Journal articles: 'Antimitotic'

1

Campos, Susana M., and Don S. Dizon. "Antimitotic Inhibitors." Hematology/Oncology Clinics of North America 26, no. 3 (June 2012): 607–28. http://dx.doi.org/10.1016/j.hoc.2012.01.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Groult, Hugo, Isabel García-Álvarez, Lorenzo Romero-Ramírez, Manuel Nieto-Sampedro, Fernando Herranz, Alfonso Fernández-Mayoralas, and Jesús Ruiz-Cabello. "Micellar Iron Oxide Nanoparticles Coated with Anti-Tumor Glycosides." Nanomaterials 8, no. 8 (July 25, 2018): 567. http://dx.doi.org/10.3390/nano8080567.

Full text

Abstract:

The synthesis procedure of nanoparticles based on thermal degradation produces organic solvent dispersible iron oxide nanoparticles (OA-IONP) with oleic acid coating and unique physicochemical properties of the core. Some glycosides with hydrophilic sugar moieties bound to oleyl hydrophobic chains have antimitotic activity on cancer cells but reduced in vivo applications because of the intrinsic low solubility in physiological media, and are prone to enzymatic hydrolysis. In this manuscript, we have synthetized and characterized OA-IONP-based micelles encapsulated within amphiphilic bioactive glycosides. The glycoside-coated IONP micelles were tested as Magnetic Resonance Imaging (MRI) contrast agents as well as antimitotics on rat glioma (C6) and human lung carcinoma (A549) cell lines. Micelle antimitotic activity was compared with the activity of the corresponding free glycosides. In general, all OA-IONP-based micellar formulations of these glycosides maintained their anti-tumor effects, and, in one case, showed an unusual therapeutic improvement. Finally, the micelles presented optimal relaxometric properties for their use as T2-weighed MRI contrast agents. Our results suggest that these bioactive hydrophilic nano-formulations are theranostic agents with synergistic properties obtained from two entities, which separately are not ready for in vivo applications, and strengthen the possibility of using biomolecules as both a coating for OA-IONP micellar stabilization and as drugs for therapy.

APA, Harvard, Vancouver, ISO, and other styles

3

Hamel, Ernest, and David Covell. "Antimitotic Peptides and Depsipeptides." Current Medicinal Chemistry-Anti-Cancer Agents 2, no. 1 (November 14, 2012): 19–53. http://dx.doi.org/10.2174/1568011023354263.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Santhakumari, G., and J. Stephen. "Antimitotic effects of holothurin." CYTOLOGIA 53, no. 1 (1988): 163–68. http://dx.doi.org/10.1508/cytologia.53.163.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

R. A. Ahirrao, B. S. Patange, and S. V. More. "Evaluation of Antimitotic Activity of Momordica Dioica Fruits on Allium Cepa Root Meristamatic Cells." Journal of Pharmaceutical Technology, Research and Management 7, no. 2 (November 5, 2019): 67–71. http://dx.doi.org/10.15415/jptrm.2019.72009.

Full text

Abstract:

Objective: Natural occurring phenolic compounds play an important role in cancer prevention and shows antimitotic activity. Number of active constituents like phenolic acid, curcuminoids, coumarine, ligans, quinones, etc. is showing antimitotic activity of Momordica dioica. The present work is on phytochemical investigation and examines antimitotic activity of aqueous extract of fruits Momordica dioica at concentration of 15 mg/ml on Allium cepa root meristamatic cells.Methods: The fruits are air dried and extracted with solvents like water by maceration method. The evaluation of antimitotic activity is done by using Allium cepa root meristamatic cells parameters where and methotrexate was used as a standard drugs. Result and discussion: In Allium assay, aqueous extract of fruits of Momordica diocia (15 mg/ml) and methotrexate act against cells of allium roots and lesser the growth of root and mitotic index when compared with distilled water as control group. The result indicated that cytotoxic property is due to presence of phenolic, alkaloids and flavonoids compounds in 15 mg/ml concentration of aqueous extract of Momordica diocia fruits extract.Conclusion: On the basis of result, we concluded that, 15 mg/ml concentration of Momordica dioica fruits shows good antimitotic activity on the Allium cepa root tip assay.

APA, Harvard, Vancouver, ISO, and other styles

6

Sundaresan, K., M. Thangavel, and K. Tharini. "Synthesis, characterization and antimitotic activity of N-benzyl piperidin 4-one oxime." Journal of Drug Delivery and Therapeutics 9, no. 1 (January 15, 2019): 233–36. http://dx.doi.org/10.22270/jddt.v9i1.2228.

