIENTS AND METHODS: Efficacy data from a large randomized phase ...
... pegylated liposomal doxorubicin hydrochloride [pegylated liposomal doxorubicin] [PLD] and atezolizumab and PLD/bevacizumab and ... Phase II/III Study of Pegylated Liposomal Doxorubicin and CTEP-Supplied Atezolizumab Versus Pegylated Liposomal Doxorubicin, ... ARM III: Patients receive pegylated liposomal doxorubicin hydrochloride IV over 60 minutes on day 1 and bevacizumab IV over 30- ... Closed to accrual as of February 09, 2021) ARM II: Patients receive pegylated liposomal doxorubicin hydrochloride IV over 60 ...
0.18±0.012µg/g). Significant decreases in doxorubicin concentration were noted for RFA zones after 72 hours (0.366±0.088µg/g vs ... 0.18±0,012µg/g) (p,0.05). Doxorubicin concentrations in IRE zones were not significantly different from untreated liver (0.191± ... Doxorubicin concentrations were analyzed using fluorescence spectrofluorimetry of homogenized tissue. Results RFA treatment ... Purpose To compare the accumulation of liposomal doxorubicin in liver tissue treated by radiofrequency ablation (RFA) and ...
Guo CH, Shih MY, Chung CH, Lin YC, Fan CT, Peng CL, Chen PC, Hsia S. Fish Oil and Selenium with Doxorubicin Modulates ... Guo CH, Shih MY, Chung CH, Lin YC, Fan CT, Peng CL, Chen PC, Hsia S. Fish Oil and Selenium with Doxorubicin Modulates ... Doxorubicin-FO/Se combination treatment decreased expression of membrane EGFR and FGFR, down-regulated downstream PI3K/AKT/mTOR ... Compared with doxorubicin alone, combination treatment resulted in lower tumor sizes and fewer overall metastasis, lower GPR-40 ...
Final overall survival results of a randomized trial comparing bortezomib plus pegylated liposomal doxorubicin with bortezomib ... Final overall survival results of a randomized trial comparing bortezomib plus pegylated liposomal doxorubicin with bortezomib ... Final overall survival results of a randomized trial comparing bortezomib plus pegylated liposomal doxorubicin with bortezomib ...
Doxorubicin-induced cardiomyopathy: From molecular mechanisms to therapeutic strategies. Yanti Octavia, Carlo G. Tocchetti, ... Octavia, Y., Tocchetti, C. G., Gabrielson, K. L., Janssens, S., Crijns, H. J., & Moens, A. L. (2012). Doxorubicin-induced ... Doxorubicin-induced cardiomyopathy: From molecular mechanisms to therapeutic strategies. Journal of Molecular and Cellular ... Doxorubicin-induced cardiomyopathy : From molecular mechanisms to therapeutic strategies. / Octavia, Yanti; Tocchetti, Carlo G. ...
Doxorubicin, Hydrochloride - CAS 25316-40-9 - Calbiochem - Find MSDS or SDS, a COA, data sheets and more information. ... Doxorubicin, Hydrochloride - CAS 25316-40-9 - Calbiochem. 324380-10MG Sigma-AldrichDoxorubicin, Hydrochloride - CAS 25316-40-9 ...
Doxorubicin (Dox) is one of the most commonly used anthracyclines for the treatment of solid and hematological tumors such as B ... Doxorubicin (Dox) is one of the most commonly used anthracyclines for the treatment of solid and hematological tumors such as B ... Exploring the ATR-CHK1 Pathway in the Response of Doxorubicin-induced DNA Damages in Acute Lymphoblastic Leukemia Cells ...
Mitochondria; Doxorubicin; Carvedilol; Atenolol; Permeability transition pore; Oxidative damage; Mitochondrionopathy. Issue ... The cardiotoxicity associated with doxorubicin (DOX) therapy limits the total cumulative dose and therapeutic success of active ... Carvedilol-mediated antioxidant protection against doxorubicin-induced cardiac mitochondrial toxicity. Authors: Oliveira, Paulo ...
