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1.  Breakthrough cancer medicine and its impact on novel drug development in China: report of the US Chinese Anti-Cancer Association (USCACA) and Chinese Society of Clinical Oncology (CSCO) Joint Session at the 17th CSCO Annual Meeting 
Chinese Journal of Cancer  2014;33(12):620-624.
The US Chinese Anti-Cancer Association (USCACA) teamed up with Chinese Society of Clinical Oncology (CSCO) to host a joint session at the17th CSCO Annual Meeting on September 20th, 2014 in Xiamen, China. With a focus on breakthrough cancer medicines, the session featured innovative approaches to evaluate breakthrough agents and established a platform to interactively share successful experiences from case studies of 6 novel agents from both the United States and China. The goal of the session is to inspire scientific and practical considerations for clinical trial design and strategy to expedite cancer drug development in China. A panel discussion further provided in-depth advice on advancing both early and full development of novel cancer medicines in China.
PMCID: PMC4308658  PMID: 25418191
Breakthrough; clinical trial; cancer medicine
2.  Preclinical Models of Wound Healing: Is Man the Model? Proceedings of the Wound Healing Society Symposium 
Advances in Wound Care  2013;2(1):1-4.
A review of therapeutic effects in preclinical and clinical studies suggests that concordance between large animal (pig=78%), small laboratory animal (53%) and in vitro (57%) results with those observed in humans is only partial. Pig models of wound healing provide major advantages over other animal models. Since the vast majority of wound-healing research is done in rodents and in vitro, the low concordance rate is a significant impediment to research that will have any clinical impact.
Critical Issues
To generate clinically relevant experimental data, hypothesis generation should begin, or at least involve human wound tissue samples. Such tissue could be used to test a predetermined hypothesis generated based on, say, murine data. Alternatively, such tissue could be analyzed using high-throughput cell biology techniques (e.g., genomics, proteomics, or metabolomics) to identify novel mechanisms involved in human wounds. Once the hypothesis has been formulated and confirmed using human samples, identification of these same mechanisms in animals represents a valid approach that could be used for more in-depth investigations and experimental manipulations not feasible with humans.
Future Directions
This consensus statement issued by the Wound Healing Society symposium strongly encourages all wound researchers to involve human wound tissue validation studies to make their animal and cell biology studies more translationally and clinically significant.
PMCID: PMC3840478  PMID: 24527316
3.  Will Periodic Intravenous Injections of Conditioned Bone Marrow Cells Effectively Reduce Atherosclerosis? 
Antioxidants & Redox Signaling  2012;16(1):85-91.
Maintenance of healthy arteries requires a balance between injuries to the arterial wall and processes of intrinsic arterial repair. Such repair requires the availability of progenitor cells that are local to the wall itself. Progenitor cells from distant reservoirs like the bone marrow may also contribute to repair. Arterial repair seems to degrade over a lifetime, particularly with risk factors such as smoking and diabetes. Hence, a potential preventive/therapeutic strategy for atherosclerosis could be transfusion of competent bone marrow cells (BMCs) to restore effective repair in the face of arterial injury and depleted endogenous repair reservoirs. The challenge with this strategy has been the reliable collection and/or generation of BMCs that support arterial repair. In this study, we describe a set of experiments to elucidate a method of culturing BMCs that robustly retards atherosclerosis development in apolipoprotein E knockout mice. Identifying such a method would represent an important step in developing cell-based treatments for patients with proclivity for developing atherosclerosis. Antioxid. Redox Signal. 16, 85–91.
PMCID: PMC3218380  PMID: 21740335
4.  Transcriptional Control of Serotonin-Modulated Behavior and Physiology 
Neuropsychopharmacology  2010;36(1):361-362.
PMCID: PMC3055526  PMID: 21116255

Results 1-4 (4)