Colchicine
Tubulin Modulators
Tubulin
Vinca Alkaloids
Mitosis
Microtubules
Paclitaxel
Structure-Activity Relationship
Depsipeptides
Intercalating Agents
Encyclopedias as Topic
Nitracrine
Random Amplified Polymorphic DNA Technique
Sarcoma Viruses, Murine
DNA-Directed DNA Polymerase
Emi1 class of proteins regulate entry into meiosis and the meiosis I to meiosis II transition in Xenopus oocytes. (1/74)
Xenopus oocytes are arrested at the G2/prophase boundary of meiosis I and enter meiosis in response to progesterone. A hallmark of meiosis is the absence of DNA replication between the successive cell division phases meiosis I (MI) and meiosis II (MII). After the MI-MII transition, Xenopus eggs are locked in metaphase II by the cytostatic factor (CSF) arrest to prevent parthenogenesis. Early Mitotic Inhibitor 1 (Emi1) maintains CSF arrest by inhibiting the ability of the Anaphase Promoting Complex (APC) to direct the destruction of cyclin B. To investigate whether Emi1 has an earlier role in meiosis, we injected Xenopus oocytes with neutralizing antibodies against Emi1 at G2/prophase and during the MI-MII transition. Progesterone-treated G2/prophase oocytes injected with anti-Emi1 antibody fail to activate Maturation Promoting Factor (MPF), a complex of cdc2/cyclin B, and the MAPK pathway, and do not undergo germinal vesicle breakdown (GVBD). Injection of purified Delta90 cyclin B protein or blocking anti-Emi1 antibody with purified Emi1 protein rescues these meiotic processes in Emi1-neutralized oocytes. Acute inhibition of Emi1 in progesterone treated oocytes immediately after GVBD causes rapid loss of cdc2 activity with simultaneous loss of cyclin B levels and inactivation of the MAPK pathway. These oocytes decondense their chromosomes and enter a DNA replication phase instead of progressing to MII. Prior ablation of Cdc20, addition of methyl-ubiquitin, or addition of nondestructible Delta90 cyclin B rescues the MI-MII transition in Emi1-inhibited oocytes. (+info)Rapamycin inhibits human in stent restenosis vascular smooth muscle cells independently of pRB phosphorylation and p53. (2/74)
OBJECTIVE: Drug-eluting stents containing the immunosuppressant rapamycin markedly inhibit in stent restenosis (ISR). However, the molecular mechanisms that underlie its effect on ISR-derived vascular smooth muscle cells (VSMCs), as opposed to normal VSMCs, are unknown. Specifically, as ISR-VSMCs have altered cell cycle regulation, rapamycin may arrest these cells via novel molecular pathways. METHODS: We isolated human VSMCs from sites of ISR, and examined the effect of rapamycin on cell proliferation using MTT assay, time lapse videomicroscopy and flow cytometry. Regulation of G(1)-S transition was examined using Western blotting, and cell size and protein synthesis examined using flow cytometry and collagen assay, respectively. The requirement for pRB and p53 was examined using ISR VSMCs expressing E1A and a dominant negative p53, respectively. RESULTS: ISR-VSMC proliferation was potently inhibited by rapamycin. Arrest was confined to G(1), as cell proliferation (but not cell size) of S/G(2)-arrested cells was unaffected by rapamycin. Moreover, ISR-VSMC lines generated with disrupted p53 or pRB function still arrested in the presence of rapamycin, suggesting that these genes are dispensable for rapamycin-induced arrest. Significantly, rapamycin completely inhibited the phosphorylation of p70(S6K), an mTOR-regulated kinase implicated in the control of proliferation, but had no effect on collagen or total protein synthesis. CONCLUSIONS: We demonstrate that rapamycin is a potent inhibitor of ISR VSMC proliferation during G(1). Rapamycin's action does not require p53 or pRB. We show that p70(S6K) is markedly inhibited in rapamycin-arrested ISR cells, suggesting that regulation of its upstream kinase, mTOR, is important for the control of proliferation in ISR cells. (+info)The primary antimitotic mechanism of action of the synthetic halichondrin E7389 is suppression of microtubule growth. (3/74)
E7389, which is in phase I and II clinical trials, is a synthetic macrocyclic ketone analogue of the marine sponge natural product halichondrin B. Whereas its mechanism of action has not been fully elucidated, its main target seems to be tubulin and/or the microtubules responsible for the construction and proper function of the mitotic spindle. Like most microtubule-targeted antitumor drugs, it inhibits tumor cell proliferation in association with G(2)-M arrest. It binds to tubulin and inhibits microtubule polymerization. We examined the mechanism of action of E7389 with purified microtubules and in living cells and found that, unlike antimitotic drugs including vinblastine and paclitaxel that suppress both the shortening and growth phases of microtubule dynamic instability, E7389 seems to work by an end-poisoning mechanism that results predominantly in inhibition of microtubule growth, but not shortening, in association with sequestration of tubulin into aggregates. In living MCF7 cells at the concentration that half-maximally blocked cell proliferation and mitosis (1 nmol/L), E7389 did not affect the shortening events of microtubule dynamic instability nor the catastrophe or rescue frequencies, but it significantly suppressed the rate and extent of microtubule growth. Vinblastine, but not E7389, inhibited the dilution-induced microtubule disassembly rate. The results suggest that, at its lowest effective concentrations, E7389 may suppress mitosis by directly binding to microtubule ends as unliganded E7389 or by competition of E7389-induced tubulin aggregates with unliganded soluble tubulin for addition to growing microtubule ends. The result is formation of abnormal mitotic spindles that cannot pass the metaphase/anaphase checkpoint. (+info)The mitotic checkpoint in cancer therapy. (4/74)