Full text

Abstract:

The aim of this study was to synthesize, characterization and antimitotic activity of N-Benzyl piperidin 4-one oxime derivative. The synthesized compound was characterized by IR, 13C and 1H NMR spectral studies. The synthesized compound was subjected to antimitotic studies of alliumcepa root meristamatic cells. The mitotic activity was observed in 3 different concentrations of N-Benzyl piperidin 4-one oxime. Our findings support the reported therapeutic use of this compound as a antimitotic or anticancer agent in the Indian system of medicine. Keywords: N-Benzyl piperidin 4-one oxime, meristamatic cells, mitotic index.

APA, Harvard, Vancouver, ISO, and other styles

7

Nagle, Advait, Wooyoung Hur, and Nathanael Gray. "Antimitotic Agents of Natural Origin." Current Drug Targets 7, no. 3 (March 1, 2006): 305–26. http://dx.doi.org/10.2174/138945006776054933.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Tarkowska, Jadwiga A. "Sodium cacodylate as antimitotic agent." Acta Societatis Botanicorum Poloniae 57, no. 3 (2014): 329–40. http://dx.doi.org/10.5586/asbp.1988.032.

Full text

Abstract:

The effect of pure sodium cacodylate on dividing cells was studied. The root meristematic cells of Allium cepa L. (the roots were squashed in acetoorcein) and endosperm cells of Haemanthus katherinae Bak. (in vitro observations) were used. Serious disturbances in karyokinesis and cytokinesis were found that led most often to the formation of polyploid or multinucleate (A. cepa) cells. These results point to damage of the mitotic spindle and phragmoplast. Careful use of cacodylate buffer in ultrastructural studies of microtubules is advised.

APA, Harvard, Vancouver, ISO, and other styles

9

Dall'Acqua, Stefano. "Natural Products As Antimitotic Agents." Current Topics in Medicinal Chemistry 14, no. 20 (December 12, 2014): 2272–85. http://dx.doi.org/10.2174/1568026614666141130095311.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Perez-Melero, Concepcion. "KSP Inhibitors as Antimitotic Agents." Current Topics in Medicinal Chemistry 14, no. 20 (December 12, 2014): 2286–311. http://dx.doi.org/10.2174/1568026614666141130095532.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Leslie, Benjamin J., Clinton R. Holaday, Tran Nguyen, and Paul J. Hergenrother. "Phenylcinnamides as Novel Antimitotic Agents." Journal of Medicinal Chemistry 53, no. 10 (May 27, 2010): 3964–72. http://dx.doi.org/10.1021/jm901805m.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Orth, James D., Alexander Loewer, Galit Lahav, and Timothy J. Mitchison. "Prolonged mitotic arrest triggers partial activation of apoptosis, resulting in DNA damage and p53 induction." Molecular Biology of the Cell 23, no. 4 (February 15, 2012): 567–76. http://dx.doi.org/10.1091/mbc.e11-09-0781.

Full text

Abstract:

Mitotic arrest induced by antimitotic drugs can cause apoptosis or p53-dependent cell cycle arrest. It can also cause DNA damage, but the relationship between these events has been unclear. Live, single-cell imaging in human cancer cells responding to an antimitotic kinesin-5 inhibitor and additional antimitotic drugs revealed strong induction of p53 after cells slipped from prolonged mitotic arrest into G1. We investigated the cause of this induction. We detected DNA damage late in mitotic arrest and also after slippage. This damage was inhibited by treatment with caspase inhibitors and by stable expression of mutant, noncleavable inhibitor of caspase-activated DNase, which prevents activation of the apoptosis-associated nuclease caspase-activated DNase (CAD). These treatments also inhibited induction of p53 after slippage from prolonged arrest. DNA damage was not due to full apoptosis, since most cytochrome C was still sequestered in mitochondria when damage occurred. We conclude that prolonged mitotic arrest partially activates the apoptotic pathway. This partly activates CAD, causing limited DNA damage and p53 induction after slippage. Increased DNA damage via caspases and CAD may be an important aspect of antimitotic drug action. More speculatively, partial activation of CAD may explain the DNA-damaging effects of diverse cellular stresses that do not immediately trigger apoptosis.

