Antineoplastic Agents, Phytogenic
Leukemia P388
Amaryllidaceae Alkaloids
Ellipticines
Doxorubicin
Drug Screening Assays, Antitumor
Antibiotics, Antineoplastic
Bryostatins
Antineoplastic Agents, Alkylating
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)
Ancitabine
Neoplasms
Gallium
Depsipeptides
Tumor Cells, Cultured
Cisplatin
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.
Paclitaxel
6-Mercaptopurine
Apoptosis
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.
Aminoacridines
Epothilones
Cell Survival
Molecular Structure
Lactones
Daunorubicin
Fluorouracil
Bleomycin
Dose-Response Relationship, Drug
Etoposide
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.
Antineoplastic Combined Chemotherapy Protocols
Drug Resistance, Neoplasm
Prodrugs
Drug Evaluation, Preclinical
Drug Evaluation
Cell Division
Xenograft Model Antitumor Assays
Drug Resistance
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.
Macrolides
Neoplasms, Experimental
Methotrexate
Camptothecin
Cell Cycle
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
Mice, Nude
HL-60 Cells
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
Enzyme Inhibitors
Drug Administration Schedule
Isoquinolines
Neoplasm Transplantation
Biotransformation
The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alterations may be divided into METABOLIC DETOXICATION, PHASE I and METABOLIC DETOXICATION, PHASE II.
Drug Interactions
DNA Damage
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.
Cyclophosphamide
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.
Stereoisomerism
Clinical Trials as Topic
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
Leukemia
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
Ovarian Neoplasms
Caspases
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
Taxoids
Structure-Activity Relationship
DNA
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Phospholipid Ethers
Phospholipids which have an alcohol moiety in ethereal linkage with a saturated or unsaturated aliphatic alcohol. They are usually derivatives of phosphoglycerols or phosphatidates. The other two alcohol groups of the glycerol backbone are usually in ester linkage. These compounds are widely distributed in animal tissues.
RNA, Messenger
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Reactive Oxygen Species
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
Cells, Cultured
Gloves, Protective
Coverings for the hands, usually with separations for the fingers, made of various materials, for protection against infections, toxic substances, extremes of hot and cold, radiations, water immersion, etc. The gloves may be worn by patients, care givers, housewives, laboratory and industrial workers, police, etc.
Aster Plant
Occupational Exposure
Treatment Outcome
Medical Secretaries
Oncology Nursing
Sulindac
A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.
Protective Devices
Protective Clothing
Equipment Contamination
Amsacrine
Decontamination
Phlebitis
Environmental Monitoring
Hazardous Substances
Inhibitory Concentration 50
Carcinoma, Ehrlich Tumor
Floxuridine
An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.
Drug Compounding
2-Propanol
Tumor Stem Cell Assay
Carmustine
A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed)
Cytarabine
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
Topoisomerase II Inhibitors
Drug Resistance, Multiple
Farnesyltranstransferase
Oncology Service, Hospital
Comet Assay
A genotoxicological technique for measuring DNA damage in an individual cell using single-cell gel electrophoresis. Cell DNA fragments assume a "comet with tail" formation on electrophoresis and are detected with an image analysis system. Alkaline assay conditions facilitate sensitive detection of single-strand damage.
Drugs, Investigational
Isocoumarins
Nitrogen Mustard Compounds
Nurses
Suramin
A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties.
Alkaloids
Plant Extracts
Mitomycin
Azacitidine
DNA Adducts
DNA Topoisomerases, Type II
Anti-Inflammatory Agents, Non-Steroidal
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
Pharmacists
Lethal Dose 50
Gene Expression Regulation, Neoplastic
Mutagenicity Tests
Metabolic Detoxication, Drug
HT29 Cells
Blotting, Western
Hydrazones
Alkylating Agents
Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases.