  • A randomized trial comparing cisplatin plus cyclophosphamide versus cisplatin, doxorubicin, and cyclophosphamide in advanced ovarian cancer. (
  • After primary surgery, 125 patients with epithelial ovarian cancer (International Federation of Gynaecology and Obstetrics [FIGO] 1c + IIb + IIc = 22 patients, FIGO III = 82 patients, FIGO IV = 21 patients) were randomly allocated to receive PC (cisplatin 50 mg/m2 + cyclophosphamide 600 mg/m2 on day 1 every 28 days) (corrected) or PAC (PC + doxorubicin 45 mg/m2). (
  • This randomized phase III trial studies how well doxorubicin hydrochloride and cyclophosphamide followed by paclitaxel with or without carboplatin work in treating patients with triple-negative breast cancer. (
  • It is not yet known whether doxorubicin hydrochloride and cyclophosphamide is more effective when followed by paclitaxel alone or paclitaxel and carboplatin in treating triple-negative breast cancer. (
  • I. To determine whether the addition of carboplatin to an adjuvant chemotherapy regimen of doxorubicin (doxorubicin hydrochloride)/cyclophosphamide followed by paclitaxel will improve the invasive disease-free survival (IDFS) compared to doxorubicin/cyclophosphamide followed by paclitaxel when administered to patients with operable node-positive or high-risk node-negative triple-negative breast cancer. (
  • V. To determine the toxicity of doxorubicin/cyclophosphamide followed by paclitaxel administered concurrently with carboplatin compared to the toxicity of doxorubicin/cyclophosphamide followed by paclitaxel alone. (
  • To collect tissue and blood samples at several occasions for future biomarkers development in predicting risk of breast cancer recurrence in patients with operable node-positive or high-risk node-negative triple-negative breast cancer treated with doxorubicin/cyclophosphamide followed by paclitaxel with or without carboplatin and predicting benefit from the addition of carboplatin among these patients. (
  • Patients receive doxorubicin hydrochloride intravenously (IV) over 15 minutes and cyclophosphamide IV over 30 minutes on day 1. (
  • We also collected surface wipe samples for cyclophosphamide, ifosfamide, and doxorubicin at the beginning of the work day before the chemotherapy drugs were unpacked and at the end of the work day after the last chemotherapy treatment was completed. (
  • Doxorubicin and cyclophosphamide, or methotrexate. (
  • Cyclophosphamide, methotrexate, fluorouracil, and prednisone (CMP + P). The alternate drugs are doxorubicin and cyclophosphamide. (
  • Standard of care Srituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone plus second-line salvage therapy ± autologous stem-cell transplant). (
  • The optimal doses of Doxorubicin and Cyclophosphamide (AC) regimen in pre-operation Neoadjuvant chemotherapy for the patients suffering from stage III breast cancer were investigated. (
  • Adriamycin is the common name for the drug doxorubicin hydrochloride that is thought to bind DNA and inhibit nucleic acid synthesis. (
  • Doxorubicin-also known by its brand names Adriamycin and Doxil-is the oldest FDA approved chemotherapy drug in the United States. (
  • In addition, doxorubicin (Adriamycin)-induced nephrosis in rats is a commonly used experimental model for pharmacological studies of human chronic renal diseases. (
  • The combination of methotrexate, vinblastine, doxorubicin (Adriamycin), and cisplatin (MVAC) is the standard treatment for metastatic bladder cancer. (
  • Using a powerful combination of two chemotherapy agents - doxorubicin (brand names Adriamycin, Rubex ) and ifosfamide (Mitoxana) - does not help soft-tissue cancer patients live longer. (
  • PURPOSE: To compare long-term survival in patients with locally advanced or metastatic transitional cell carcinoma (TCC) of the urothelium treated with gemcitabine/cisplatin (GC) or methotrexate/vinblastine/doxorubicin/cisplatin (MVAC). (
  • To determine the efficacy of Stealth liposomal doxorubicin hydrochloride (DOX-SL) in the treatment of moderate to severe AIDS-related Kaposi's sarcoma (KS) by comparison with the established therapy BV (bleomycin/vincristine). (
  • Selective delivery of doxorubicin to tumor tissues was analyzed by measuring the auto-fluorescence of doxorubicin by in vivo imaging system. (
  • Selective distribution of targeted doxorubicin-loaded exosomes in the target tissues of the murine breast cancer model suggested specific delivery of doxorubicin by targeted exosomes, rather than untargeted exosomes. (
