Portland, OR, United States

Oregon Health And Science University

www.ohsu.edu
Portland, OR, United States

Oregon Health & Science University is a public university in Oregon with a main campus, including two hospitals, in Portland. It was formed in 1974 as the University of Oregon Health science Center, combining state dentistry, medicine, and nursing programs into a single center Wikipedia.


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Patent
Oregon Health And Science University | Date: 2016-11-18

Mutant mono ADP-ribose-polymerases (mono-PARP) proteins and small molecule compound substrates specific for the mutant mono-PARP proteins as well as methods of using these compositions to identify protein targets of the mono-PARPs and to screen for antagonists of the mono-PARPs are described.


Patent
Oregon Health And Science University | Date: 2016-11-18

Immunohistochemical (IHC) techniques that enable the sequential evaluation of at least seven biomarkers in one formalin-fixed paraffin-embedded (FFPE) tissue section are disclosed. The methods involve high-throughput multiplexed, quantitative IHC imaging, sequential IHC with iterative labeling, digital scanning, image coregistration and merging, and subsequent stripping of sections.


Patent
Pdx Pharmaceuticals, Llc and Oregon Health And Science University | Date: 2017-02-10

Disclosed herein are nanoconstructs comprising a nanoparticle, coated with additional agents such as cationic polymers, stabilizers, targeting molecules, labels, oligonucleotides and small molecules. These constructs may be used to deliver compounds to treat solid tumors and to diagnose cancer and other diseases. Further disclosed are methods of making such compounds and use of such compounds to treat or diagnose human disease.


Jacques S.L.,Oregon Health And Science University
Physics in Medicine and Biology | Year: 2013

A review of reported tissue optical properties summarizes the wavelength-dependent behavior of scattering and absorption. Formulae are presented for generating the optical properties of a generic tissue with variable amounts of absorbing chromophores (blood, water, melanin, fat, yellow pigments) and a variable balance between small-scale scatterers and large-scale scatterers in the ultrastructures of cells and tissues. © 2013 Institute of Physics and Engineering in Medicine.


Corless C.L.,Oregon Health And Science University
Modern Pathology | Year: 2014

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the GI tract, arising from the interstitial cells of Cajal, primarily in the stomach and small intestine. They manifest a wide range of morphologies, from spindle cell to epithelioid, but are immunopositive for KIT (CD117) and/or DOG1 in essentially all cases. Although most tumors are localized at presentation, up to half will recur in the abdomen or spread to the liver. The growth of most GISTs is driven by oncogenic mutations in either of two receptor tyrosine kinases: KIT (75% of cases) or PDGFRA (10%). Treatment with tyrosine kinase inhibitors (TKIs) such as imatinib, sunitinib, and regorafenib is effective in controlling unresectable disease; however, drug resistance caused by secondary KIT or PDGFRA mutations eventually develops in 90% of cases. Adjuvant therapy with imatinib is commonly used to reduce the likelihood of disease recurrence after primary surgery, and for this reason assessing the prognosis of newly resected tumors is one of the most important roles for pathologists. Approximately 15% of GISTs are negative for mutations in KIT and PDGFRA. Recent studies of these so-called wild-type GISTs have uncovered a number of other oncogenic drivers, including mutations in neurofibromatosis type I, RAS genes, BRAF, and subunits of the succinate dehydrogenase complex. Routine genotyping is strongly recommended for optimal management of GISTs, as the type and dose of TKI used for treatment is dependent on the mutation identified. © 2014 USCAP, Inc.