The mitotic checkpoint is a key cell cycle control mechanism that ensures an accurate segregation of chromosomes during mitosis by delaying the onset of anaphase until all chromosomes are properly attached to a bipolar mitotic spindle. While complete loss of this checkpoint is lethal in vertebrates, a weakened mitotic checkpoint is frequently seen in cancer cells and it may contribute to tumorigenesis. Many anti-tumor drugs, including spindle assembly inhibitors and DNA damaging agents, can activate the mitotic checkpoint. However, since these drugs influence interphase events besides activating the mitotic checkpoint, the role of the mitotic checkpoint in drug-induced cell death remained unclear. Using a KSP antagonist that specifically acts on mitotic cells, we have recently shown that activation of the mitotic checkpoint followed by mitotic slippage or adaptation, activates Bax and initiates apoptosis. Notably, cells with a weakened mitotic checkpoint incur much less apoptotic death than their checkpoint-proficient counterparts, indicating the requirement of a competent mitotic checkpoint in the induction of apoptosis. In light of these findings and other recent reports, the potential influence of the mitotic checkpoint in response to chemotherapies, and the strategy to target the mitotic checkpoint for cancer therapeutics are discussed. (+info)Sichuan pepper extracts block the PAK1/cyclin D1 pathway and the growth of NF1-deficient cancer xenograft in mice. (5/74)
There is increasing evidence that more than 70% of cancers including pancreatic, breast and prostate cancers as well as neurofibromatosis (NF) are highly addicted to abnormal activation of the Ser/Thr kinase PAK1 for their growth. So far FK228 is the most potent among the HDAC (histone deacetylase) inhibitors that block the activation of both PAK1 and another kinase AKT, downstream of PI-3 kinase. However, FK228 is still in clinical trials (phase 2) for a variety of cancers (but not for NF as yet), and not available for most cancer/NF patients. Thus, we have been exploring an alternative which is already in the market, and therefore immediately useful for the treatment of those desperate cancer/NF patients. Here we provide the first evidence that extracts of Chinese/ Japanese peppercorns (Zanthoxyli Fructus) from the plant Zanthoxylum piperitum called "Hua Jiao"/"Sansho", block selectively the key kinase PAK1, leading to the downregulation of cyclin D1. Unlike FK228, these extracts do not inhibit AKT activation at the concentrations that block either cancer growth or PAK1 activation. The Chinese pepper extract selectively inhibits the growth of NF1-deficient malignant peripheral nerve sheath tumor (MPNST) cells, without affecting the growth of normal fibroblasts, and suppresses the growth of NF1-deficient human breast cancer (MDA-MB-231) xenograft in mice. Our data suggest that these peppercorn extracts would be potentially useful for the treatment of PAK1-dependent NF such as MPNST, in addition to a variety of PAK1-dependent cancers including breast cancers. (+info)Increased therapeutic potential of an experimental anti-mitotic inhibitor SB715992 by genistein in PC-3 human prostate cancer cell line. (6/74)
BACKGROUND: Kinesin spindle proteins (KSP) are motor proteins that play an essential role in mitotic spindle formation. HsEg5, a KSP, is responsible for the formation of the bipolar spindle, which is critical for proper cell division during mitosis. The function of HsEg5 provides a novel target for the manipulation of the cell cycle and the induction of apoptosis. SB715992, an experimental KSP inhibitor, has been shown to perturb bipolar spindle formation, thus making it an excellent candidate for anti-cancer agent. Our major objective was a) to investigate the cell growth inhibitory effects of SB715992 on PC-3 human prostate cancer cell line, b) to investigate whether the growth inhibitory effects of SB715992 could be enhanced when combined with genistein, a naturally occurring isoflavone and, c) to determine gene expression profile to establish molecular mechanism of action of SB715992. METHODS: PC-3 cells were treated with varying concentration of SB715992, 30 microM of genistein, and SB715992 plus 30 microM of genistein. After treatments, PC-3 cells were assayed for cell proliferation, induction of apoptosis, and alteration in gene and protein expression using cell inhibition assay, apoptosis assay, microarray analysis, real-time RT-PCR, and Western Blot analysis. RESULTS: SB715992 inhibited cell proliferation and induced apoptosis in PC-3 cells. SB715992 was found to regulate the expression of genes related to the control of cell proliferation, cell cycle, cell signaling pathways, and apoptosis. In addition, our results showed that combination treatment with SB715992 and genistein caused significantly greater cell growth inhibition and induction of apoptosis compared to the effects of either agent alone. CONCLUSION: Our results clearly show that SB715992 is a potent anti-tumor agent whose therapeutic effects could be enhanced by genistein. Hence, we believe that SB715992 could be a novel agent for the treatment of prostate cancer with greater success when combined with a non-toxic natural agent like genistein. (+info)Preplaced cell division: a critical mechanism of autoprotection against S-1,2-dichlorovinyl-L-cysteine-induced acute renal failure and death in mice. (7/74)