  • In this study, we covalently conjugated polyethylene glycol-linked lactobionic acid (PEG-LA) onto the surface of laponite (LAP) nanodisks for the targeted delivery of doxorubicin (DOX) to liver cancer cells. (
  • Delivery of Doxorubicin from Hyaluronic Acid-Modified Glutathione-Responsive Ferrocene Micelles for Combination Cancer Therapy. (
  • Unfortunately, the use of doxorubicin is associated with several adverse effects, particularly severe cardiotoxicity that can be life-threatening, which greatly limits its clinical use. (
  • The concrete molecular mechanism of doxorubicin-induced cardiotoxicity is still to be unraveled, yet endothelial damage is gradually being identified as an important mechanism triggering the development and progression of doxorubicin-induced cardiotoxicity. (
  • Mounting evidence suggests that endothelial-mesenchymal transition may play a non-negligible role in doxorubicin-induced cardiotoxicity. (
  • In this paper, we reviewed the molecular mechanisms and signaling pathways of EndMT and outlined the molecular mechanisms of doxorubicin-induced cardiotoxicity and the current therapeutic advances. (
  • Furthermore, we summarized the basic principles of doxorubicin-induced endothelial-mesenchymal transition that lead to endothelial dysfunction and cardiotoxicity, aiming to provide suggestions or new ideas for the prevention and treatment of doxorubicin-induced endothelial and cardiac injury. (
  • [ 6 , 7 ] Some studies have been conducted on the underlying mechanisms of doxorubicin-induced cardiotoxicity, but mostly on contractile impairment due to cardiomyocyte injury. (
  • [ 8 ] However, the latest research has identified endothelial damage as a possible novel target for doxorubicin-induced cardiotoxicity and is now a major focus of research. (
  • [ 13 , 14 ] Hence, while identifying the mechanisms and cytokines responsible for doxorubicin-induced cardiotoxicity, it is of great significance to seek therapeutic approaches to alleviate their cardiotoxicity in oncology patients. (
  • However, interventions reducing oxidative stress have not been successful at reducing the incidence of cardiotoxicity in patients treated with doxorubicin. (
  • In this review, the authors have reviewed the molecular mechanisms of the pathogenesis of acute and chronic doxorubicin-induced cardiotoxicity and propose potential pharmacological interventions and treatment options to prevent or reverse this specific type of heart failure. (
  • The cardiotoxicity associated with doxorubicin (DOX) therapy limits the total cumulative dose and therapeutic success of active anticancer chemotherapy. (
  • Tocopherol 200 mg/kg bodyweight respectively for ten days before injection of doxorubicin.Results: Doxorubicin produced marked cardiotoxicity represented by raised levels of serum biomarkers (cTnI, LDH and CK-MB) and severe necrosis of cardiomyocytes on microscopic examination. (
  • Prevention of doxorubicin-induced experimental cardiotoxicity by Nigella sativa in rats. (
  • Moreover, tumor growth inhibition and body weight were monitored following injection of free doxorubicin, and targeted and untargeted doxorubicin-loaded exosomes in a TUBO breast cancer model. (
  • Doxorubicin Injection is used in the treatment of various types of cancers of blood, breast, lung, ovaries and soft tissues. (
  • Doxorubicin Injection helps to treat certain kinds of cancer. (
  • Doxorubicin Injection kills or stops the growth of cancer cells and also prevents the multiplication of cancer cells. (
  • Your doctor will order tests before and during your treatment to see if your heart is working well enough for you to safely receive doxorubicin. (
  • They were randomly selected to receive either doxorubicin by itself or in combination with ifosfamide. (
  • The in vitro cytotoxicity effect of targeted doxorubicin-loaded exosomes on TUBO cells was determined using MTT assay. (
  • The results of MTT assay showed that cytotoxicity of targeted doxorubicin-loaded exosomes was higher than free doxorubicin at 72 hours. (
  • Free doxorubicin and untargeted doxorubicin-loaded exosomes showed insignificant effects, whereas targeted doxorubicin-loaded exosomes reduced the tumor growth rate. (
  • Herein, we report efficient delivery of targeted doxorubicin-loaded exosomes in vitro, corroborated with a significant reduction of murine breast cancer model tumor growth rate. (
  • This phase II/III trial studies how well pegylated liposomal doxorubicin hydrochloride with atezolizumab and/or bevacizumab work in treating patients with ovarian, fallopian tube, or primary peritoneal cancer that has come back (recurrent). (