McCormick J.A.,Oregon Health And Science University | Ellison D.H.,Oregon Health And Science University
Physiological Reviews | Year: 2011

WNKs are serine/threonine kinases that comprise a unique branch of the kinome. They are so-named owing to the unusual placement of an essential catalytic lysine. WNKs have now been identified in diverse organisms. In humans and other mammals, four genes encode WNKs. WNKs are widely expressed at the message level, although data on protein expression is more limited. Soon after the WNKs were identified, mutations in genes encoding WNK1 and -4 were determined to cause the human disease familial hyperkalemic hypertension (also known as pseudohypoaldosteronism II, or Gordon's Syndrome). For this reason, a major focus of investigation has been to dissect the role of WNK kinases in renal regulation of ion transport. More recently, a different mutation in WNK1 was identified as the cause of hereditary sensory and autonomic neuropathy type II, an early-onset autosomal disease of peripheral sensory nerves. Thus the WNKs represent an important family of potential targets for the treatment of human disease, and further elucidation of their physiological actions outside of the kidney and brain is necessary. In this review, we describe the gene structure and mechanisms regulating expression and activity of the WNKs. Subsequently, we outline substrates and targets of WNKs as well as effects of WNKs on cellular physiology, both in the kidney and elsewhere. Next, consequences of these effects on integrated physiological function are outlined. Finally, we discuss the known and putative pathophysiological relevance of the WNKs. Copyright © 2011 the American Physiological Society.


Hanahan D.,Ecole Polytechnique Federale de Lausanne | Coussens L.,Oregon Health And Science University
Cancer Cell | Year: 2012

Mutationally corrupted cancer (stem) cells are the driving force of tumor development and progression. Yet, these transformed cells cannot do it alone. Assemblages of ostensibly normal tissue and bone marrow-derived (stromal) cells are recruited to constitute tumorigenic microenvironments. Most of the hallmarks of cancer are enabled and sustained to varying degrees through contributions from repertoires of stromal cell types and distinctive subcell types. Their contributory functions to hallmark capabilities are increasingly well understood, as are the reciprocal communications with neoplastic cancer cells that mediate their recruitment, activation, programming, and persistence. This enhanced understanding presents interesting new targets for anticancer therapy. © 2012 Elsevier Inc.


Rotwein P.,Oregon Health And Science University
Trends in Endocrinology and Metabolism | Year: 2012

Growth hormone (GH) and insulin-like growth factor-I (IGF-I) exert powerful influences on somatic growth, metabolism, and tissue repair, and have been implicated in aging and carcinogenesis. Since the formulation of the somatomedin hypothesis over 50 years ago, GH and IGF-I have been linked intimately to one another. Recent studies have established that GH potently stimulates IGF-I gene transcription, and through this mechanism controls production of IGF-I. A key mediator of the GH-IGF-I biosynthetic pathway is the latent transcription factor Stat5b. This review summarizes the potentially complex mechanistic relationship between GH action, Stat5b, and IGF-I gene activation, and suggests that Stat5b may have a broad role in mediating IGF-I gene regulation in response to diverse physiological inputs. © 2012 Elsevier Ltd.


Sack R.L.,Oregon Health And Science University
New England Journal of Medicine | Year: 2010

A 55-year-old physician is planning a trip from Los Angeles to London to attend a scientific conference. His previous trip to Europe was complicated by sleepiness during meetings and difficulty falling asleep and remaining asleep at night. He wants to know what he can do to avoid jet lag. What would you advise? Copyright © 2010 Massachusetts Medical Society.


Lieberman D.,Oregon Health And Science University
Gastroenterology | Year: 2010

Colorectal cancer is a leading cause of cancer death throughout the world. There is evidence that screening of average-risk individuals can result in mortality reduction with early cancer detection and cancer prevention by detection and removal of cancer precursor lesions. The optimal form of screening is not clear. Fecal screening tests can be performed at home at low initial cost, but current versions lack high sensitivity for cancer precursor lesions, and tests need to be repeated at regular intervals. Adherence to repeat testing for negative tests and referral for colonoscopy for positive tests are important elements of program effectiveness. Structural examinations of the colon are more invasive and may result in detection of both early cancer and cancer precursor lesions. Every screening program has advantages and limitations, but each program ultimately depends on quality and patient adherence. © 2010 AGA Institute.

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