APA, Harvard, Vancouver, ISO, and other styles

13

Cores, Angel, Carlos Carbajales, and Alberto Coelho. "Multicomponent Reactions in Antimitotic Drug Discovery." Current Topics in Medicinal Chemistry 14, no. 20 (December 12, 2014): 2209–30. http://dx.doi.org/10.2174/1568026614666141127115130.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Gwaltney, Stephen L., Hovis M. Imade, Qun Li, Laura Gehrke, R. Bruce Credo, Robert B. Warner, Jang Yun Lee, et al. "Novel sulfonate Derivatives: potent antimitotic agents." Bioorganic & Medicinal Chemistry Letters 11, no. 13 (July 2001): 1671–73. http://dx.doi.org/10.1016/s0960-894x(01)00279-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Badria, Farid A., Waell E. Houssein, Mona G. Zaghloul, and Ahmed F. Halim. "Antimitotic Activity of Gossypol and Gossypolone." Pharmaceutical Biology 39, no. 2 (January 2001): 120–26. http://dx.doi.org/10.1076/phbi.39.2.120.6257.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Montagnac, A., J. Provost, M. Litaudon, and M. Païs. "Antimitotic and Cytotoxic Constituents ofMyodocarpus gracilis." Planta Medica 63, no. 04 (August 1997): 365–66. http://dx.doi.org/10.1055/s-2006-957704.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Remigio, Antonia C., Janet Piloto, Yamile Vega, Alicia Lagarto, Carlos Rodriguez, Caridad Carballo, Micaela Couret, and Isbel Guerra. "Toxigenetic screening of medicinal plants antimitotic." Toxicology Letters 180 (October 2008): S241—S242. http://dx.doi.org/10.1016/j.toxlet.2008.06.073.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Akdeniz, Duygu, and Ali Özmen. "Antimitotic effects of the biopesticide oxymatrine." Caryologia 64, no. 1 (January 2011): 117–20. http://dx.doi.org/10.1080/00087114.2011.10589771.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Miernik, A., A. Santa-Maria, and F. Marano. "The antimitotic activities of some benzodiazepines." Experientia 42, no. 8 (August 1986): 956–58. http://dx.doi.org/10.1007/bf01941778.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Morita, Hiroshi, Yusuke Hirasawa, Akihiro Muto, Tadashi Yoshida, Setsuko Sekita, and Osamu Shirota. "Antimitotic quinoid triterpenes from Maytenus chuchuhuasca." Bioorganic & Medicinal Chemistry Letters 18, no. 3 (February 2008): 1050–52. http://dx.doi.org/10.1016/j.bmcl.2007.12.016.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Bhunia, Debmalya, Saswat Mohapatra, Prashant Kurkute, Subhajit Ghosh, Batakrishna Jana, Prasenjit Mondal, Abhijit Saha, Gaurav Das, and Surajit Ghosh. "Novel tubulin-targeted cell penetrating antimitotic octapeptide." Chemical Communications 52, no. 85 (2016): 12657–60. http://dx.doi.org/10.1039/c6cc05110c.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Schnerch, Dominik, Julia Felthaus, Monika Engelhardt, and Ralph Wäsch. "A Rationale to Enhance the Response to Antimitotic Therapy in Acute Myeloid Leukemia." Blood 120, no. 21 (November 16, 2012): 1332. http://dx.doi.org/10.1182/blood.v120.21.1332.1332.

Full text

Abstract:

