The Sanford-Burnham Medical Research Institute, previously Burnham Institute for Medical Research, is a non-profit medical research institute with locations in La Jolla, California, Orlando, Florida, and Santa Barbara, California. There are more than 850 scientists at Sanford-Burnham; they work on the fundamental molecular causes of various diseases, with research including topics such as cancer, neuroscience, stem cell research, diabetes and obesity.Research at Sanford-Burnham is supported by funding from National Institutes of Health, National Cancer Institute, and Juvenile Diabetes Research Foundation among others, and partnerships with pharmaceutical companies such as Johnson & Johnson Pharmaceutical Research and Development. In 2008, Sanford-Burnham was awarded a $97.9 million grant by NIH to establish a high-throughput screening screening center. Wikipedia.
Towler D.A.,Sanford Burnham Institute for Medical Research
Calcific aortic valve disease (CAVD) increasingly afflicts our aging population. One third of our elderly have echocardiographic or radiological evidence of calcific aortic valve sclerosis, an early and subclinical form of CAVD. Age, sex, tobacco use, hypercholesterolemia, hypertension, and type II diabetes mellitus all contribute to the risk of disease that has worldwide distribution. On progression to its most severe form, calcific aortic stenosis, CAVD becomes debilitating and devastating, and 2% of individuals >60 years are affected by calcific aortic stenosis to the extent that surgical intervention is required. No effective pharmacotherapies exist for treating those at risk for clinical progression. It is becoming increasingly apparent that a diverse spectrum of cellular and molecular mechanisms converge to regulate valvular calcium load; this is evidenced not only in histopathologic heterogeneity of CAVD, but also from the multiplicity of cell types that can participate in valve biomineralization. In this review, we highlight our current understanding of CAVD disease biology, emphasizing molecular and cellular aspects of its regulation. We end by pointing to important biological and clinical questions that must be answered to enable sophisticated disease staging and the development of new strategies to treat CAVD medically. © 2013 American Heart Association, Inc. Source
Back S.H.,University of Ulsan |
Kaufman R.J.,Sanford Burnham Institute for Medical Research
Annual Review of Biochemistry
Given the functional importance of the endoplasmic reticulum (ER), an organelle that performs folding, modification, and trafficking of secretory and membrane proteins to the Golgi compartment, the maintenance of ER homeostasis in insulin-secreting β-cells is very important. When ER homeostasis is disrupted, the ER generates adaptive signaling pathways, called the unfolded protein response (UPR), to maintain homeostasis of this organelle. However, if homeostasis fails to be restored, the ER initiates death signaling pathways. New observations suggest that both chronic hyperglycemia and hyperlipidemia, known as important causative factors of type 2 diabetes (T2D), disrupt ER homeostasis to induce unresolvable UPR activation and β-cell death. This review examines how the UPR pathways, induced by high glucose and free fatty acids (FFAs), interact to disrupt ER function and cause β-cell dysfunction and death. © 2012 by Annual Reviews. All rights reserved. Source
Wolf D.A.,Sanford Burnham Institute for Medical Research
A series of recent reports has suggested PGC1α-driven upregulation of mitochondrial oxidative phosphorylation as a selective vulnerability of drug-resistant cancers. Accordingly, chemical inhibitors of respiration led to selective eradication of such cancer cells due to their preferential sensitivity to mitochondrial production of reactive oxygen species. These insights create a timely opportunity for a biomarker guided application of already existing and newly emerging mitochondrial inhibitors in recurrent drug-resistant cancer, including lymphomas, melanomas, and other malignant diseases marked by increased mitochondrial respiration. © 2014 Elsevier Inc. Source
Sanford Burnham Institute for Medical Research | Date: 2014-07-14
Disclosed are compositions and methods useful for targeting tumors, sites of injury and blood clots. The compositions and methods are based on peptide sequences that selectively bind to and home to tumors, sties of injury and blood clots in animals. The disclosed targeting is useful for delivering therapeutic and detectable agents to tumors, sites of injury and blood clots.
Sanford Burnham Institute for Medical Research | Date: 2014-11-26
We used ACCUTASE, a commercially available cell detachment solution, for single cell propagation of pluripotent hESCs. Unlike trypsin dissociation, ACCUTASE treatment does not significantly affect the plating efficiency of hESC dissociation into single cells. Cultures dissociated with ACCUTASE to single cells at each passage maintain a higher proportion of pluripotent cells as compared to collagenase-passaged hESCs. ACCUTASE-treated hESCs can be grown to a high density as monolayers, and yet retain their pluripotency.