Home About us Contact
|
Home About us Contact | ||
|
|
||
Effective Anticancer Drug (effective + anticancer_drug)
Selected AbstractsExperimental design comparison of studies evaluating doxorubicin nanoparticles in breast cancer therapyHUMAN FACTORS AND ERGONOMICS IN MANUFACTURING & SERVICE INDUSTRIES, Issue 3 2008Farman A. Moayed Background The unique properties of nanoparticles (NP) qualify these colloidal systems for a wide range of medical applications, including diagnosis and treatment. Particularly in cancer therapy, NP have significantly enhanced the potential of conventional imaging, radiotherapy, and chemotherapy and, consequently, offered new avenues for early interventions. So far, breast cancer has been one of the most studied cancer types with NP research, which can benefit the occupational breast cancer for the increasing number of women in the labor force in industry. Objectives The objective of this study is to compare the experimental designs of preclinical studies that assessed the effect of doxorubicin NP (DOX-NP) on the estrogen-dependent MCF-7 breast cancer cell line using a recently established quantitative Experimental Appraisal Instrument (ExpAI). Methods A systematic review of research articles published between August 2004 and August 2005 on NP and breast cancer treatment with doxorubicin was performed using various online databases and indexes available through the University of Cincinnati. Restrictive inclusion and exclusion criteria were defined leading to selection of four relevant articles that used comparable experimental designs. Critical appraisal of those studies was performed by five independent assessors using the ExpAI version 2.0 and the results were summarized in a table of evidence. Results The study design in the selected articles was either between groups or mixed, with sample sizes varying from n = 3,6, and the evaluation of the effect of DOX-NP either in vitro or in vivo. The cytotoxic drug doxorubicin was the input variable in all studies, whereas different end points such as pharmacokinetic parameters, cytotoxicity surrogates (e.g., growth inhibition, mitochondrial activity), and quantitative analysis of messenger RNA were used as output variables. Conclusions Although the articles assessed in this article were preclinical experimental studies, the results showed that doxorubicin NP drugs can be used effectively to enhance the delivery process in MCF-7 breast cancer cells by increasing the circulation time and targeting the tumor tissues. Considering the rising number of women in the labor force and the risk of occupational breast cancer, it can be concluded that DOX-NP may potentially be used as an effective anticancer drug on humans, but further research and studies are required to understand how DOX-NP drugs might react in the human body before using it on breast cancer patients. © 2008 Wiley Periodicals, Inc. [source] Increase of lipid peroxidation by cisplatin in WI38 cells but not in SV40-transformed WI38 cellsJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 1 2003Hsiu-Chuan Yen Abstract Cisplatin (CPT) is an effective anticancer drug that causes cumulative toxicity to normal tissues. It has been suggested that CPT damages normal cells by causing oxidative stress, but it is not known whether it can induce similar oxidative damage to tumor cells. In this study, by using normal human lung fibroblast (W138) cells and SV40-transformed WI38 (VA13) cells as a model, we compared the effect of CPT on cytotoxicity, apoptosis, lipid peroxidation, and mitochondrial gene expression, which could be regulated by oxidative stress, between normal and tumor cells. CPT induced greater growth inhibition and percentage of apoptotic cells in VA13 cells. However, levels of esterified F2 -isoprostanes and 4-hydroxy-2-nonenal, two specific products of lipid peroxidation, were increased by CPT in WI38 cells, but not in VA13 cells. Furthermore, the transcript level of mitochondrial 12S rRNA was augmented by CPT in both cells, but to a higher degree in WI38 cells. The data suggest a correlation between lipid peroxidation and cytotoxicity or increased mitochondrial transcript levels in WI38 cells but not in VA13 cells. The results also indicate an altered response of oxidative damage and mitochondrial gene regulation to CPT in the transformed phenotype of WI38 cells. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:39,46, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10059 [source] Gold compounds as anticancer agents: chemistry, cellular pharmacology, and preclinical studiesMEDICINAL RESEARCH REVIEWS, Issue 3 2010Stefania Nobili Abstract Gold compounds are a class of metallodrugs with great potential for cancer treatment. During the last two decades, a large variety of gold(I) and gold(III) compounds are reported to possess relevant antiproliferative properties in vitro against selected human tumor cell lines, qualifying themselves as excellent candidates for further pharmacological evaluation. The unique chemical properties of the gold center confer very interesting and innovative pharmacological profiles to gold-based metallodrugs. The primary goal of this review is to define the state of the art of preclinical studies on anticancer gold compounds, carried out either in vitro or in vivo. The available investigations of anticancer gold compounds are analyzed in detail, and particular attention is devoted to underlying molecular mechanisms. Notably, a few biophysical studies reveal that the interactions of cytotoxic gold compounds with DNA are generally far weaker than those of platinum drugs, implying the occurrence of a substantially different mode of action. A variety of alternative mechanisms were thus proposed, of which those involving either direct mitochondrial damage or proteasome inhibition or modulation of specific kinases are now highly credited. The overall perspectives on the development of gold compounds as effective anticancer drugs with an innovative mechanism of action are critically discussed on the basis of the available experimental evidence. © 2009 Wiley Periodicals, Inc. Med Res Rev, 30, No. 3, 550,580, 2010 [source] Antimetabolite incorporation into DNA: Structural and thermodynamic basis for anticancer activityBIOPOLYMERS, Issue 3 2002William H. Gmeiner Abstract Antimetabolites are a class of effective anticancer drugs that structurally resemble naturally occurring biochemicals and interfere in essential biochemical processes. In this review, the recent literature describing investigations of the structural and thermodynamic basis for the anticancer activity of three antipyrimidines [1-,- D -arabinofuranosyl cytidine (AraC). 2,,2,-difluoro deoxycytidine (dFdC), and 5-fluoro-2,-deoxyuridine (FdUrd)] is summarized. Our laboratory, and others, have shown that misincorporation of any of these three antipyrimidines into DNA perturbs the structure and decreases the stability of duplex DNA. These data are useful for rationalizing the effects of antipyrimidine misincorporation on the activities of proteins required for DNA replication and repair such as DNA topoisomerase 1 and DNA polymerases. The studies completed to date and summarized in this review demonstrate the utility of investigations into the structure,function relationships between antipyrimidine-substituted DNA complexed with DNA-modifying proteins for the purpose of understanding the basis for effective antipyrimidine cancer chemotherapy and the future design of novel anticancer drugs. © 2002 Wiley Periodicals, Inc. Biopolymers (Nucleic Acid Sci) 65: 180,189, 2002 [source] | ||||||||||