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Cancer Clinical Trials (cancer + clinical_trials)
Selected AbstractsExact Tests using Two Correlated Binomial Variables in Contemporary Cancer Clinical TrialsBIOMETRICAL JOURNAL, Issue 6 2009Jihnhee Yu Abstract New therapy strategies for the treatment of cancer are rapidly emerging because of recent technology advances in genetics and molecular biology. Although newer targeted therapies can improve survival without measurable changes in tumor size, clinical trial conduct has remained nearly unchanged. When potentially efficacious therapies are tested, current clinical trial design and analysis methods may not be suitable for detecting therapeutic effects. We propose an exact method with respect to testing cytostatic cancer treatment using correlated bivariate binomial random variables to simultaneously assess two primary outcomes. The method is easy to implement. It does not increase the sample size over that of the univariate exact test and in most cases reduces the sample size required. Sample size calculations are provided for selected designs. [source] Antiangiogenic drugs: Current knowledge and new approaches to cancer therapyJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 10 2008Jose L. Mauriz Abstract Angiogenesis,process of new blood-vessel growth from existing vasculature,is an integral part of both normal developmental processes and numerous pathologies such as cancer, ischemic diseases and chronic inflammation. Angiogenesis plays a crucial role facilitating tumour growth and the metastatic process, and it is the result of a dynamic balance between proangiogenic and antiangiogenic factors. The potential to block tumour growth and metastases by angiogenesis inhibition represents an intriguing approach to the cancer treatment. Angiogenesis continues to be a topic of major scientific interest; and there are currently more antiangiogenic drugs in cancer clinical trials than those that fit into any other mechanistic category. Based on preclinical studies, researchers believe that targeting the blood vessels which support tumour growth could help treatment of a broad range of cancers. Angiogenic factors or their receptors, endothelial cell proliferation, matrix metalloproteinases or endothelial cell adhesion, are the main targets of an increasing number of clinical trials approved to test the tolerance and therapeutic efficacy of antiangiogenic agents. Unfortunately, contrary to initial expectations, it has been described that antiangiogenic treatment can cause different toxicities in cancer patients. The purpose of this article is to provide an overview of current attempts to inhibit tumour angiogenesis for cancer therapy. © 2008 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 97:4129,4154, 2008 [source] Solamargine upregulation of Fas, downregulation of HER2, and enhancement of cytotoxicity using epirubicin in NSCLC cellsMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 8 2007Chia-Hua Liang Abstract Nonsmall-cell lung cancer (NSCLC) is not generally a chemosensitive tumor, and the mechanism of resistance to the relevant anticancer drugs has not been fully elucidated. Solamargine (SM), the major steroidal glycoalkaloids extracted from the Chinese herb Solanum, inhibits the growth of human tumor cells. We have previously demonstrated that SM regulates tumor necrosis factor receptors (TNFRs)- and mitochondria-mediated pathways and sensitizes NSCLC cells to initiate apoptosis. Interestingly, this investigation reveals that SM up-regulated Fas expression and down-regulated the expression of HER2, whose overexpression is associated with resistance to drugs, and promotes chemotherapy-induced apoptosis in NSCLC A549 and H441 cells. After treatment with SM, the expression of HER2 mRNA was correlated with the expression of topoisomerase II, (TOP2A) mRNA. The combinatory use of low concentrations of SM with low-toxic topoisomerase II inhibitor epirubicin accelerated apoptotic cell death. Therefore, the downregulation of the HER2 and TOP2A expression by SM with epirubicin may partially explain the SM and epirubicin cytotoxicity synergy effect in NSCLC. Results of this study suggest that SM induces Fas and TNFR-induced NSCLC cell apoptosis and reduces HER2 expression. These findings provide the synergistic therapeutic interaction between SM and epirubicin, suggesting that such combinations may be effectively exploited in future human cancer clinical trials. [source] Recruitment to breast cancer clinical trials: What makes a difference?CA: A CANCER JOURNAL FOR CLINICIANS, Issue 1 2009Mary Desmond Pinkowish News & Views Editor No abstract is available for this article. [source] From the Editors: Encouraging participation in cancer clinical trials, one step at a timeCA: A CANCER JOURNAL FOR CLINICIANS, Issue 6 2000T. Gansler First page of article [source] Clinical trial accrual among new cancer patients at a community-based cancer center,CANCER, Issue 2 2006A prospective study Abstract BACKGROUND To the authors' knowledge, only limited data are available regarding clinical trial accrual patterns and the barriers encountered among newly diagnosed patients seen at community-based cancer centers. METHODS In the current study, the authors prospectively collected clinical and sociodemographic data from all adult patients seen at a community-based cancer center who had new cancers diagnosed between 2003,2004. Clinical trial enrollment decisions were noted and factors that prevented accrual were identified. RESULTS There was a total of 1012 new cancer patients. In 587 patients (58%), clinical trials appropriate for the diagnosis and stage of disease were not available. Among those patients for whom trials were available, 19.8% did not meet eligibility criteria, and only 9.9% of patients were enrolled. Although more trials were found to be available for women compared with men (51% vs. 32%; P < 0.01), the accrual rates were equal (11.2% vs. 7.6%; P = 0.24). Elderly patients comprised approximately 59.4% of those patients with available trials, but they were less likely to be enrolled (5.1% vs. 16.8%; P < 0.01). The major barriers to nonparticipation can be grouped into protocol limitations (68.1%), physician triage (16%), and patient decisions (15.9%). The overall accrual rate when all patients were included was 4% (42 of 1012 patients). CONCLUSIONS At the study institution, participation in clinical trials is reported to be low. The unavailability of appropriate clinical trials represents the most significant barrier. Continuing efforts to encourage physicians and to educate patients remain necessary. If the current study findings are found to be applicable to other community-based cancer centers, making a larger variety of clinical trials available to the community may help to improve the accrual of patients to national cancer clinical trials. Cancer 2006. © 2005 American Cancer Society. [source] | ||||||||||