Previous studies have shown that renal injury initiated by a lethal dose of S-1,2-dichlorovinyl-l-cysteine (DCVC) progresses due to inhibition of cell division and hence renal repair, leading to acute renal failure (ARF) and death in mice. Renal injury initiated by low to moderate doses of DCVC is repaired by timely and adequate stimulation of renal cell division, tubular repair, restoration of renal structure and function leading to survival of mice. Recent studies have established that mice primed with a low dose of DCVC (15 mg/kg i.p.) 72 h before administration of a normally lethal dose (75 mg/kg i.p.) are protected from ARF and death (nephro-autoprotection). We showed that renal cell division and tissue repair stimulated by the low dose are sustained even after the lethal dose administration resulting in survival from ARF and death. If renal cell division induced by the low dose is indeed the critical mechanism of this autoprotection, then its ablation by the antimitotic agent colchicine (1.5 mg CLC/kg i.p.) should abolish autoprotection. The present interventional experiments were designed to test the hypothesis that DCVC autoprotection is due to stimulated cell division and tissue repair by the priming low dose. CLC intervention at 42 and 66 h after the priming dose resulted in marked progressive elevation of plasma blood urea nitrogen and creatinine resulting in ARF and death of mice. Light microscopic examination of hematoxylin and eosin-stained kidney sections revealed progression of renal necrosis concordant with progressively failing renal function. With CLC intervention, S-phase stimulation (as assessed by BrdU pulse labeling), G(1)-to-S phase clearance, and cell division were diminished essentially abolishing the promitogenic effect of the priming low dose of DCVC. Phospho-retinoblastoma protein (P-pRB), a crucial protein for S-phase stimulation, and other cellular signaling mechanisms regulating P-pRB were investigated. We report that decreased P-pRB via activation of protein phosphatase-1 by CLC is the critical mechanism of this inhibited S-phase stimulation and ablation of autoprotection with CLC intervention. These findings lend additional support to the notion that stimulated cell division and renal tissue repair by the priming dose of DCVC are the critical mechanisms that allow sustained compensatory tissue repair and survival of mice in nephro-autoprotection. (+info)A thalidomide analogue with in vitro antiproliferative, antimitotic, and microtubule-stabilizing activities. (8/74)
We discovered a thalidomide analogue [5-hydroxy-(2,6-diisopropylphenyl)-1H-isoindole-1,3-dione (5HPP-33)] with antiproliferative activity against nine cancer cell lines in vitro. Flow cytometric analyses showed that the compound caused G2-M arrest, which occurred mainly at the mitotic phase. In addition, immunofluorescence microscopy and in vitro tubulin polymerization studies showed that 5HPP-33 has antimicrotubule activity with a paclitaxel-like mode of action. It is effective against four different paclitaxel-resistant cell lines. Thus, 5HPP-33 represents a potential antitumor agent. (+info)Antimitotic agents are a class of chemotherapeutic drugs that work by disrupting the normal mitosis (cell division) process in cells. These agents bind to and inhibit the function of specific proteins involved in the formation of the mitotic spindle, which is essential for proper chromosome separation during cell division.
By doing so, antimitotic agents prevent cancer cells from dividing and growing, ultimately leading to their death. However, these drugs can also affect normal cells that divide rapidly, such as those in the bone marrow, digestive tract, and hair follicles, which can result in side effects like anemia, nausea, vomiting, and hair loss.
Examples of antimitotic agents include vincristine, vinblastine, paclitaxel, docetaxel, and ixabepilone. They are often used to treat various types of cancer, such as leukemia, lymphoma, breast cancer, ovarian cancer, and lung cancer.
Colchicine is a medication that is primarily used to treat gout, a type of arthritis characterized by sudden and severe attacks of pain, swelling, redness, and tenderness in the joints. It works by reducing inflammation and preventing the formation of uric acid crystals that cause gout symptoms.
Colchicine is also used to treat familial Mediterranean fever (FMF), a genetic disorder that causes recurrent fevers and inflammation in the abdomen, chest, and joints. It can help prevent FMF attacks and reduce their severity.
The medication comes in the form of tablets or capsules that are taken by mouth. Common side effects of colchicine include diarrhea, nausea, vomiting, and abdominal pain. In rare cases, it can cause more serious side effects such as muscle weakness, nerve damage, and bone marrow suppression.
It is important to follow the dosage instructions carefully when taking colchicine, as taking too much of the medication can be toxic. People with certain health conditions, such as liver or kidney disease, may need to take a lower dose or avoid using colchicine altogether.
Tubulin modulators are a class of drugs that target and alter the function or structure of tubulin, which is a key component of microtubules in cells. These drugs can either stabilize or destabilize microtubules by interacting with tubulin, leading to various effects on cell division and other processes that rely on microtubule dynamics.
There are two main types of tubulin modulators:
1. Microtubule stabilizers: These drugs promote the assembly and stability of microtubules by binding to tubulin, preventing its disassembly. Examples include taxanes (e.g., paclitaxel) and vinca alkaloids (e.g., vinblastine). They are primarily used as anticancer agents because they interfere with the division of cancer cells.
2. Microtubule destabilizers: These drugs inhibit the formation and stability of microtubules by binding to tubulin, promoting its disassembly. Examples include colchicine, vinca alkaloids (e.g., vinorelbine), and combretastatins. They can also be used as anticancer agents because they disrupt the mitotic spindle during cell division, leading to cancer cell death.