Mammary Neoplasms, Experimental
Organoplatinum Compounds
Octreotide
Glutathione Transferase
Mitomycins
Dehydroascorbic Acid
Anthracyclines
Tyrosine kinase inhibitor emodin suppresses growth of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. (1/4985)
Overexpression of the HER-2/neu proto-oncogene, which encodes the tyrosine kinase receptor p185neu, has been observed in tumors from breast cancer patients. We demonstrated previously that emodin, a tyrosine kinase inhibitor, suppresses tyrosine kinase activity in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. We found that emodin significantly inhibited tumor growth and prolonged survival in mice bearing HER-2/neu-overexpressing human breast cancer cells. Furthermore, the combination of emodin and paclitaxel synergistically inhibited the anchorage-dependent and -independent growth of HER-2/neu-overexpressing breast cancer cells in vitro and synergistically inhibited tumor growth and prolonged survival in athymic mice bearing s.c. xenografts of human tumor cells expressing high levels of p185neu. Both immunohistochemical staining and Western blot analysis showed that emodin decreases tyrosine phosphorylation of HER-2/neu in tumor tissue. Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. The results may have important implications in chemotherapy for HER-2/neu-overexpressing breast tumors. (+info)CLIP-170 highlights growing microtubule ends in vivo. (2/4985)
A chimera with the green fluorescent protein (GFP) has been constructed to visualize the dynamic properties of the endosome-microtubule linker protein CLIP170 (GFP-CLIP170). GFP-CLIP170 binds in stretches along a subset of microtubule ends. These fluorescent stretches appear to move with the growing tips of microtubules at 0.15-0.4 microm/s, comparable to microtubule elongation in vivo. Analysis of speckles along dynamic GFP-CLIP170 stretches suggests that CLIP170 treadmills on growing microtubule ends, rather than being continuously transported toward these ends. Drugs affecting microtubule dynamics rapidly inhibit movement of GFP-CLIP170 dashes. We propose that GFP-CLIP170 highlights growing microtubule ends by specifically recognizing the structure of a segment of newly polymerized tubulin. (+info)The topoisomerase-related function gene TRF4 affects cellular sensitivity to the antitumor agent camptothecin. (3/4985)
Camptothecin is an antitumor agent that kills cells by converting DNA topoisomerase I into a DNA-damaging poison. Although camptothecin derivatives are now being used to treat tumors in a variety of clinical protocols, the cellular factors that influence sensitivity to the drug are only beginning to be understood. We report here that two genes required for sister chromatid cohesion, TRF4 and MCD1/SCC1, are also required to repair camptothecin-mediated damage to DNA. The hypersensitivity to camptothecin in the trf4 mutant does not result from elevated expression of DNA topoisomerase I. We show that Trf4 is a nuclear protein whose expression is cell cycle-regulated at a post-transcriptional level. Suppression of camptothecin hypersensitivity in the trf4 mutant by gene overexpression resulted in the isolation of three genes: another member of the TRF4 gene family, TRF5, and two genes that may influence higher order chromosome structure, ZDS1 and ZDS2. We have isolated and sequenced two human TRF4 family members, hTRF4-1 and hTRF4-2. The hTRF4-1 gene maps to chromosome 5p15, a region of frequent copy number alteration in several tumor types. The evolutionary conservation of TRF4 suggests that it may also influence mammalian cell sensitivity to camptothecin. (+info)Fractionated administration of irinotecan and cisplatin for treatment of lung cancer: a phase I study. (4/4985)
A combination chemotherapy of irinotecan (CPT-11) and cisplatin (CDDP) has been reported to be active for lung cancer. In the previous trial, however, diarrhoea and leucopenia became the major obstacle for sufficient dose escalation of CPT-11 to improve the treatment outcome. We conducted a phase I study to investigate whether the fractionated administration of CDDP and CPT-11 at escalated dose was feasible and could improve the treatment outcome. Twenty-four previously untreated patients with unresectable non-small-cell lung cancer (NSCLC) or extensive disease of small-cell lung cancer (SCLC) were eligible. Both CDDP and CPT-11 were given on days 1 and 8, and repeated every 