  • Chemotherapy drugs, such as pegylated liposomal doxorubicin hydrochloride, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. (
  • PRIMARY OBJECTIVES: I. Estimate the probability of a dose limiting toxicity (DLT) following cycle 1 of experimental regimens (pegylated liposomal doxorubicin hydrochloride [pegylated liposomal doxorubicin] [PLD] and atezolizumab and PLD/bevacizumab and atezolizumab). (
  • ARM I: Patients receive pegylated liposomal doxorubicin hydrochloride intravenously (IV) over 60 minutes on day 1 and atezolizumab IV over 30-60 minutes on days 1 and 15. (
  • PLD is a unique doxorubicin formulation in which a polyethylene glycol layer surrounds a doxorubicin-containing liposome. (
  • The pegylation process protects the liposome from detection by the immune system, thereby increasing the plasma half-life relative to conventional doxorubicin. (
  • The molecules of doxorubicin are coated in a fatty capsule called as liposome. (
  • This liposome protects the body and allows the doxorubicin to remain in the blood circulation for a longer duration. (
  • Doxorubicin is in a class of medications called anthracyclines. (
  • Doxorubicin (Dox) is one of the most commonly used anthracyclines for the treatment of solid and hematological tumors such as B-/T-cell acute lymphoblastic leukemia (ALL). (
  • He Y, Khan M, Yang J, Yao M, Yu S, Gao H. Proscillaridin A induces apoptosis, inhibits STAT3 activation and augments doxorubicin toxicity in prostate cancer cells. (
  • Moreover, we found that PSN-A inhibits JAK2/STAT3 signaling and augments doxorubicin toxicity in prostate cancer cells. (
  • Doxorubicin is an anthracycline, a class of drugs researchers developed from streptomyces, a fungus that grows naturally in soil. (
  • Doxorubicin is an anthracycline antibiotic that is used widely as a chemotherapeutic agent. (
  • Doxorubicin is an anthracycline antineoplastic that causes DNA strand breakage through effects on topoisomerase II and direct intercalation into DNA, which causes DNA polymerase inhibition. (
  • Doxil (doxorubicin liposomal) infusion carries the risk of developing severe complications. (
  • The following four studies, which discuss pegylated liposomal doxorubicin (PLD) (Doxil) in combination with bortezomib, were presented at this year's 49th ASH Annual Meeting in Atlanta in December 2007. (
  • please see reference below ), which demonstrated that the combination of pegylated liposomal doxorubicin (PLD) (Doxil) plus bortezomib (Velcade) improved time to progression (TTP), compared with B monotherapy, in patients with multiple myeloma (MM) who relapse within 12 months of autologous stem-cell transplantation (SCT). (
  • Doxorubicin is a chemotherapy drug most effective in treating patients with advanced mesothelioma. (
  • Because of its tumor shrinking ability, doctors use doxorubicin as a palliative treatment to help patients with advanced mesothelioma improve their quality of life. (
  • In a recent study carried out in Belgium, researchers combined doxorubicin and valproate, a drug normally used for epilepsy, to treat patients diagnosed with mesothelioma. (
  • Researchers have also shown that doxorubicin works well as a treatment for patients with advanced stage mesothelioma that doctors can't remove with surgery. (
  • While this side effect is uncommon, it's serious, and the reason why patients can only receive a maximum amount of doxorubicin during a lifetime. (
  • Final overall survival results of a randomized trial comparing bortezomib plus pegylated liposomal doxorubicin with bortezomib alone in patients with relapsed or refractory multiple myeloma. (
  • It has been calculated that approximately 10% of patients treated with doxorubicin or its derivatives will develop cardiac complications up to 10. (
  • In 23 patients with limb sarcomas (2 patients International Union Against Cancer Stage IIA, 4 stage IIB, 1 stage IIIA, 11 stage IIIB, and 5 stage IVB) doxorubicin was administered via HAP 4-6 weeks before surgery. (
  • Conclusion These pectin structures with stronger TLR2-inhibiting properties may prevent the development of doxorubicin-induced intestinal damage in patients undergoing chemotherapeutic treatment with doxorubicin. (
  • In this study, patients will receive pembrolizumab with three chemotherapy drugs: gemcitabine, vinorelbine, and liposomal doxorubicin. (
  • These observations suggest that the nutritional supplements FO/Se increase the chemotherapeutic efficacy of doxorubicin against TNBC by modulating GPR-40 and selenoprotein and targeting multiple signaling pathways in tumor tissues. (
