The Biomarkers Core contributes to the overall program project in the;a) collection of large numbers of biologic samples in support of Projects 1, 2, and 3, b) storage and archiving of all biologic samples, c) histologic services for the sectioning of tissue blocks in support of Projects 1, 2, and 3, d) pathology review of ail tissue samples (Projects 1, 2, and 3), d) standardization of sample acquisition, fixation and/or time to freezing, and sample storage, e) distribution of samples from Projects 1, 2, and 3 to co-Investigators/collaborators, in the case of assays done off-site, f) measurement of biomarker expression in skin biopsies (Projects 1, 2, and 3), and g) measurement of agent levels in blood and periodic quality control of agents developed for clinical application in support of Core D (Project 3). We have evaluated, analyzed, and optimized assays used in the Biomarker Core and have an extensive history of measurement of analytes in both plasma and serum. In collaboration with Biometry and Data Management (Core B), the Biomarker Core has carried out the sample analyses and interacted with each Project on the transfer and/or analysis of samples, as well as on the management and interpretation of the results. Assays provided by the Core will include immunohistochemical method development and analysis, karyometric sample preparation, as well as the measurement of agent levels in skin and blood. The Core has added a proteomic methodology, Reverse Phase Protein Microarray (RPMA), a novel application for multiplexed quantitative measurement of multiple signaling proteins, many of which are phosphoproteins, from biological specimens. RPMA represents a novel means of measurement of hundreds of proteins from a single specimen. A second novel methodology in this Program Project is quantitative Nuclease Protection Assay (qNPA), a method for mRNA analysis from small tissue sections of formalin fixed paraffin embedded (FFPE) samples of selected genes arrayed onto a platform. qNPA will be a developmental aim in the Program Project and each project selected specific genes to be arrayed onto this platform including genes associated with skin cells and their transition into cancer and metastasis. This highly interactive and clinically translational research program project focuses on the successful preclinical testing of targeted chemoprevention agents in innovative mouse models (Projects 1 and 2) followed by the design and implementation of clinical trials in at risk human populations (Project 3). Detailed descriptions of the decision-tree selection process as well as the interactions between Projects and Cores are found on the Resources Format Page.

Public Health Relevance

The overall goal of our Chemoprevention of Skin Cancer Program Project is to develop new strategies to eradicate intraepithelial neoplasias (lENs) in the skin and dramatically reduce the risk of nonmelanoma and melanoma skin cancers (NMSC),

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
3P01CA027502-29S1
Application #
8504923
Study Section
Special Emphasis Panel (ZCA1-GRB-P)
Project Start
Project End
2016-06-30
Budget Start
2012-07-01
Budget End
2013-06-30
Support Year
29
Fiscal Year
2012
Total Cost
$8,485
Indirect Cost
$2,536
Name
University of Arizona
Department
Type
DUNS #
806345617
City
Tucson
State
AZ
Country
United States
Zip Code
85721
Blohm-Mangone, Karen; Burkett, Nichole B; Tahsin, Shekha et al. (2018) Pharmacological TLR4 Antagonism Using Topical Resatorvid Blocks Solar UV-Induced Skin Tumorigenesis in SKH-1 Mice. Cancer Prev Res (Phila) 11:265-278
Knights-Mitchell, Shellie S; Romanowski, Marek (2018) Near-Infrared Activated Release of Doxorubicin from Plasmon Resonant Liposomes. Nanotheranostics 2:295-305
Roh, Eunmiri; Lee, Mee-Hyun; Zykova, Tatyana A et al. (2018) Targeting PRPK and TOPK for skin cancer prevention and therapy. Oncogene 37:5633-5647
Chen, Yin; Vasquez, Monica M; Zhu, Lingxiang et al. (2017) Effects of Retinoids on Augmentation of Club Cell Secretory Protein. Am J Respir Crit Care Med 196:928-931
Yamamoto, Hiroyuki; Ryu, Joohyun; Min, Eli et al. (2017) TRAF1 Is Critical for DMBA/Solar UVR-Induced Skin Carcinogenesis. J Invest Dermatol 137:1322-1332
Zykova, Tatyana A; Zhu, Feng; Wang, Lei et al. (2017) The T-LAK Cell-originated Protein Kinase Signal Pathway Promotes Colorectal Cancer Metastasis. EBioMedicine 18:73-82
Einspahr, Janine G; Curiel-Lewandrowski, Clara; Calvert, Valerie S et al. (2017) Protein activation mapping of human sun-protected epidermis after an acute dose of erythemic solar simulated light. NPJ Precis Oncol 1:
Gao, Ge; Zhang, Tianshun; Wang, Qiushi et al. (2017) ADA-07 Suppresses Solar Ultraviolet-Induced Skin Carcinogenesis by Directly Inhibiting TOPK. Mol Cancer Ther 16:1843-1854
Janda, Jaroslav; Burkett, Nichole B; Blohm-Mangone, Karen et al. (2016) Resatorvid-based Pharmacological Antagonism of Cutaneous TLR4 Blocks UV-induced NF-?B and AP-1 Signaling in Keratinocytes and Mouse Skin. Photochem Photobiol 92:816-825
Peng, C; Zeng, W; Su, J et al. (2016) Cyclin-dependent kinase 2 (CDK2) is a key mediator for EGF-induced cell transformation mediated through the ELK4/c-Fos signaling pathway. Oncogene 35:1170-9

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