Abstract Abstract 1332 Acute myeloid leukemia (AML) is known to respond only moderately to antimitotic therapy while acute lymphoblastic leukemias can be efficiently targeted using spindle-disrupting agents. The underlying molecular cause for this clinical phenomenon is unknown. Recent evidence suggests that response to antimitotic therapy substantially depends on the stability of the critical mitotic regulator cyclin B. The ability to keep cyclin B expression levels stable during a mitotic block is associated with a good response leading to cell death in mitosis. At the metaphase to anaphase transition of an unperturbed cell division, cyclin B is targeted for degradation by the anaphase-promoting complex/cyclosome (APC/C) to trigger chromosome separation. The spindle assembly checkpoint (SAC) is a surveillance mechanism to ensure that APC/C-mediated ubiquitylation is restricted to cells that show proper attachment of all chromosomes to a functional mitotic spindle. In case of spindle disruption or unattached chromosomes, the spindle checkpoint stays active which leads to interference with APC/C-dependent proteolysis of cyclin B blocking cells in prometaphase until every chromosome is attached to the mitotic spindle. We recently developed a cell line-based reporter system which allows monitoring of cyclin B degradation under various conditions (Schnerch et al. Cell Cycle 2012). Here, we identified a pattern of slow degradation of cyclin B which continues through a mitotic block in case of chromosomal misalignment in unperturbed cell cycles. Remarkably, we also found prolonged slow degradation to trigger aberrant exit from mitosis in such cells giving rise to tetraploid cells. Therefore, a reduction in slow degradation appears as a promising rationale to foster a mitotic arrest and enhance cell death in mitosis during antimitotic therapy by preventing such mitotic slippage. We exposed our reporter cells to low concentrations of proteasome inhibitor during a spindle poison induced mitotic block to assess whether proteasome inhibition is capable of modulating slow degradation. Importantly, very low doses of proteasome inhibitor were sufficient to reduced the extent of cyclin B slow degradation during the mitotic block. Moreover, we demonstrate that low doses of proteasome inhibitor render the AML cell line Kasumi-1 responsive to low, non-disruptive concentrations of spindle poison (nocodazole and vincristine) leading to remarkable increases in the G2M-fraction. To the best of our knowledge there is no evidence so far that low doses of proteasome inhibitor exert antimitotic effects by interference with protein degradation during mitosis. Importantly, concentration of bortezomib of 1–2ng/ml (such as found in the serum of patients for up to 72h following administration of 1.3mg/m2 bortezomib subcutaneously) were found to exert synergistic effects with antimitotic therapy. Increases in the percentage of G2M cells by 38% were observed in Kasumi-1 cells for the combination of vincristine and bortezomib. Based on these findings, we currently apply our system to probe combinations of proteasome inhibitor with modern tailored therapies that exert their antimitotic effects by activation of the SAC, such as inhibitors of the motor protein Eg5 or of the mitotic kinases Polo-like kinase 1 (Plk1) or Aurora A and B. Using our cell line-based reporter system, we provide evidence in the in vitro setting that modulating slow degradation during antimitotic therapy by proteasome inhibition is a promising rationale to enhance the efficacy of antimitotic drugs. Drug concentrations used are based on published pharmacokinetics in humans and suggest feasibility of the drug combination in vivo. Our approach of targeted drug combinations may provide highly efficient treatment alternatives for patients that are not eligible for induction treatment. Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

23

Shivasharanappa, Kirankumar, and Ramesh Londonkar. "Clot Lysis and Antimitotic Study of Ficus glomerata Roxb Fruit Extracts." ISRN Pharmacology 2014 (March 31, 2014): 1–4. http://dx.doi.org/10.1155/2014/975303.

Full text

Abstract:

The present study was carried out to investigate the thrombolytic and antimitotic potentiality of various extracts of fruits of Ficus glomerata, a traditional medicinal plant, using an in vitro assay method. Three crude extracts such as petroleum ether (FGPE), chloroform (FGCE), and methanol (FGME) were used for the study, with a standard (streptokinase) and negative control (sterile distilled water) to validate the method. The thrombolytic nature of the plant was found significant with methanol extract and chloroform and petroleum ether extracts have recorded mild activity, when compared with the negative control (sterile distilled water). The extracts have shown mild clot lysis, that is, 2.16%, 23.06%, 27.60%, and 47.74% of sterile distilled water, FGPE, FGCE, and FGME, respectively, while the standard (streptokinase) has shown 74.22% clot lysis. FGME inhibited the root growth in number as well as length effectively, followed by FGPE, while FGCE exhibited moderate antimitotic activity and it was supported by mitotic index. Therefore, the obtained results suggest that among all the extracts of plant the methanolic extract has shown highest thrombolytic and antimitotic activity.

APA, Harvard, Vancouver, ISO, and other styles

24

Maneh, Nidain, Kokou Vonor, Bénédicte Marèbe Diatewa, Nonon Saa Kassoula Batomaguela, Kokou Messan Amedomé, Yawa Edebah Nagbe, Ayena Koffi Didier, Meba Banla, and Komi Patrice Balo. "Résultats De La Trabéculectomie Dans Le Glaucome Infantile Au Chu Campus De Lomé (Togo)." European Scientific Journal, ESJ 13, no. 12 (April 30, 2017): 119. http://dx.doi.org/10.19044/esj.2017.v13n12p119.