Tubulin modulators have various other effects on cells beyond their impact on microtubules, such as interfering with intracellular transport and signaling pathways. These diverse actions contribute to their therapeutic potential in treating diseases like cancer, but they can also lead to side effects that limit their clinical use.
Tubulin is a type of protein that forms microtubules, which are hollow cylindrical structures involved in the cell's cytoskeleton. These structures play important roles in various cellular processes, including maintaining cell shape, cell division, and intracellular transport. There are two main types of tubulin proteins: alpha-tubulin and beta-tubulin. They polymerize to form heterodimers, which then assemble into microtubules. The assembly and disassembly of microtubules are dynamic processes that are regulated by various factors, including GTP hydrolysis, motor proteins, and microtubule-associated proteins (MAPs). Tubulin is an essential component of the eukaryotic cell and has been a target for anti-cancer drugs such as taxanes and vinca alkaloids.
Griseofulvin is an antifungal medication used to treat various fungal infections, including those affecting the skin, hair, and nails. It works by inhibiting the growth of fungi, particularly dermatophytes, which cause these infections. Griseofulvin can be obtained through a prescription and is available in oral (by mouth) and topical (on the skin) forms.
The primary mechanism of action for griseofulvin involves binding to tubulin, a protein necessary for fungal cell division. This interaction disrupts the formation of microtubules, which are crucial for the fungal cell's structural integrity and growth. As a result, the fungi cannot grow and multiply, allowing the infected tissue to heal and the infection to resolve.
Common side effects associated with griseofulvin use include gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea), headache, dizziness, and skin rashes. It is essential to follow the prescribing physician's instructions carefully when taking griseofulvin, as improper usage may lead to reduced effectiveness or increased risk of side effects.
It is important to note that griseofulvin has limited use in modern medicine due to the development of newer and more effective antifungal agents. However, it remains a valuable option for specific fungal infections, particularly those resistant to other treatments.
Vinca alkaloids are a group of naturally occurring chemicals derived from the Madagascar periwinkle plant, Catharanthus roseus. They are known for their antineoplastic (cancer-fighting) properties and are used in chemotherapy to treat various types of cancer. Some examples of vinca alkaloids include vinblastine, vincristine, and vinorelbine. These agents work by disrupting the normal function of microtubules, which are important components of the cell's structure and play a critical role in cell division. By binding to tubulin, a protein that makes up microtubules, vinca alkaloids prevent the formation of mitotic spindles, which are necessary for cell division. This leads to cell cycle arrest and apoptosis (programmed cell death) in cancer cells. However, vinca alkaloids can also affect normal cells, leading to side effects such as neurotoxicity, myelosuppression, and gastrointestinal disturbances.
Mitosis is a type of cell division in which the genetic material of a single cell, called the mother cell, is equally distributed into two identical daughter cells. It's a fundamental process that occurs in multicellular organisms for growth, maintenance, and repair, as well as in unicellular organisms for reproduction.
The process of mitosis can be broken down into several stages: prophase, prometaphase, metaphase, anaphase, and telophase. During prophase, the chromosomes condense and become visible, and the nuclear envelope breaks down. In prometaphase, the nuclear membrane is completely disassembled, and the mitotic spindle fibers attach to the chromosomes at their centromeres.
During metaphase, the chromosomes align at the metaphase plate, an imaginary line equidistant from the two spindle poles. In anaphase, sister chromatids are pulled apart by the spindle fibers and move toward opposite poles of the cell. Finally, in telophase, new nuclear envelopes form around each set of chromosomes, and the chromosomes decondense and become less visible.
Mitosis is followed by cytokinesis, a process that divides the cytoplasm of the mother cell into two separate daughter cells. The result of mitosis and cytokinesis is two genetically identical cells, each with the same number and kind of chromosomes as the original parent cell.
Vinblastine is an alkaloid derived from the Madagascar periwinkle plant (Catharanthus roseus) and is primarily used in cancer chemotherapy. It is classified as a vinca alkaloid, along with vincristine, vinorelbine, and others.
Medically, vinblastine is an antimicrotubule agent that binds to tubulin, a protein involved in the formation of microtubules during cell division. By binding to tubulin, vinblastine prevents the assembly of microtubules, which are essential for mitosis (cell division). This leads to the inhibition of cell division and ultimately results in the death of rapidly dividing cells, such as cancer cells.
Vinblastine is used to treat various types of cancers, including Hodgkin's lymphoma, non-Hodgkin's lymphoma, testicular cancer, breast cancer, and others. It is often administered intravenously in a healthcare setting and may be given as part of a combination chemotherapy regimen with other anticancer drugs.
As with any medication, vinblastine can have side effects, including bone marrow suppression (leading to an increased risk of infection, anemia, and bleeding), neurotoxicity (resulting in peripheral neuropathy, constipation, and jaw pain), nausea, vomiting, hair loss, and mouth sores. Regular monitoring by a healthcare professional is necessary during vinblastine treatment to manage side effects and ensure the safe and effective use of this medication.
Microtubules are hollow, cylindrical structures composed of tubulin proteins in the cytoskeleton of eukaryotic cells. They play crucial roles in various cellular processes such as maintaining cell shape, intracellular transport, and cell division (mitosis and meiosis). Microtubules are dynamic, undergoing continuous assembly and disassembly, which allows them to rapidly reorganize in response to cellular needs. They also form part of important cellular structures like centrioles, basal bodies, and cilia/flagella.
