Energy balance &cancer: markers and mechanisms in rats

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Project Title: Energy balance &cancer: markers and mechanisms in rats
Project Number: 5U54CA116847-05-0002
Project web address: Follow on NIH
Parent Project: 5U54CA116847-05
 
Project Description:
The goal of this project is to determine the effects of controlling weight gain by energy restriction, physical activity, or their combination on the carcinogenic process in an experimental model for breast cancer, and to assess how dietary carbohydrate availability modulates responses as outlined in the followings aims. Aim 1. Determine the effects of energy restriction or physical activity alone or in combination on the carcinogenic response in the mammary gland and on candidate markers for cancer risk. This model is built on the human model in Project 4 but extends observation to related pathways/processes in the target tissue. This work will be conducted using a well characterized rodent model for breast cancer and a rodent exercise device newly developed by our laboratory in which a variable speed, motorized activity wheel is linked, under computer control, to a food pellet dispenser so that physical activity behavior is maintained by positive food reward. Effects of these interventions on the carcinogenic process, on factors involved in glucose homeostasis, and on indicators of inflammation and oxidative damage will be measured. As in Project 1 we will seek to determine how cell proliferation, apoptosis, and angiogenesis are modulated. Aim 2. Assess the effect of carbohydrate availability on the carcinogenic response and systemic biomarkers when weight control is mediated by energy restriction and observe of pathways and processes in the target tissue. There is considerable speculation but few experimental data to inform the debate about the consequences on disease risk of popular weight loss/maintenance diets that differ in carbohydrate availability. Preliminary studies have established the feasibility of feeding the same diets used in the human feeding study proposed in Project 3 in our pre-clinical animal model. Aim 3. Investigate candidate mechanisms and markers using genomic and proteomic technologies in order to elucidate target pathways for prevention. Human beings vary in the amount (dose) of energy restriction or physical activity in which they engage to control weight. Available pre-clinical data indicate that different mechanisms may underlie the prevention of cancer by these interventions depending on intervention dose. cDNA microarray analyses will be used to detect differences in the pathways induced in response to energy restriction or physical activity dose and proteomic technologies performed in Core C will be employed to discover serum biomarker profiles that reflect the modulation of the carcinogenic response by these interventions.
 
Project Terms:
accounting adult angiogenesis animal model apoptosis base behavior biochemical biological markers blood glucose regulation body weight body weight decreased breast cancer model cancer prevention cancer prevention intervention cancer risk cancer type candidate marker carbohydrates carcinogenesis cdna arrays cell culture techniques cell physiology cell proliferation cells chronic disease clinical clinical data clinical research computers data devices diet dietary carbohydrates disorder risk dose energy balance energy intake energy metabolism epidemiologic studies exercise experimental models failure (biologic function) feeding food genomics glucose goals human individual inflammation intervention intervention effect intervention studies investigation laboratories link maintenance malignant - descriptor malignant breast neoplasm malignant neoplasms mammary gland measurement measures mediating mediator of activation protein modeling molecular nitrosourea compounds obesity overweight oxidative damage oxidative stress pathology pathway interactions physical activity population based pre-clinical pre-clinical model premalignant prevent prevention procedures process proteomics public health medicine (field) rat-1 rattus recommendation regulation relative (related person) research study response rewards risk risk reduction rodent rodent model serum speed (motion) technology time tissues translations weight gain weight gain prevention weight maintenance regimen work biotechnology breast cancer nutrition cancer
Project Title: Energy balance &cancer: markers and mechanisms in rats
Project Number: 5U54CA116847-05-0002
Project web address: Follow on NIH
Parent Project: 5U54CA116847-05
Organization: Fred Hutchinson Cancer Research Center, United States, Washington, SEATTLE
Principal Investigators (PI): Thompson Henry J, US
 
Project Categories:
Natural Sciences
 
Other Information:
Fiscal Year: 2009
Project Start Date: 1 September 2009
Project End Date: 31 August 2010
Project program: Specialized Center--Cooperative Agreements
 
Project Funding Information:
Funding Mechanism: Research Centers
Year Funding Organization Total Funding, $
2009 NIH - National Cancer Institute $374,901
Project Title: Energy balance &cancer: markers and mechanisms in rats
Project Number: 5U54CA116847-05-0002
Project web address: Follow on NIH
Parent Project: 5U54CA116847-05
 
Title FY Funding
There are no results for this project in database.
Project Title: Energy balance &cancer: markers and mechanisms in rats
Project Number: 5U54CA116847-05-0002
Project web address: Follow on NIH
Parent Project: 5U54CA116847-05
 
Project Title Organization FY Funding
Project Title: Energy balance &cancer: markers and mechanisms in rats
Project Number: 5U54CA116847-05-0002
Project web address: Follow on NIH
Parent Project: 5U54CA116847-05
 
Title Journal Year Country Rel
Project Title: Energy balance &cancer: markers and mechanisms in rats
Project Number: 5U54CA116847-05-0002
Project web address: Follow on NIH
Parent Project: 5U54CA116847-05
 
Title Year
Project Title: Energy balance &cancer: markers and mechanisms in rats
Project Number: 5U54CA116847-05-0002
Project web address: Follow on NIH
Parent Project: 5U54CA116847-05
 
Title Phase Year