Abstract

The Proteomics Shared Resource provides modern tools of mass spectrometry to Knight Cancer Institute members so that they may determine the identity, abundance, and modifications occurring in proteins, the building blocks of the cell. These analyses are crucial to understanding the cause of cancer and devising improved treatments for the disease, since changes in proteins occur in all forms of cancer. Support will be used to partially fund salaries of five staff and four state-of-the-art mass spectrometers to assist Knight investigators studying cancer-causing changes in proteins, including phosphorylation, acetylation, changes in abundance and altered binding to other proteins. A wide array of informatics tools and expertise will also be provided to Knight members to increase their research productivity. The results from the Proteomics Shared Resource will be used to better treat cancer patients by providing earlier diagnosis of the disease and discovering more effective treatments that are personalized for individual patients.

Public Health Relevance

Alterations in proteins occur in all forms of cancer, and the study of proteins is crucial to devising new treatments and allowing early detection of the disease. The requested support will provide state-of-the-art mass spectrometry and proteomics technologies to Knight Cancer Institute members at The Oregon Health &Science University to speed progress in cancer research.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA069533-17
Application #
8712379
Study Section
Subcommittee B - Comprehensiveness (NCI)
Project Start
Project End
Budget Start
2014-07-01
Budget End
2015-06-30
Support Year
17
Fiscal Year
2014
Total Cost
Indirect Cost

  Institution

Name
Oregon Health and Science University
Department
Type
DUNS #
City
Portland
State
OR
Country
United States
Zip Code
97239

  Publications

Lane, Ryan S; Femel, Julia; Breazeale, Alec P et al. (2018) IFN?-activated dermal lymphatic vessels inhibit cytotoxic T cells in melanoma and inflamed skin. J Exp Med 215:3057-3074
Smith, Nicholas R; Swain, John R; Davies, Paige S et al. (2018) Monoclonal Antibodies Reveal Dynamic Plasticity Between Lgr5- and Bmi1-Expressing Intestinal Cell Populations. Cell Mol Gastroenterol Hepatol 6:79-96
Langer, E M; Kendsersky, N D; Daniel, C J et al. (2018) ZEB1-repressed microRNAs inhibit autocrine signaling that promotes vascular mimicry of breast cancer cells. Oncogene 37:1005-1019
Sorace, Anna G; Partridge, Savannah C; Li, Xia et al. (2018) Distinguishing benign and malignant breast tumors: preliminary comparison of kinetic modeling approaches using multi-institutional dynamic contrast-enhanced MRI data from the International Breast MR Consortium 6883 trial. J Med Imaging (Bellingham) 5:011019
Medler, Terry R; Murugan, Dhaarini; Horton, Wesley et al. (2018) Complement C5a Fosters Squamous Carcinogenesis and Limits T Cell Response to Chemotherapy. Cancer Cell 34:561-578.e6
Kelley, Katherine A; Wieghard, Nicole; Chin, Yuki et al. (2018) MiR-486-5p Downregulation Marks an Early Event in Colorectal Carcinogenesis. Dis Colon Rectum 61:1290-1296
Davare, Monika A; Henderson, Jacob J; Agarwal, Anupriya et al. (2018) Rare but Recurrent ROS1 Fusions Resulting From Chromosome 6q22 Microdeletions are Targetable Oncogenes in Glioma. Clin Cancer Res 24:6471-6482
Kurtz, Stephen E; Eide, Christopher A; Kaempf, Andy et al. (2018) Dual inhibition of JAK1/2 kinases and BCL2: a promising therapeutic strategy for acute myeloid leukemia. Leukemia 32:2025-2028
Sehrawat, Archana; Gao, Lina; Wang, Yuliang et al. (2018) LSD1 activates a lethal prostate cancer gene network independently of its demethylase function. Proc Natl Acad Sci U S A 115:E4179-E4188
Watson, Spencer S; Dane, Mark; Chin, Koei et al. (2018) Microenvironment-Mediated Mechanisms of Resistance to HER2 Inhibitors Differ between HER2+ Breast Cancer Subtypes. Cell Syst 6:329-342.e6

Showing the most recent 10 out of 277 publications