4 weeks. The dose of CDDP was fixed at 60 mg m(-2) and given by 1-h infusion before CPT-11 administration. The starting dose of CPT-11 was 40 mg m(-2), and the dose was escalated by an increase of 10 mg m(-2). The maximally tolerated dose of CPT-11 was determined as 60 mg m(-2) because grade 4 haematological or grade 3 or 4 non-haematological toxicities developed in six patients out of 11 patients evaluated. Diarrhoea became a dose-limiting toxicity. The objective response rates were 76% for NSCLC and 100% for SCLC. The recommended dose of CPT-11 and CDDP in a phase II study will be 50 mg m(-2) and 60 mg m(-2) respectively. (+info)A novel taxane with improved tolerability and therapeutic activity in a panel of human tumor xenografts. (5/4985)
Clinically available taxanes represent one of the most promising class of antitumor agents, despite several problems with their solubility and toxicity. In an attempt to improve the pharmacological profile of taxanes, a new series of analogues was synthesized from 14beta-hydroxy-10-deacetylbaccatin III and tested in a panel of human tumor cell lines. On the basis of the pattern of cytotoxicity and lack of cross-resistance in tumor cell lines expressing the typical multidrug-resistant phenotype, a compound (IDN5109) was selected for preclinical development. A comparative efficacy study of IDN5109 and paclitaxel was performed using a large panel of human tumor xenografts, characterized by intrinsic (seven tumors) or acquired (four tumors) resistance to cisplatin or doxorubicin, including four ovarian, one breast, one cervical, three lung, one colon, and one prostatic carcinoma. Drugs were delivered i.v. according to the same schedule (four times every 4th day). IDN5109 achieved a very high level of activity (percentage tumor weight inhibition >70%; log10 cell kill >1) in all but one of the tested tumors. Compared to paclitaxel, IDN5109 exhibited a significantly superior activity in six tumors (including the four tumors that were resistant to paclitaxel) and a comparable activity against the other five paclitaxel-responsive tumors. Additional advantages of IDN5109 over paclitaxel were also suggested by its toxicity profile. IDN5109 was not only less toxic (maximal tolerated doses were 90 and 54 mg/kg for IDN5109 and paclitaxel, respectively), but it also appeared to be endowed with a reduced neurotoxic potential and an improved profile of tolerability compared to the parent drug. Furthermore, the best antitumor efficacy was often already reached with doses lower than the maximal tolerated dose, suggesting an improved therapeutic index for the new drug. In conclusion, the results support the preclinical interest of IDN5109 in terms of the toxicity profile and of the efficacy with particular reference to the ability to overcome multiple mechanisms of drug resistance. (+info)Enhanced antitumor activity of 6-hydroxymethylacylfulvene in combination with irinotecan and 5-fluorouracil in the HT29 human colon tumor xenograft model. (6/4985)
6-Hydroxymethylacylfulvene (MGI-114) is a semisynthetic analogue of the toxin illudin S, a product of the Omphalotus mushroom. MGI-114 induces cytotoxicity in a variety of solid tumors in vivo, including the refractory HT29 human colon cancer xenograft. In this study, the potential application of MGI-114 in the treatment of colon cancer was further explored by evaluating the activity of MGI-114 in combination with irinotecan (CPT-11) and 5-fluorouracil (5FU). Groups of 9 nude mice bearing HT29 xenografts were treated with either single agent MGI-114, CPT-11, or 5FU, or MGI-114 in combination with CPT-11 or 5FU. MGI-114 was administered at doses of 3.5 and 7 mg/kg i.p. daily on days 1 through 5, and CPT-11 and 5FU were administered at doses of 50 and 100 mg/kg i.p. on days 1, 12, and 19. In the single agent studies, MGI-114, CPT-11, and 5FU all resulted in decreased final tumor weights compared with vehicle-treated controls (P<0.05), but only MGI-114 at 7 mg/kg produced partial responses. When MGI-114 at 3.5 mg/kg was combined with CPT-11, significant decrements in final tumor weights occurred compared with monotherapy with the same doses of MGI-114 and CPT-11 (P< or =0.001). Also, administration of the low-dose combination (MGI-114 at 35 mg/kg and CPT-11 at 50 mg/kg) resulted in final tumor weights similar to those achieved after administration of high-dose MGI-114 as a single agent. Moreover, the combination of MGI-114 and CPT-11 produced partial responses in nearly all of the animals, with some animals achieving complete responses. The outcome with the combination of MGI-114 and 5FU was less striking, with fewer partial responses and no complete responses. These results suggest enhanced activity when MGI-114 is combined with CPT-11, and clinical trials to further evaluate this combination regimen are planned. (+info)Cyclosporine inhibited calcium-mediated apoptosis of HL-60 cells. (7/4985)
