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Bioarray Therapeutics
Boston, MA, United States
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Salgado D.M.,South Colombian University | Eltit J.M.,Brigham and Women's Hospital | Eltit J.M.,University of Chile | Mansfield K.,Harvard University | And 11 more authors.
Pediatric Infectious Disease Journal | Year: 2010

Background: Dengue fever is one of the most significant re-emerging tropical diseases, despite our expanding knowledge of the disease, viral tropism is still not known to target heart tissues or muscle. Methods: A prospective pediatric clinical cohort of 102 dengue hemorrhagic fever patients from Colombia, South America, was followed for 1 year. Clinical diagnosis of myocarditis was routinely performed. Electrocardiograph and echocardiograph analysis were performed to confirm those cases. Immunohistochemistry for detection of dengue virus and inflammatory markers was performed on autopsied heart tissue. In vitro studies of human striated skeletal fibers (myotubes) infected with dengue virus were used as a model for myocyte infection. Measurements of intracellular Ca concentration as well as immunodetection of dengue virus and inflammation markers in infected myotubes were performed. Results: Eleven children with dengue hemorrhagic fever presented with symptoms of myocarditis. Widespread viral infection of the heart, myocardial endothelium, and cardiomyocytes, accompanied by inflammation was observed in 1 fatal case. Immunofluorescence confocal microscopy showed that myotubes were infected by dengue virus and had increased expression of the inflammatory genes and protein IP-10. The infected myotubes also had increases in intracellular Ca concentration. Conclusions: Vigorous infection of heart tissues in vivo and striated skeletal cells in vitro are demonstrated. Derangements of Ca storage in the infected cells may directly contribute to the presentation of myocarditis in pediatric patients. © 2010 Lippincott Williams & Wilkins.

Martin K.J.,Bioarray Therapeutics | Fournier M.V.,Bioarray Therapeutics | Veer Reddy G.P.,Ford Motor Company | Pardee A.B.,Dana-Farber Cancer Institute
Cancer Research | Year: 2010

Cancer continues to be a major cause of mortality despite decades of effort and expense. The problem reviewed here is that before many cancers are discovered they have already progressed to become drug resistant or metastatic. Biomarkers found in blood or other body fluids could supplement current clinical indicators to permit earlier detection and thereby reduce cancer mortality. ©2010 AACR.

Fata J.E.,CUNY - College of Staten Island | Fata J.E.,City University of New York | Debnath S.,CUNY - College of Staten Island | Debnath S.,City University of New York | And 3 more authors.
International Journal of Cell Biology | Year: 2012

A large amount of data supports the view that PTEN is a bona fide tumor suppressor gene. However, recent evidence suggests that derailment of cellular localization and expression levels of functional nonmutated PTEN is a determining force in inducing abnormal cellular and tissue outcomes. As the cellular mechanisms that regulate normal PTEN enzymatic activity resolve, it is evident that deregulation of these mechanisms can alter cellular processes and tissue architecture and ultimately lead to oncogenic transformation. Here we discuss PTEN ubiquitination, PTEN complex formation with components of the adherens junction, PTEN nuclear localization, and microRNA regulation of PTEN as essential regulatory mechanisms that determine PTEN function independent of gene mutations and epigenetic events. Copyright 2012 Jimmie E. Fata et al.

Methods and compositions for determining and/or predicting a response to a therapy, prognosis of a cancer subject or survival of a cancer and kits for performing the same are described herein.

PubMed | Bioarray Therapeutics
Type: Journal Article | Journal: Journal of clinical oncology : official journal of the American Society of Clinical Oncology | Year: 2016

e21071 Background: Accurate stratification of patients prior to treatment with combination chemotherapy would allow non-responders to receive an alternative treatment in a timely manner and potentially improve clinical outcomes. We describe a 22-gene signature that accurately predicts response to antimitotic combination chemotherapy for breast cancer. This signature was selected in a well characterized system that models a key step disrupted in tumorigenesis: the formation of spatially accurate mammary ductal units by breast epithelial cells. Hence the 22 genes represent a biological process that is independent of any specific patient set or predefined clinical classification.To determine whether genes with differential expression during human mammary acinar morphogenesis predict response to combination chemotherapy in breast cancer, we have analyzed results from two published microarray datasets (Fournier, et al., 2006; Popovici et al., 2010). Expression levels of the majority of genes that were coordinately down regulated during acini formation were significantly associated with response to combination chemotherapy treatment. A 22-gene signature representing the down regulated genes was evaluated independently in each of three breast cancer clinical subgroups, ER-positive (n=146), HER2-positive (n=41), and triple negative (n=90) using two methods of analysis, hierarchical clustering and logistic regression.Hierarchical cluster analysis results showed that the 22 genes accurately stratified patients in each of the three subgroups by response (Fishers Exact p<0.05). Logistic regression with 3-fold cross validation demonstrated that different models accurately predicted response in these subgroups (AUC 0.7). We have observed that the 22-gene signature is broadly effective across independent patient clinical subgroups in its ability to stratify patients according to chemotherapy response in breast cancer.The 22-gene signature has the potential to provide patients, early in the care process, with accurate and personalized information to predict response to combination chemotherapy.

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