Full text

Abstract:

Purpose: To evaluate the results of the trabeculectomy without antimitotic in children aged 5 to 15 years and identify the factors of success of this technique. Method: we have conducted a retrospective study based on records of children of 5 to 15 years, operated from January 2011 to December 2013 for glaucoma excepted congenital glaucoma. The trabeculectomy was performed without antimitotic and the follow up was done during 6 months. Nineteen children (35 eyes) were included over 23 children (43 eyes) operated. Surgical success was defined for intra ocular (IOP) ≤ 20mmhg (target pressure) pressure associated with a pressure reduction over 30% with or without topical medication and major postoperative complications. Results: On the 19 included Sham children (35 eyes) the mean age was 9.05 years [5;15], 11 were of boys and 8 girls and the sex ratio was 0.73. The mean cup/disc of the papillary excavation was 0.54 [0.2; 0.8]. The mean preoperative IOP was 20.08 mm Hg [11;30]. Postoperative complications was seen in 17% (6 eyes) with 11.4% (4 eyes) of hypothalamy. The mean post operative IOP at 6 months was 12.86 mm Hg [10; 23]. The success rate was 62.86% (22 eyes). IOP control was the only factor influencing the success of surgery (p = 0. 0055). Conclusion: The trabeculectomy without antimitotic allowed a substantial reduction in IOP. The control of IOP determine the success of the surgery at 6 months. The spreading of the technique with the use of an antimitotic will optimize our results.

APA, Harvard, Vancouver, ISO, and other styles

25

Klíma, M., M. Vyvadilová, and V. Kučera. "Chromosome doubling effects of selected antimitotic agents in Brassica napus microspore culture." Czech Journal of Genetics and Plant Breeding 44, No. 1 (March 28, 2008): 30–36. http://dx.doi.org/10.17221/1328-cjgpb.

Full text

Abstract:

Effects of microspore culture treatment with antimitotic agents colchicine, trifluralin and oryzalin on the frequency of embryo formation, embryo development, plant regeneration and diploidization rate in three F1 hybrids of winter rapeseed cultivars were compared. The ploidy level analysis of 1709 flowering microspore-derived plants showed that in vitro applications of all antimitotic drugs increased the rate of doubled haploid (DH) plants significantly. The mean rate of DH plants from the trifluralin treatment was 85.7%, from colchicine 74.1% and 66.5% in the case of oryzalin, while only 42.3% in the untreated control variant whereas in vivo additional application of colchicine at the plantlet stage did not significantly increase the mean rate of DH plants (55.6%). Although there were no significant differences in diploidization efficiency between the in vitro applications of particular antimitotic agents, trifluralin showed to be the most suitable because of its positive effect on embryo development and conversion into whole plants. In addition, the diploidization rate was sufficient and stable in all genotypes tested. The results indicate that the trifluralin treatment of microspore cultures could provide efficient chromosome doubling for the production of doubled haploid lines from winter oilseed rape breeding materials.

APA, Harvard, Vancouver, ISO, and other styles

26

Bergnes, Gustave, Katjusa Brejc, and Lisa Belmont. "Mitotic Kinesins: Prospects for Antimitotic Drug Discovery." Current Topics in Medicinal Chemistry 5, no. 2 (April 1, 2005): 127–45. http://dx.doi.org/10.2174/1568026053507697.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Correia, J., and S. Lobert. "Physiochemical Aspects of Tubulin-Interacting Antimitotic Drugs." Current Pharmaceutical Design 7, no. 13 (September 1, 2001): 1213–28. http://dx.doi.org/10.2174/1381612013397438.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Mohan, Gottumukkala Krishna, Malavika Yadav, M. Sandhya Rani, and Kalakotla Shanker. "Antimitotic activity of Borassus flabellifer Seed Coat." Research Journal of Pharmacognosy and Phytochemistry 8, no. 4 (2016): 223. http://dx.doi.org/10.5958/0975-4385.2016.00033.9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Suzuki, Takahiro, Kenji Usui, Yoshiharu Miyake, Michio Namikoshi, and Masahisa Nakada. "First Total Synthesis of Antimitotic Compound, (+)-Phomopsidin." Organic Letters 6, no. 4 (February 2004): 553–56. http://dx.doi.org/10.1021/ol036338q.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Weiderhold, Kimberly N., Deborah A. Randall-Hlubek, Lisa A. Polin, Ernest Hamel, and Susan L. Mooberry. "CB694, a novel antimitotic with antitumor activities." International Journal of Cancer 118, no. 4 (September 8, 2005): 1032–40. http://dx.doi.org/10.1002/ijc.21424.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Mitchison, Timothy J. "The proliferation rate paradox in antimitotic chemotherapy." Molecular Biology of the Cell 23, no. 1 (January 2012): 1–6. http://dx.doi.org/10.1091/mbc.e10-04-0335.