AIM: To study the effects of cyclosporine (Cyc) on apoptosis of HL-60 cells. METHODS: Apoptotic cells induced by harringtonine (Har), camptothecin (Cam), or calcimycin (Cal), thapsigargin (Tha) were identified with DNA electrophoresis, morphology, and flow cytometry. Relative [Ca2+]i alteration of apoptotic HL-60 cells were determined with flow cytometry. RESULTS: Cal 1 mg.L-1 or Tha 0.5 mg.L-1 induced apoptosis of HL-60 cells. This effect was inhibited by nontoxic concentration of Cyc 1 mg.L-1. Cyc did not inhibit Har- or Cam-induced apoptosis of HL-60 cells. Both Cal and Tha increased intracellular calcium, whereas Har or Cam did not. CONCLUSION: Cyc inhibited apoptosis only induced by calcium increasement in HL-60 cells. The mechanism of apoptosis induced by Cal or Tha was different from that by Har or Cam. (+info)Quercetin induced apoptosis in human leukemia HL-60 cells. (8/4985)
AIM: To examine whether quercetin (Que) might induce apoptosis in human leukemia HL-60 cells. METHODS: DNA fragmentation was visualized by agarose gel electrophoresis. Inhibition of proliferation was measured with a colorimetric MTT-assay. The DNA degradation was determined using flow cytometry, and the microscopic changes were observed by an electron microscope. RESULTS: Que 15-120 mumol.L-1 elicited typical apoptosis morphological changes including condensed chromatin, nuclear fragmentation, and reduction in volume. DNA fragmentation and DNA degradation in a concentration-dependent manner in HL-60 cells. Que inhibited HL-60 cell proliferation. The values of IC50 and 95% confidence limits were 43 (30-61) mumol.L-1 after 48-h treatment with Que. CONCLUSION: Que induced apoptosis in HL-60 cells. (+info)
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Antimitotic Agents. *Antineoplastic Agents. *Antineoplastic Agents, Phytogenic. *Mitosis Modulators. *Tubulin Modulators. ... This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell ... NCI: A compound extracted from the Pacific yew tree Taxus brevifolia with antineoplastic activity. Paclitaxel binds to tubulin ...
tupichinolide | Semantic Scholar
Superiority of sequential versus concurrent administration of paclitaxel with etoposide in advanced non-small cell lung cancer:...
Paclitaxel and etoposide are two chemotherapy agents with broad cytotoxic activity and different mechanisms of action and ... Antineoplastic Agents, Phytogenic, Antineoplastic Combined Chemotherapy Protocols, Treatment Outcome, Drug Administration ... Paclitaxel and etoposide are two chemotherapy agents with broad cytotoxic activity and different mechanisms of action and ...
Drug Resistance, Multiple, Fungal | Harvard Catalyst Profiles | Harvard Catalyst
topic:"Drug Synergism" found 94 records • Arctic Health
Antineoplastic Agents, Phytogenic - therapeutic use Cathepsin B - metabolism Cyclophosphamide - therapeutic use Cysteine ... Abortifacient Agents, Steroidal Carboprost - administration & dosage Contraceptives, Oral, Synthetic Drug Synergism Female ... has additive effects as an ocular hypotensive agent with timolol, a beta-adrenergic antagonist, even though both drugs are ...
Medicinas Tradicionais, Complementares e Integrativas | RefNet
OR management OR treatment OR antineoplastic* OR preparation* OR terapia* OR tratamento*)) OR ti:herbal* OR "phytogenic agents ... "antineoplastic agents" OR cancer OR analgesic OR antihelminthic)) OR "chitosan weight loss" OR (("thymus extract" OR " ... medicinal OR therapy OR antifungal OR antineoplastic)) OR "medicinal fungi" OR "purple sweet potato anthocyanin" OR ephedra OR ...
Isocoumarins | Profiles RNS
Marie Stiborova - NeL.edu
David Orlicky's research topics | Colorado PROFILES
SPOP Promotes Ubiquitination and Degradation of the ERG Oncoprotein to Suppress Prostate Cancer Progression. | [email protected]
Camptothecin targets WRN protein: mechanism and relevance in clinical breast cancer. - MRC Weatherall Institute of Molecular...
