@article {642,
	title = {Anticancer agents from unique natural products sources},
	journal = {Pharmaceutical Biology},
	volume = {41},
	year = {2003},
	note = {ISI Document Delivery No.: 877RKTimes Cited: 5Cited Reference Count: 8344th Annual Meeting of the American-Society-of-PharmacognosyJUL 12-16, 2003Chapel Hill, NCAmer Soc PharmacognosySuppl. S},
	pages = {15-38},
	type = {Proceedings Paper},
	abstract = {The National Cooperative Natural Products Drug Discovery Group (NCNPDDG) "Anticancer Agents from Unique Natural Products Sources, CA 67786" was first awarded in September 1995. The goal of the project is to discover and develop novel anticancer agents from a variety of natural products sources. The key accomplishments of this NCDDG which will be highlighted in this manuscript include: Development of tools to probe fungi for the production of novel natural products by DNA-based probes. Discovery that the majority of these fungi can produce natural products via nonribosomal peptide synthetases, polyketide synthases, or both - a much larger percentage than current culturing techniques reveal. Identification of the MDR-selective cytotoxic agent austocystin D, and use of a novel yeast deletion strain approach to help identify its molecular target(s). Identification of hemiasterlin and other naturally occurring analogs as potent antimitotic agents with excellent in vivo activity against human solid tumors in mouse models. Development of a total synthesis of hemiasterlin. The utilization of this methodology to provide the first SAR for the hemiasterlin family of antimitotic agents and to identify the synthetic analog HTI-286, which is being examined in clinical trials as an anticancer agent. To provided technology transfer, educational opportunities and compensation to countries of origin for collection and study of their natural product resources. This NCNPDDG program has provided funding to research programs at the University of the Philippines, The University of the South Pacific in the Fiji Islands, Colombo University in Sri Lanka, the Instituto de Quimica de Sao Carlos, Universidade de Sao Paulo, Brazil, and the University of Papua New Guinea.},
	keywords = {ACTIVATED PROTEIN-KINASE, antitumor agents, austocystins, CYCLIN-DEPENDENT KINASES, CYTOTOXIC PEPTIDES, fungi, GROWTH-FACTOR RECEPTOR, hemiasterlins, IN-VIVO, LINKED-IMMUNOSORBENT-ASSAY, MARINE, MICROORGANISMS, MULTIDRUG-RESISTANCE, natural products, NCDDG, sponges, TRIPEPTIDE HEMIASTERLIN, TUMOR-CELL LINES, TYROSINE KINASE},
	isbn = {1388-0209},
	url = {<Go to ISI>://000225587500004},
	author = {Ireland, C. M. and Aalbersberg, W. and Andersen, R. J. and Ayral-Kaloustian, S. and Berlinck, R. G. S. and Bernan, V. and Carter, G. and Churchill, A. C. L. and Clardy, J. and Concepcion, G. P. and De Silva, E. D. and Discafani, C. and Fojo, T. and Frost, P. and Gibson, D. and Greenberger, L. M. and Greenstein, M. and Harper, M. K. and Mallon, R. and Loganzo, F. and Nunes, M. and Poruchynsky, M. S. and Zask, A.}
}
@article {5181,
	title = {G(2) DNA damage checkpoint inhibition and antimitotic activity of 13-hydroxy-15-oxozoapatlin},
	journal = {Journal of Biological Chemistry},
	volume = {276},
	number = {51},
	year = {2001},
	note = {ISI Document Delivery No.: 505QLTimes Cited: 24Cited Reference Count: 51},
	month = {Dec},
	pages = {48231-48236},
	type = {Article},
	abstract = {Checkpoints activated in response to DNA damage cause arrest in the G(1) and G(2) phases of the cell cycle. Inhibitors of the G(2) checkpoint may be used as tools to study this response and also to increase the effectiveness of DNA-damaging therapies against cancers lacking p53 function. Using a cell-based assay for G(2) check. point inhibitors, we have screened extracts from the NCI National Institutes of Health Natural Products Repository and have identified 13-hydroxy-15-oxozoapatlin (OZ) from the African tree Parinari curatellifolia. Flow cytometry with a mitosis-specific antibody showed that checkpoint inhibition by OZ was maximal at 10 muM, which released 20\% of irradiated MCF-7 cells expressing defective p53 and 30\% of irradiated HCT116p53(-/-) cells from G(2) arrest. OZ additively increased the response to the checkpoint inhibitors isogranulatimide and debromohymenialdisine, but it did not augment the effects of UCN-01 or caffeine. Unlike other checkpoint inhibitors, OZ did not inhibit ataxia-telangiectasia mutated (ATM), ATM and Rad3-related (ATR), Chk1, Chk2, Plk1, or Ser/Thr protein phosphatases in vitro. Treatment with OZ also caused G(2)-arrested and cycling cells to arrest in mitosis in a state resembling prometaphase. In these cells, the chromosomes were condensed and scattered over disordered mitotic spindles. The results demonstrate that OZ is both a G(2) checkpoint inhibitor and an antimitotic agent.},
	keywords = {ARREST, BHK CELLS, CAFFEINE, CELL-CYCLE CHECKPOINTS, CHROMOSOME ALIGNMENT, G2, P34(CDC2) KINASE, PROTEIN-KINASE, RADIOSENSITIZING AGENT, TYROSINE KINASE, UCN-01},
	isbn = {0021-9258},
	url = {<Go to ISI>://000172927000066},
	author = {Rundle, N. T. and Xu, L. and Andersen, R. J. and Roberge, M.}
}