  • Scope Intestinal mucositis is a common side effect of the chemotherapeutic agent doxorubicin, which is characterized by severe Toll-like receptor (TLR) 2-mediated inflammation. (
  • The purpose of the present study was to determine the in vivo and in vitro effects of doxorubicin exposure on sarcoplasmic reticulum (SR) Ca2+-content and contractile protein function. (
  • The Ca2+-content of SR is shown to have a biphasic response to in vivo and in vitro doxorubicin exposure that is time- and dose-dependent. (
  • In vitro doxorubicin exposure initially reduces the SR Ca2+-content, but the predominant action to block the SR Ca2+-release channel increases SR Ca2+-content within 60 min. (
  • Methods and Results Four structurally different pectins that differed in DM and DB are tested on inhibitory effects on murine TLR2 in vitro, and on doxorubicin-induced intestinal mucositis in mice. (
  • Therefore, it is hypothesized that the degree of methyl-esterification (DM) and the degree of blockiness (DB) of pectins determine attenuating efficacy on doxorubicin-induced intestinal mucositis. (
  • As one of the most popular chemotherapy drugs, doxorubicin plays a substantial role in the treatment of tumors. (
  • Doxorubicin causes side effects similar to those produced by other chemotherapy drugs . (
  • Background: Doxorubicin, an effective anticancer drug used to treat multiple solid tumours and childhood malignancies since many decades but its cardiac adverse effects limits its use in full therapeutic dose. (
  • 2011). Acute exercise protects against calcium-induced cardiac mitochondrial permeability transition pore opening in doxorubicin-treated rats . (
  • Palliative treatments like doxorubicin stop the growth of mesothelioma, reducing the symptoms caused by large tumors. (
  • Intraoperative doxorubicin helps shrink mesothelioma tumors while doctors perform surgery . (
  • Guo CH, Shih MY, Chung CH, Lin YC, Fan CT, Peng CL, Chen PC, Hsia S. Fish Oil and Selenium with Doxorubicin Modulates Expression of Fatty Acid Receptors and Selenoproteins, and Targets Multiple Anti-Cancer Signaling in Triple-negative Breast Cancer Tumors. (
  • The authors' aim was to ascertain the activity of HAP with doxorubicin against intermediate or high grade limb tumors. (
  • In these cells, doxorubicin (DOX) caused rapid apoptsis, whereas GA-induced heat-shock protein-70 (Hsp70) (a potent inhibitor of apoptosis) and G1 arrest without significant apoptosis. (
  • Peroxisomal proliferator-activated receptor-alpha protects renal tubular cells from doxorubicin-induced apoptosis. (
  • In this study, we investigated the protective effect of PPAR-alpha on doxorubicin-induced apoptosis and its detailed mechanism in NRK-52E cells and animal models. (
  • PPAR-alpha overexpression in NRK-52E cells significantly inhibited doxorubicin-induced apoptosis and the quantity of cleaved caspase-3. (
  • Endogenous prostacyclin (PGI(2)) augmentation, which has been reported to protect NRK-52E cells from doxorubicin-induced apoptosis, induced the translocation and activation of PPAR-alpha. (
  • Therefore, PPAR-alpha is capable of inhibiting doxorubicin-induced ROS and NF-kappaB activity and protecting NRK-52E cells from doxorubicin-induced apoptosis. (
  • These data are consistent with the view that doxorubicin acts in a similar manner to ryanodine and results in cardiomyopathy due to Ca2+-overload. (
  • Doxorubicin may cause serious or life-threatening heart problems at any time during your treatment or months to years after your treatment has ended. (
  • Before treatment begins, doctors give their patient an anti-nausea drug to help reduce any side effects caused by doxorubicin. (
  • If you're considering adding doxorubicin, or any other chemotherapy, to your treatment regimen, make sure you speak to a doctor who has experience treating mesothelioma first. (
  • Compared with doxorubicin alone, combination treatment resulted in lower tumor sizes and fewer overall metastasis, lower GPR-40 mRNA levels, and higher expression of all selenoproteins. (
  • Doxorubicin-FO/Se combination treatment decreased expression of membrane EGFR and FGFR, down-regulated downstream PI3K/AKT/mTOR, MAPK/ERK, and JAK2/c-Src/STAT3 signaling, increased tumor suppressor PTEN/TSC1/TSC2 expression and P53 activation, and suppressed oncogenic transcription factor expression. (
  • Our findings show that HAP with doxorubicin is an active and well-tolerated procedure within a multidisciplinary approach to treatment of limb sarcomas. (