Full text

Abstract:

Cytotoxic cancer chemotherapy drugs are believed to gain selectivity by targeting cells that proliferate rapidly. However, the proliferation rate is low in many chemosensitive human cancers, and it is not clear how a drug that only kills dividing cells could promote tumor regression. Four potential solutions to this “proliferation rate paradox” are discussed for the microtubule-stabilizing drug paclitaxel: drug retention in tumors, killing of quiescent cells, targeting of noncancer cells in the tumor, and bystander effects. Testing these potential mechanisms of drug action will facilitate rational improvement of antimitotic chemotherapy and perhaps cytotoxic chemotherapy more generally.

APA, Harvard, Vancouver, ISO, and other styles

32

Edwards, Michael L., David M. Stemerick, and Prasad S. Sunkara. "Chalcones: a new class of antimitotic agents." Journal of Medicinal Chemistry 33, no. 7 (July 1990): 1948–54. http://dx.doi.org/10.1021/jm00169a021.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Delacour, Quentin, and Olivier Gavet. "Re-investigating PLK1 inhibitors as antimitotic agents." Molecular & Cellular Oncology 4, no. 6 (October 20, 2017): e1356430. http://dx.doi.org/10.1080/23723556.2017.1356430.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Compton, D. A. "CELL CYCLE:New Tools for the Antimitotic Toolbox." Science 286, no. 5441 (October 29, 1999): 913–14. http://dx.doi.org/10.1126/science.286.5441.913.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Kim, Semi, Ji Hyun Park, Sun-Young Koo, Jung In Kim, Min-Hyeung Kim, Ji Eun Kim, Kiwon Jo, Hwan Geun Choi, Sung Bae Lee, and Sang-Hun Jung. "Novel diarylsulfonylurea derivatives as potent antimitotic agents." Bioorganic & Medicinal Chemistry Letters 14, no. 24 (December 2004): 6075–78. http://dx.doi.org/10.1016/j.bmcl.2004.09.069.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

van Vuuren, Rustelle Janse, Michelle H. Visagie, Anne E. Theron, and Annie M. Joubert. "Antimitotic drugs in the treatment of cancer." Cancer Chemotherapy and Pharmacology 76, no. 6 (November 12, 2015): 1101–12. http://dx.doi.org/10.1007/s00280-015-2903-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Gallet, Sebastien, Nathalie Flouquet, Pascal Carato, Bruno Pfeiffer, Pierre Renard, Stéphane Léonce, Alain Pierré, Pascal Berthelot, and Nicolas Lebegue. "Benzopyridooxathiazepine derivatives as novel potent antimitotic agents." Bioorganic & Medicinal Chemistry 17, no. 3 (February 2009): 1132–38. http://dx.doi.org/10.1016/j.bmc.2008.12.039.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Tu, Shih-Hsin, Yi-Shiou Chiou, Nagabhushanam Kalyanam, Chi-Tang Ho, Li-Ching Chen, and Min-Hsiung Pan. "Garcinol sensitizes breast cancer cells to Taxol through the suppression of caspase-3/iPLA2and NF-κB/Twist1 signaling pathways in a mouse 4T1 breast tumor model." Food & Function 8, no. 3 (2017): 1067–79. http://dx.doi.org/10.1039/c6fo01588c.

Full text

Abstract:

Garcinol sensitizes breast cancer cells to Taxolviasynergistically inducing antimitotic effects and effectively repressing the activation of caspase-3/iPLA₂and Taxol-promoted NF-κB/Twist1 signaling pathways.

APA, Harvard, Vancouver, ISO, and other styles

39

Abraham, I., R. J. Hunter, K. E. Sampson, S. Smith, M. M. Gottesman, and J. K. Mayo. "Cyclic AMP-dependent protein kinase regulates sensitivity of cells to multiple drugs." Molecular and Cellular Biology 7, no. 9 (September 1987): 3098–106. http://dx.doi.org/10.1128/mcb.7.9.3098.

Full text

Abstract:

The isolation of mutant cell lines affecting the activity of cyclic AMP (cAMP)-dependent protein kinase (PK-A) has made it possible to determine the function of this kinase in mammalian cells. We found that both a CHO cell mutant with a defective regulatory subunit (RI) for PK-A and a transfectant cell line expressing the same mutant kinase were sensitive to multiple drugs, including puromycin, adriamycin, actinomycin D, and some antimitotic drugs. The mutant and transfectant cells, after treatment with a concentration of the antimitotic drug colcemid that had no marked effect on the wild-type parent cell, had a severely disrupted microtubule network. The phenotype of hypersensitivity to the antimitotic drug colcemid was used to select revertants of the transfectant and the original mutant. These revertants simultaneously regained normal multiple drug resistance and cAMP sensitivity, thus establishing that the characteristics of colcemid sensitivity and cAMP resistance are linked. Four revertants of the transfectant reverted because of loss or rearrangement of the transfected mutant RI gene. These revertants, as well as one revertant selected from the original mutant, had PK-A activities equal to or higher than that of the parent. In these genetic studies, in which linkage of expression of a PK-A mutation with drug sensitivity is demonstrated, it was established that the PK-A system is involved in regulating resistance of mammalian cells to multiple drugs.