Rangaswamy Govindarajan's research topics | Profiles RNS
Down-regulation
... phytogenic - isolation & purification ; Antineoplastic agents, phytogenic - pharmacology ; Antineoplastic agents, phytogenic - ... Antineoplastic agents, phytogenic - pharmacology ; Cell line, tumor ; Collagen - biosynthesis ; Dipeptidases - antagonists & ... Photosensitizing agents - therapeutic use ; Psoriasis - blood ; Psoriasis - drug therapy ; Psoriasis - pathology ; Psoriasis - ...
Apoptosis1
- This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2). (nih.gov)
Paclitaxel2
- The distribution of paclitaxel (Taxol) within the central and peripheral nervous system after repeated administration of this antineoplastic agent is still largely unknown. (hunimed.eu)
- Paclitaxel and etoposide are two chemotherapy agents with broad cytotoxic activity and different mechanisms of action and resistance. (ox.ac.uk)
Nausea1
- International(NANDA-I)in1999(4)anditwentthroughrevisionsinthesubsequenteditionsthatresultedin changesinitsdefinition,aswel as,itsdefiningcharacteristicsandinthefactorsrelatedtoit(5-7).Withinits editionsthatpresentednausearelatedchanges,theNANDA-Iof2007and2008(6)broughtalargerquantity of reviews and almost al diagnoses presented few changes in its defining characteristics and in factors relatedtoitor,ofriskfactors.Itwasinthiseditionthatitwasobservedtheremovalof"chemotherapeutic agents"fromthenusingdiagnosis"nausea",whichisstil absentinthecurrentedition(7). (bvsalud.org)
Effects1
- CONCLUSIONS: Dorzolamide, a carbonic anhydrase inhibitor, has additive effects as an ocular hypotensive agent with timolol, a beta-adrenergic antagonist, even though both drugs are suppressors of aqueous humor flow. (arctichealth.org)
Activity1
- NCI: A compound extracted from the Pacific yew tree Taxus brevifolia with antineoplastic activity. (nih.gov)
High1
- The agent demonstrated sub-nanomolar EC50 binding concentrations, with high specificity and binding could be inhibited by GLP-1R agonists. (perkinelmer.com)
Substances1
- Agents and endogenous substances that antagonize or inhibit the development of new blood vessels. (uams.edu)
Drugs3
- This study is exploring a new combination of drugs fosbretabulin, a vascular disrupting agent and pazopanib, a tyrosine kinase inhibitor. (clinicaltrials.gov)
- Both drugs contain the same active agent, but Abraxane is delivered by a nanoparticle technology that binds to albumin, a natural protein, rather than the toxic solvent known as Cremophor. (t3db.ca)
- A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. (rush.edu)
MeSH1
- Antineoplastic Agents, Alkylating" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (rush.edu)
Therapeutic2
- Although considerable efforts have been made to develop effective therapeutic agents for AD therapy, drug development has not met significant clinical success. (omeka.net)
- A considerable effort has been spent investigating the therapeutic potential of antioxidants and anti-inflammatory agents, several of natural products and dietary origin, in AD treatment. (omeka.net)
Anticancer agent1
- Paris Saponin II (PSII), a major steroidal saponin extracted from Rhizoma Paris polyphylla, has emerged as a potential anticancer agent. (nih.gov)
Clinically2
- Drug interactions are quite common with these agents, some of which are sequence-dependent and clinically significant. (nih.gov)
- PURPOSE: ART and its derivatives, clinically used antimalarial agents, have recently shown antitumor activities. (isharonline.org)
Toxicity1
- Toxicity profiles for these agents are somewhat different. (nih.gov)
Profiles1
- Below are the most recent publications written about "Antineoplastic Agents, Alkylating" by people in Profiles. (rush.edu)
Therapy1
- The phase 1 protocol will have 2 parts: a single agent dose escalation phase (Part 1) and a combination therapy phase (Part 2). (clinicaltrials.gov)
Dose1
- Both agents undergo hepatic metabolism and biliary excretion and require dose adjustment in the setting of liver dysfunction. (nih.gov)
Cell1
- Modified weekly regimen with vinorelbine as a single agent in unresectable non-small cell lung cancer. (ox.ac.uk)