  • The mRNA level of PPAR-alpha was found to be reduced by doxorubicin treatment in NRK-52E cells. (
  • If cancer cells don't respond to doxorubicin, Taxotere may also be a treatment option. (
  • ABSTRACT Objective: To analyze wound contraction and histomorphometric pattern of lesions in Wistar rats undergoing doxorubicin extravasation. (
  • Doxorubicin is used to treat a number of cancers, including bladder, breast, lung, stomach and ovarian cancer, as well as lymphoma and certain types of leukemia, multiple myeloma and soft-tissue cancers. (
  • Trabectedin coupled with pegylated liposomal doxorubicin in relapsed ovarian cancer: outcomes in the entirely platinum-sensitive (platinum-free delay 6В-12 months) subpopulation of OVA-301 phase III randomized trial. (
  • In clinical practice, 40 mg/m 2 of pegylated liposomal doxorubicin (PLD40) has been used as an initial dosage for treating recurrent epithelial ovarian cancer (OC) instead of the recommended dose of 50 mg/m 2 (PLD50). (
  • Also, the size of the doxorubicin-containing vesicles allows leakage of the drug through the abnormally permeable tumor vessels, resulting in preferential concentration of doxorubicin at the tumor sites. (
  • Doxorubicin 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 and radiation (x-ray) therapy. (
  • Mice were randomized into 5 groups (n = 7/group) and treated with physiological saline (control), low-dose doxorubicin, and doxorubicin in combination with low, medium, or high doses of FO/Se. (
  • This study aims to determine whether FO/Se modulates G-protein-coupled polyunsaturated fatty acid receptors (GPR-40 and GPR-120) and selenoproteins (Sel-H, Sel-W, and GPx4), and increases the therapeutic effect of doxorubicin in a dose-dependent manner on triple-negative breast cancer (TNBC) mouse. (
  • An anti-cancer drug ( i.e. , doxorubicin (DOX)) was covalently conjugated onto PEGylated (PEG: polyethylene glycol) GNR nanocarriers via a hydrazone bond to achieve pH-sensitive controlled drug release. (
  • Cardiac expression of human type 2 iodothyronine deiodinase increases glucose metabolism and protects against doxorubicin-induced cardiac dysfunction in male mice. (
  • Purpose To compare the accumulation of liposomal doxorubicin in liver tissue treated by radiofrequency ablation (RFA) and irreversible electroporation (IRE) in in vivo porcine models. (
  • Doxorubicin concentrations in IRE zones were not significantly different from untreated liver (0.191±0.049µg/g and 0.210±0.049µg/g vs. 0.18±0.012µg/g). (
  • Abstract Objective: to investigate the effect of using different agents (topical hyaluronidase, photobiomodulation, and the association of photobiomodulation with topical hyaluronidase) in preventing the formation of lesions caused by doxorubicin extravasation, as well as in the reduction of lesions fo. (
  • Finally, mouse tissues were examined for the presence of intrinsic fluorescence of doxorubicin. (
  • Doxorubicin is also used alone and in combination with other medications to treat certain types of thyroid cancer and certain types of soft tissue or bone sarcomas (cancer that forms in muscles and bones). (
  • Doxorubicin can't, however, tell the difference between cancer cells and healthy cells that also divide rapidly, like hair cells. (
  • Like any chemotherapy, the effectiveness of doxorubicin depends on your diagnosis-the location, cancer stage, and cell type of the mesothelioma-and overall health. (
  • The anti-cancer drug Doxorubicin was loaded into the new drug carrier to assess its quality. (
  • Doxorubicin and Anti-PD-L1 Antibody Conjugated Gold Nanoparticles for Colorectal Cancer Photochemotherapy. (
  • LncRNA XIST promotes chemoresistance of breast cancer cells to doxorubicin by sponging miR-200c-3p to upregulate ANLN. (
  • Here, we study the function mechanisms of long non-coding RNA XIST in chemoresistance of breast cancer to doxorubicin. (
  • Doxorubicin can cause a severe decrease in the number of blood cells in your bone marrow. (
  • Similar results are observed with in vivo doxorubicin exposure: it leads to Ca2+-overload. (
  • To confirm the protective role of PPAR-alpha in vivo, PPAR-alpha activator docosahexaenoic acid (DHA) was administered to doxorubicin-treated mice, and it has been shown to significantly reduce the doxorubicin-induced apoptotic cells in renal cortex. (
  • Los experimentos in Vivo de Lai y Singh (1995, 1996) ameritan especial atención, teniendo en cuenta el interés que despertaron. (