APA, Harvard, Vancouver, ISO, and other styles

40

Abraham, I., R. J. Hunter, K. E. Sampson, S. Smith, M. M. Gottesman, and J. K. Mayo. "Cyclic AMP-dependent protein kinase regulates sensitivity of cells to multiple drugs." Molecular and Cellular Biology 7, no. 9 (September 1987): 3098–106. http://dx.doi.org/10.1128/mcb.7.9.3098-3106.1987.

Full text

Abstract:

The isolation of mutant cell lines affecting the activity of cyclic AMP (cAMP)-dependent protein kinase (PK-A) has made it possible to determine the function of this kinase in mammalian cells. We found that both a CHO cell mutant with a defective regulatory subunit (RI) for PK-A and a transfectant cell line expressing the same mutant kinase were sensitive to multiple drugs, including puromycin, adriamycin, actinomycin D, and some antimitotic drugs. The mutant and transfectant cells, after treatment with a concentration of the antimitotic drug colcemid that had no marked effect on the wild-type parent cell, had a severely disrupted microtubule network. The phenotype of hypersensitivity to the antimitotic drug colcemid was used to select revertants of the transfectant and the original mutant. These revertants simultaneously regained normal multiple drug resistance and cAMP sensitivity, thus establishing that the characteristics of colcemid sensitivity and cAMP resistance are linked. Four revertants of the transfectant reverted because of loss or rearrangement of the transfected mutant RI gene. These revertants, as well as one revertant selected from the original mutant, had PK-A activities equal to or higher than that of the parent. In these genetic studies, in which linkage of expression of a PK-A mutation with drug sensitivity is demonstrated, it was established that the PK-A system is involved in regulating resistance of mammalian cells to multiple drugs.

APA, Harvard, Vancouver, ISO, and other styles

41

Jana, Batakrishna, Atanu Biswas, Saswat Mohapatra, Abhijit Saha, and Surajit Ghosh. "Single functionalized graphene oxide reconstitutes kinesin mediated intracellular cargo transport and delivers multiple cytoskeleton proteins and therapeutic molecules into the cell." Chem. Commun. 50, no. 78 (2014): 11595–98. http://dx.doi.org/10.1039/c4cc04924a.

Full text

Abstract:

Kinesin-1 mediated intracellular cargo transport is reconstituted using EGFP–Tris-NTA-GO (EGFP–TGO) as cargo. This functionalized nanoparticle can deliver multiple cytoskeleton proteins and antimitotic peptides into the cancer cell.

APA, Harvard, Vancouver, ISO, and other styles

42

Gupta, Radhey S. "Microtubules, mitochondria, and molecular chaperones: a new hypothesis for in vivo assembly of microtubules." Biochemistry and Cell Biology 68, no. 12 (December 1, 1990): 1352–63. http://dx.doi.org/10.1139/o90-198.

Full text

Abstract:

In Chinese hamster ovary cells, a number of independent mutants selected for resistance to antimitotic drugs have been found to be specifically altered in two major cellular proteins, designated P1 (relative mass (Mr) ≈ 60–63 kilodaltons (kDa)) and P2 (Mr ≈ 69–70 kDa), which appeared microtubule related by a number of genetic and biochemical criteria. Antibodies to P1 have been found to bind specifically to mitochondria that showed specific association with microtubules in interphase cells. Biochemical and cDNA sequence studies on P1 showed that this protein, which is localized in the matrix compartment, is the mammalian homolog of the highly conserved chaperonin family of proteins (other members include the GroEL protein of Escherichia coli, the 60-kDa heat-shock protein of yeast, and the rubisco subunit binding protein of plant chloroplasts). The chaperonin proteins in various systems play a transient but essential molecular chaperone role in the proper folding of polypeptide chains and their assembly into oligomeric protein complexes. Our studies on P2 protein established that it corresponds to the constitutive form of the major 70-kDa heat-shock protein of mammalian cells (i.e., hsc70), which also acts as a molecular chaperone in the intracellular transport of nascent proteins to organelles such as mitochondria and endoplasmic reticulum. To account for the above, as well as a number of other observations (e.g., binding of fluorescent-labeled antimitotic drugs to mitochondria, association of tubulin with mitochondria as well as other membranes, and high affinity binding of antimitotic drugs to free tubulin but not to assembled microtubules), a new model for the in vivo assembly of interphase microtubules is proposed. The model ascribes a central role to the mitochondrially localized chaperonin (i.e., P1) protein in the intracellular formation of tubulin dimers and in their addition to the growth sites in microtubules. The proposed model also explains a number of other observations related to microtubule assembly in the literature.Key words: microtubule assembly, mitochondria, molecular chaperones, heat-shock proteins, antimitotic drugs.

