Nature has been a source of medical treatments for thousands of years, and plant based systems continue to play an essential role in the primary health care of 80% of the world’ population. Nature has provided many of the effective anticancer agents in current use, such as the microbial derived drugs, dactinomycin, bleomycin, and doxorubicin, and the plant derived drugs vinblastine, irinotecan, topotecan, etoposide and paclitaxel. The search for novel anti-cancer from nature source continues with botanists, marine biologists and microbiologist team-ing up with chemists, pharmacologist, toxicologists and clinicans in the investigation of coral reefs, rain forests, and deep subsurface thermal vents for novel bioactive compounds. The wealth of anticancer drugs of nature origin and critical aspects of the ongoing discovery and development process are discussed.
Medicine, Traditional ; Neoplasms ; Antimitotic Agents

In Vietnam, some medicinal plants have been administrated for cancer treatment. But those medicinal plants have only been used based on experiences and their actual anticancer efficacy have not been proven yet. For that reason, studying to prove anticancer efficacy of those plants is very necessary. In 16 selected medicinal plants had been researched, there were 14 medicinal plants having effect on anti cellular division rate on schizogenous tissue of raphanus sativus L. higher than 50%. They were agave americana L., acanthopanax aculeatus seem, angelica decursiva (Miq) Fr.et Sav., spilanthes acmella (L.) Murr., garcinia cambodgiensis vesque, gleditsia australis hemsl, hippeastrum equestre (Ait.) herb., grium sp. (X2, X3, X4), amarathus tricolor L. and allium sativum L..
Neoplasms ; Plants, Medicinal ; Medicine, Traditional ; Antimitotic Agents

The most common cause of blurred vision after extracapsular cataract extraction is known to be an opacification of the posterior lens capsule. The pathogenesis of posterior lens capsule opacification is primarily caused by residual lens epithelial cells. For the prevention of posterior capsular opacification, several kinds of anti-mitotic drugs is being actively investigated. But the antimitotic drugs are not clinically used due to toxicity towards the intraocular tissues. The objectives of this study is to evaluate the effect of mitomycin C and tirilazad mesylate(FREEDOX(TM)) respectively for inhibiting the proliferation of rabbit lens epithelial cells when it is administered in a short period. Lens epithelial cells from white rabbits were harvested andcultured for 4 passages. Mitomycin C was applied for 3 minutes with 0.025mg/ml and 0.05mg/ml in concentration respectively. The proliferation assay was performed by [(3)H]-thymidine uptake test. Significant decrease of lens epithelial cell proliferation appeared in both drugs.When Mitomycin-C was applied with 0.025mg/ml for 3 minutes, cell proliferation was reduced to 31.5% compared with control and in 0.05mg/ml concentration, to 12.5%. When tirilazad mesylate was applied 0.15mg/ml for 3 minutes, cell proliferation was reduced to 46.5% compared with control and in 1.5mg/ml concentration, to 7.5%. If futher investigation would show the effectives and safety of these drugs, these agents could be applied into the lens capsular bad at the time of surgery to prevent the posterior capsular opacification after cataract surgery.
Antimetabolites* ; Antimitotic Agents ; Capsule Opacification ; Cataract ; Cataract Extraction ; Cell Proliferation ; Epithelial Cells* ; Mesylates ; Mitomycin ; Rabbits

BACKGROUND: Arsenic trioxide (As2O3) is a well-known and effective treatment that can result in clinical remission for patients diagnosed with acute promyelocytic leukemia (APL). The biologic efficacy of As2O3 in APL and solid tumor cells has been explained through its actions on anti-proliferation, anti-angiogenesis, and apoptotic signaling pathways. We theorize that As2O3 activates a pathway that disrupts microtubule dynamics forming abnormal, nonfunctioning mitotic spindles, thus preventing cellular division. In this study, we investigated how As2O3 induces apoptosis by causing microtubule dysfunction. METHODS: Cultured NB4 cells were treated with As2O3, paclitaxel, and vincristine. Flow cytometric analysis was then performed. An MTT assay was used to determine drug-mediated cytotoxicity. For tubulin polymerization assay, each polymerized or soluble tubulin was measured. Microtubule assembly-disassembly was measured using a tubulin polymerization kit. Cellular microtubules were also observed with fluorescence microscopy. RESULTS: As2O3 treatment disrupted tubulin assembly resulting in dysfunctional microtubules that cause death in APL cells. As2O3 markedly enhanced the amount of depolymerized microtubules. The number of microtubule posttranslational modifications on an individual tubulin decreased with As2O3 concentration. Immunocytochemistry revealed changes in the cellular microtubule network and formation of polymerized microtubules in As2O3-treated cells. CONCLUSION: The microtubules alterations found with As2O3 treatment suggest that As2O3 increases the depolymerized forms of tubulin in cells and that this is potentially due to arsenite's negative effects on spindle dynamics.
Antimitotic Agents ; Apoptosis ; Arsenic ; Arsenicals ; Cell Line ; Fluorescence ; Humans ; Immunohistochemistry ; Leukemia, Promyelocytic, Acute ; Microtubules ; Oxides ; Paclitaxel ; Polymerization ; Polymers ; Protein Processing, Post-Translational ; Tubulin ; Vincristine

The inv(16)(p13q22) is found in de novo AML and is closely associated with the FAB subtype M4eo. The inv(16) is rarely reported in therapy-related AML (t-AML) patients. Herein, we report a case of t-AML with inv(16) after combination chemotherapy using antimitotic agent and alkylating agent (cis-platin-paclitaxel) for ovarian serous cystadenocarcinoma.
Antimitotic Agents/*adverse effects/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/*adverse effects/therapeutic use ; Chromosomes, Human, Pair 16/*genetics ; Cisplatin/adverse effects/therapeutic use ; Female ; Humans ; *Inversion, Chromosome ; Leukemia, Myeloid, Acute/*chemically induced/pathology ; Middle Aged ; Taxoids/adverse effects/therapeutic use