Paclitaxel is a chemotherapeutic agent derived from the bark of the Pacific yew tree (Taxus brevifolia). It is an antimicrotubule agent that promotes the assembly and stabilization of microtubules, thereby interfering with the normal dynamic reorganization of the microtubule network that is essential for cell division.
Paclitaxel is used in the treatment of various types of cancer including ovarian, breast, lung, and pancreatic cancers. It works by inhibiting the disassembly of microtubules, which prevents the separation of chromosomes during mitosis, leading to cell cycle arrest and apoptosis (programmed cell death).
Common side effects of paclitaxel include neutropenia (low white blood cell count), anemia (low red blood cell count), alopecia (hair loss), peripheral neuropathy (nerve damage causing numbness or tingling in the hands and feet), myalgias (muscle pain), arthralgias (joint pain), and hypersensitivity reactions.
Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.
Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.
It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.
A Structure-Activity Relationship (SAR) in the context of medicinal chemistry and pharmacology refers to the relationship between the chemical structure of a drug or molecule and its biological activity or effect on a target protein, cell, or organism. SAR studies aim to identify patterns and correlations between structural features of a compound and its ability to interact with a specific biological target, leading to a desired therapeutic response or undesired side effects.
By analyzing the SAR, researchers can optimize the chemical structure of lead compounds to enhance their potency, selectivity, safety, and pharmacokinetic properties, ultimately guiding the design and development of novel drugs with improved efficacy and reduced toxicity.
A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.
Maytansine is not typically defined in a medical dictionary as it is not a medical term itself, but rather a chemical compound. Maytansine is a natural product that was initially isolated from the bark of the African shrub Maytenus ovatus. It is a potent antimitotic agent, which means it interferes with cell division and has been studied for its potential use in cancer treatment.
In medical contexts, maytansine is often discussed in relation to specific drugs or therapies that utilize this compound. For example, the drug DM1 (also known as maytansinoid 1) is a derivative of maytansine and has been conjugated with monoclonal antibodies for targeted cancer therapy.
Therefore, when discussing 'Maytansine' in a medical context, it generally refers to the chemical compound or its derivatives that have potential use as anticancer agents.
Depsipeptides are a type of naturally occurring or synthetic modified peptides that contain at least one amide bond replaced by an ester bond in their structure. These compounds exhibit diverse biological activities, including antimicrobial, antiviral, and antitumor properties. Some depsipeptides have been developed as pharmaceutical drugs for the treatment of various diseases.
Intercalating agents are chemical substances that can be inserted between the stacked bases of DNA, creating a separation or "intercalation" of the base pairs. This property is often exploited in cancer chemotherapy, where intercalating agents like doxorubicin and daunorubicin are used to inhibit the replication and transcription of cancer cells by preventing the normal functioning of their DNA. However, these agents can also have toxic effects on normal cells, particularly those that divide rapidly, such as bone marrow and gut epithelial cells. Therefore, their use must be carefully monitored and balanced against their therapeutic benefits.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
I apologize, but "Nitracrine" does not appear to be a recognized term in medical terminology or pharmacology. It's possible that there may be a spelling error or it could be a very specialized or obscure term that is not widely used or known.
If you meant "Nitracrine" as a type of chemical compound, it refers to a class of compounds known as nitroaromatics, which contain a nitro group (-NO2) attached to an aromatic ring. However, I couldn't find any specific medical or clinical use for a compound named "Nitracrine".
Please double-check the spelling and let me know if you meant a different term or if you need information on a related topic.
Random Amplified Polymorphic DNA (RAPD) technique is a type of Polymerase Chain Reaction (PCR)-based method used in molecular biology for DNA fingerprinting and genetic diversity analysis. This technique utilizes random primers of arbitrary nucleotide sequences to amplify random segments of genomic DNA. The amplified products are then separated by electrophoresis, and the resulting banding patterns are analyzed.
In RAPD analysis, the randomly chosen primers bind to multiple sites in the genome, and the intervening regions between the primer binding sites are amplified. Since the primer binding sites can vary among individuals within a species or among different species, the resulting amplicons will also differ. These differences in amplicon size and pattern can be used to distinguish between individuals or populations at the DNA level.
RAPD is a relatively simple and cost-effective technique that does not require prior knowledge of the genome sequence. However, it has some limitations, such as low reproducibility and sensitivity to experimental conditions. Despite these limitations, RAPD remains a useful tool for genetic analysis in various fields, including forensics, plant breeding, and microbial identification.
Sarcoma viruses, murine, are a group of RNA viruses that primarily affect mice and other rodents. They are classified as type C retroviruses, which means they contain an envelope, have reverse transcriptase enzyme activity, and replicate through a DNA intermediate.
The murine sarcoma viruses (MSVs) are associated with the development of various types of tumors in mice, particularly fibrosarcomas, which are malignant tumors that originate from fibroblasts, the cells that produce collagen and other fibers in connective tissue.
The MSVs are closely related to the murine leukemia viruses (MLVs), and together they form a complex called the murine leukemia virus-related viruses (MLVRVs). The MLVRVs can undergo recombination events, leading to the generation of new viral variants with altered biological properties.
The MSVs are important tools in cancer research because they can transform normal cells into tumor cells in vitro and in vivo. The study of these viruses has contributed significantly to our understanding of the molecular mechanisms underlying cancer development and progression.
DNA-directed DNA polymerase is a type of enzyme that synthesizes new strands of DNA by adding nucleotides to an existing DNA template in a 5' to 3' direction. These enzymes are essential for DNA replication, repair, and recombination. They require a single-stranded DNA template, a primer with a free 3' hydroxyl group, and the four deoxyribonucleoside triphosphates (dNTPs) as substrates to carry out the polymerization reaction.
DNA polymerases also have proofreading activity, which allows them to correct errors that occur during DNA replication by removing mismatched nucleotides and replacing them with the correct ones. This helps ensure the fidelity of the genetic information passed from one generation to the next.
There are several different types of DNA polymerases, each with specific functions and characteristics. For example, DNA polymerase I is involved in both DNA replication and repair, while DNA polymerase III is the primary enzyme responsible for DNA replication in bacteria. In eukaryotic cells, DNA polymerase alpha, beta, gamma, delta, and epsilon have distinct roles in DNA replication, repair, and maintenance.
Amikhelline
Rhizoxin
Podophyllotoxin
Fisetin
History of cancer chemotherapy
DPP7
Mike Berridge
Oryzalin
Iris cyst
Mitotic catastrophe
Maryam Jafarkhani Kermani
Plant tissue culture
Monomethyl auristatin F
Enteropathy-associated T-cell lymphoma
Monomethyl auristatin E
Mature T-cell lymphoma
Spindle poison
Neoxaline
Moroidin
Discovery and development of tubulin inhibitors
Volasertib
Vinca alkaloid
Laucysteinamide A
Curacin A
2,5-Diketopiperazine
Endogenous regeneration
List of MeSH codes (D27)
Index of oncology articles
Brentuximab vedotin
Kinesin-like protein KIF11
Rationally Designed Anti-mitotic Agents with Pro-Apoptotic Activity | Bentham Science
Amikhelline - Wikipedia
Scholarly article on Benzene, 1-(bromomethyl)-3,4,5-trimethoxy-2-nitro- 103387-07-1 from Journal of Medicinal Chemistry p. 6412...
Colchicine: Biotoxin | NIOSH | CDC
CanMED: HCPCS
CanMED: HCPCS
Nature Reviews Cancer
UA 62784 Summary Report | CureHunter
Agentes Estabilizantes de Microtúbulos / Microtubule stabilizing agents | DIGITAL.CSIC
Vincristine News, Research - Page 5
Human Papillomavirus (HPV) Treatment & Management: Approach Considerations, Considerations in Specific Patient Subgroups,...
CDC | Case Definition: Colchicine Poisoning
Plus it
Trial of NanoPac® in Subjects With Locally Advanced Pancreatic Adenocarcinoma - Full Text View - ClinicalTrials.gov
Prospective identification of functionally distinct stem cells and neurosphere-initiating cells in adult mouse forebrain | eLife
TAK-960, a Novel, Orally Available, Selective Inhibitor of Polo-Like Kinase 1, Shows Broad-spectrum Preclinical Antitumor...
Condylox (podofilox) dosing, indications, interactions, adverse effects, and more.
Cancer therapy: Gene silencing of cytoskeleton-associated protein 5 in genetically unstable cancer cells
CDC | Case Definition: Colchicine Poisoning
Publications | www.ibmc.up.pt
MarBEF Data System - ERMS - Sigmophoranema rufum (Cobb, 1933) Hope & Murphy, 1972
WoRMS - World Register of Marine Species - Anoplostoma viviparum (Bastian, 1865) Bütschli, 1874
KCS Publications
Mitotic clustering of pulverized chromosomes from micronuclei | Nature
Insulin and novel thioglycosides exert suppressive effect on human breast and colon carcinoma cells | Oncotarget
Flashcards - dmrn105c
US Patent Application for OCULAR INSERT COMPOSITION OF A SEMI-CRYSTALLINE OR CRYSTALLINE PHARMACEUTICALLY ACTIVE AGENT Patent...
Molecular Vision: Nintedanib inhibits TGF-β-induced myofibroblast transdifferentiation in human Tenon's fibroblasts
Profile: Xinli Liu - University of Houston
15.2.3.4
Chemotherapy1
- The mainstay of treatment for indolent non-Hodgkin's lymphoma is an anti-CD20 antibody rituximab in combination with chemotherapy consisting of alkylating agents, anthracyclines, antimitotic agents, or purine analogues. (esmo.org)
Vinca Alkaloid1
- It is a type of vinca alkaloid and a type of antimitotic agent. (news-medical.net)
Potent4
- Our study provides new evidence that nintedanib has potent antifibrotic effects in HTFs and suggests that it may be used as a potential therapeutic agent for subconjunctival fibrosis. (molvis.org)
- In this article, we will introduce a potent anti-mitotic agent, LP-261. (cancer-research-network.com)
- The present invention isa new solid phase method for the preparation of DAT to make this lead molecule as a new class of small molecules as a potent antimitotic agents for the control of cytoskeletal functions and cell proliferation. (rgcb.res.in)
- Dioxol and dihydrodioxin analogs of 2- and 3-phenylacetonitriles as potent anti-cancer agents with nanomolar activity against a variety of human cancer cells. (uams.edu)
Colchicine3
- Colchicine stops the process of cell division (it is an antimitotic agent). (cdc.gov)
- Determination of the antimitotic agents N-Desacetylcolchicine, demecocline and colchicine in serum and urine. (cdc.gov)
- Colchicine-like effects of other antimitotic agents. (lookformedical.com)
Compounds4
- Agents that interact with cytoskeletal elements such as tubulin include synthetic spiroketal pyrans (SPIKET), targeting the spongistatin binding site of β- tubulin, and monotetrahydrofuran compounds (COBRA compounds), targeting a unique binding cavity on α-tubulin. (eurekaselect.com)
- We try to understand the physicochemical and cellular mechanisms employed by antimitotic compounds. (csic.es)
- The field of synthesis and evaluation of sugar-conjugated anticancer agents has grown significantly in recent years, with certain compounds in advanced clinical trials [ 1 ]. (oncotarget.com)
- however, the antimitotic activity of these compounds does not always correlate with stabilization of MTs in cells. (cardiff.ac.uk)
Anticancer agent3
- Linking glucose and anticancer agent presents an approach that exploits the Warburg effect. (oncotarget.com)
- Thesis Title: Study of the Mechanism of Action of a Diaminothiazole, a Potential Anticancer Agent. (rgcb.res.in)
- Taxol is the best anticancer agent ever been isolated from plants, but its major disadvantage is the dose limiting toxicity. (rgcb.res.in)
Paclitaxel3
- Wang X, Wu E, Wu J, Wang TL, Hsieh HP, Liu X . An antimitotic and antivascular agent BPR0L075 overcomes multidrug resistance and induces mitotic catastrophe in paclitaxel-resistant ovarian cancer cells. (uh.edu)
- Thesis Title: Study of the Drug Resistance Mechanisms in Cancer Against Antimitotic Agents Using Paclitaxel and Diaminothiazoles. (rgcb.res.in)
- Paclitaxel, a unique anti-mitotic agent, has been approved by the FDA for systemic application in metastatic cases of breast cancer and refractory cases of ovarian cancer, and AIDS-KS. (aphios.com)
Tubulin4
- Targeted anti-mitotic therapies: can we improve on tubulin agents? (researchgate.net)
- The exquisite selectivity for mitosis and the distinct ways in which these new agents interfere with mitosis provides the potential to not only overcome certain limitations of current tubulin-targeted anti-mitotic drugs, but to expand the scope of clinical efficacy that those drugs have established. (researchgate.net)
- Liu L, Beck H, Wang X, Hsieh H, Mason RP, Liu X . Tubulin-destabilizing agent BPR0L075 induces vascular-disruption in human breast cancer mammary fat pad xenografts. (uh.edu)
- Agents that interact with TUBULIN to inhibit or promote polymerization of MICROTUBULES. (uams.edu)
Inhibitors2
- Promising anti-mitotic agents with pro-apoptotic activity include inhibitors of the tyrosine kinase BTK. (eurekaselect.com)
- Since the immune response to antigen requires clonal proliferation, agents that block mitosis are effective inhibitors of the immune response. (nanomedicine.com)
Agentes1
- Por tanto la búsqueda de nuevos y mejores agentes antitumorales es un campo de la mayor importancia en la investigación farmacológica. (csic.es)
Drugs6
- How do antimitotic drugs work? (csic.es)
- Podofilox belongs to a group of drugs called antimitotics. (medscape.com)
- First used as anticancer drugs, purine analogs such as 6-mercaptopurine interfere with DNA synthesis and thus are also powerful antimitotic (hence immunosuppressive) agents. (nanomedicine.com)
- Microtubule binding drugs are of special interest as they have important roles in the modulation of cellular functions and many of them act as anticancer agents. (rgcb.res.in)
- This class of carcinogens includes various hormones (e.g., estrogen and diethylstilbestrol), immunosuppressive drugs (e.g., azathioprine), solid-state carcinogens (e.g., asbestos), and promoting agents (agents that increase tumor development when given after a genotoxic chemical). (doctorlib.info)
- Microtubule destabilising agents: far more than just antimitotic anticancer drugs. (research.com)
Microtubule2
- The therapeutic potential of microtubule-associated protein targets for cancer therapy is a largely unexplored research area due to a lack of target-specific agents. (medicalxpress.com)
- 2008). 4′-Methoxy-2-styrylchromone a novel microtubule-stabilizing antimitotic agent . (up.pt)
Analogues2
- Preclinical research indicates that the active metabolite of vitamin D, 1alpha,25(OH)2D3, also known as calcitriol, or vitamin D analogues might have potential as anticancer agents because their administration has antiproliferative effects, can activate apoptotic pathways and inhibit angiogenesis. (researchgate.net)
- Here, we outline the epidemiological, preclinical and clinical studies that support the development of 1alpha,25(OH)2D3 and vitamin D analogues as preventative and therapeutic anticancer agents. (researchgate.net)
Inhibit1
- Punarnavine, an alkaloid, is known to be an anti-cancer agent and is thought to inhibit the development of cancer cells. (cowurine.com)
Interfere1
- In these cases, treatment of the disease may need to include systemic antifungal agents, which can interfere or interact with other prescribed medications (eg, ketoconazole, fluconazole, itraconazole) or compromise liver function in patients with liver disease. (medscape.com)
Mitosis2
- Many chemotherapeutic agents explore defects in the cell cycle machinery of cancer cells to halt the cycle through mitosis inhibition. (medicalxpress.com)
- However, existing mitosis-targeting chemotherapeutic agents do not discriminate between healthy and malignant cell lines, resulting in severe side-effects . (medicalxpress.com)
19961
- 1996. Threshold limit values for chemical substances and physical agents and biological indices for 1995/1996. (cdc.gov)
Antineoplastic2
- Nanosomes are ideal vehicles for the topical delivery of antineoplastic agents. (aphios.com)
- Epo folate is folate receptor-targeting antimitotic agent with potential antineoplastic activity. (targetmol.com)
Chemotherapeutic1
- The most recent chemotherapeutic agent that has been approved for use in patients with rituximab-refractory indolent non-Hodgkin's lymphoma is the alkylating agent bendamustine, but it is not currative. (esmo.org)
Therapeutic agents2
- Thanks to greater awareness, earlier detection and improving therapeutic agents, people with cancer are living longer than ever before. (news-medical.net)
- Many chemicals that are present as industrial or environmental pollutants, dietary components, combustion by-products, or therapeutic agents may increase the risk of cancer development. (doctorlib.info)
Drug3
- Amikhelline is an antimitotic drug. (wikipedia.org)
- Taxotere acts as an anti-mitotic agent, meaning that this drug works to fight cancer by disrupting cancerous cell's ability to grow and multiply, thereby allowing doctors to focus on the cancerous cells in a specific area. (charlesboyk-law.com)
- Drug treatment regimens for cancer usually involve combinations of agents given intermittently. (doctorlib.info)
Efficacy2
- This burst rate or the initial release rate compromises the efficacy of the device because prolonged delivery of the agent is undermined. (justia.com)
- Clearly, a method for monitoring the efficacy of antiangiogenic agents would aid both research and treatment planning. (ajnr.org)
Bone marrow1
- These agents also damage all tissues (e.g., gut epithelium, bone marrow) where rapid cell division is occurring, creating other undesirable side effects, thus often may not be suitable for use in medical nanorobotics. (nanomedicine.com)
Effects1
- In addition, 1alpha,25(OH)2D3 potentiates the anticancer effects of many cytotoxic and antiproliferative anticancer agents. (researchgate.net)
Infections1
- The treatment of most HPV infections involves agents that directly ablate the lesions (eg, surgical excision, chemical ablation, and cryotherapy). (medscape.com)
Rate1
- Release rate of a pharmaceutically active agent from a delivery device, for example ocular insert, in which the active agent is dispersed in a polymer matrix, can have a high day 1 burst of the agent. (justia.com)
Therapies1
- In this single-arm, open-label, phase II study, 125 patients with indolent non-Hodgkin's lymphomas who had not had a response to rituximab and an alkylating agent or had had a relapse within 6 months after receipt of those therapies were administered idelalisib, until the disease progressed or the patient withdrew from the study. (esmo.org)
Effective2
- Angiogenesis is one of the most malignant features of recurrent high-grade glioma, and the recent emergence of antiangiogenic agents offers the hope of more effective treatment. (ajnr.org)
- An understanding of the cell cycle is essential for the effective use of anticancer agents ( Fig. 34.1 ). (doctorlib.info)
Chemical6
- A Totally-Encapsulating Chemical Protective (TECP) suit that provides protection against CBRN agents. (cdc.gov)
- A hooded chemical-resistant suit that provides protection against CBRN agents. (cdc.gov)
- A case in which a potentially exposed person is being evaluated by health-care workers or public health officials for poisoning by a particular chemical agent, but no specific credible threat exists. (cdc.gov)
- The case can be confirmed if laboratory testing was not performed because either a predominant amount of clinical and nonspecific laboratory evidence of a particular chemical was present or the etiology of the agent is known with 100% certainty. (cdc.gov)
- The present disclosure further includes a method of reducing or preventing physical and chemical degradation of a semi-crystalline or crystalline active agent pharmaceutically active agent dispersed in a polymer matrix. (justia.com)
- In addition, chemical degradation of the active agent limits the duration the preparation can be stored and used. (justia.com)
Include1
- Other agents that have shown promise for cancer treatment include phorboxazoles, natural products that are extremely cytostatic towards the National Cancer Institutes panel of 60 tumor cell lines. (eurekaselect.com)
Cancer cells2
- Conjugation of glucose with metabolic agents to selectively target cancer cells was inspired by the widespread use of radiolabeled glucose analog to visualize tumors and their metastases. (oncotarget.com)
- This herb's anti-cancer agent, plumbagin has been used to stop the cancer-inflicting enhancement of prostate cancer cells. (cowurine.com)
Tissue1
- Inappropriate use of these agents may cause extensive and unnecessary tissue injury and loss. (medscape.com)
Composition1
- The present disclosure provides, inter alia, a method of reducing or preventing degradation of a semi-crystalline or crystalline pharmaceutically active agent dispersed in a polymer matrix in an ocular insert composition, the method including washing the insert with an organic solvent. (justia.com)
Target1
- Along with ibrutinib, which targets Bruton's tyrosine kinase (BTK), idelalisib represents a new class of agents that target signal transduction downstream of the B-cell receptor (BCR) in malignant B cells. (esmo.org)
Increase1
- Other agents that increase NO levels independently of ecNOS may also be used. (patentpc.com)
Administration1
- The use of these agents is further constrained by the complex procedures for their administration. (esmo.org)