APA, Harvard, Vancouver, ISO, and other styles

43

Karpov, P. A. "High-Throughput Screening of New Antimitotic Compounds Based on CSLabGrid Virtual Organization." Science and innovation 11, no. 1 (January 30, 2015): 85–93. http://dx.doi.org/10.15407/scine11.01.085.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Hsieh, H., J. Liou, and N. Mahindroo. "Pharmaceutical Design of Antimitotic Agents Based on Combretastatins." Current Pharmaceutical Design 11, no. 13 (May 1, 2005): 1655–77. http://dx.doi.org/10.2174/1381612053764751.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

IWASAKI, Shigeo. "Antimitotic Agents: Chemisrtry and Recognition of Tubulin Molecule." Journal of Synthetic Organic Chemistry, Japan 49, no. 10 (1991): 892–901. http://dx.doi.org/10.5059/yukigoseikyokaishi.49.892.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Hu, Laixing, Zhuo-rong Li, Jian-dong Jiang, and David Boykin. "Novel Diaryl or Heterocyclic Sulfonamides as Antimitotic Agents." Anti-Cancer Agents in Medicinal Chemistry 8, no. 7 (October 1, 2008): 739–45. http://dx.doi.org/10.2174/187152008785914806.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Nam, Nguyen-Hai. "Combretastatin A-4 Analogues as Antimitotic Antitumor Agents." Current Medicinal Chemistry 10, no. 17 (September 1, 2003): 1697–722. http://dx.doi.org/10.2174/0929867033457151.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Chen, Xing, Shi-Meng Wang, Gajjela Bharath Kumar, Grant A. L. Bare, Jing Leng, Syed Nasir Abbas Bukhari, and Hua-Li Qin. "Recent Developments on Phenstatins as Potent Antimitotic Agents." Current Medicinal Chemistry 25, no. 20 (June 14, 2018): 2329–52. http://dx.doi.org/10.2174/0929867324666171106162048.

Full text

Abstract:

Background: Phenstatin and their derivatives display remarkable antiproliferative activity toward a wide variety of preclinical tumor models. Structural simplicity and excellent stability of phenstatins offer a stimulating premise for developing various derivatives with profound antimitotic activity and excellent cytotoxicity. Objective: To do analysis of literature that phenstatins derivatives inhibit tubulin polymerization through their interaction at the colchicine binding site of microtubules and arrest the G2/M phase of the cell cycle. In addition, phenstatin derivatives are undergoing clinical evaluation as vascular targeting/disrupting agents and also exhibit direct antiangiogenic properties. Methods: An organised well designed and appropriately managed search of bibliographic databases for peer-reviewed research literature using a focused review question and inclusion/ exclusion criteria has been done for this article. Conclusion: In this review article, the synthesis and structure-activity relationships of phenstatin and a wide number of their reported analogues with modifications to ring A, ring B, and to the keto position are discussed in the perspective of medicinal chemistry with proper conclusion.

APA, Harvard, Vancouver, ISO, and other styles

49

Chernyshova, Natalia B., Dmitry V. Tsyganov, Victor N. Khrustalev, Mikhail M. Raihstat, Leonid D. Konyushkin, Roman V. Semenov, Marina N. Semenova, and Victor V. Semenov. "Synthesis and antimitotic properties of ortho-substituted polymethoxydiarylazolopyrimidines." Arkivoc 2017, no. 3 (June 20, 2017): 151–65. http://dx.doi.org/10.24820/ark.5550190.p010.031.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Alias, Yatimah, Khalijah Awang, A. Hamid A. Hadi, Odile Thoison, Thierry Sévenet, and Mary Païs. "An Antimitotic and Cyctotoxic Chalcone from Fissistigma lanuginosum." Journal of Natural Products 58, no. 8 (August 1995): 1160–66. http://dx.doi.org/10.1021/np50122a002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Antimitotic'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles