Epidemiological studies have demonstrated that increased cancer risk is associated with obesity, but the underlying mechanism remains poorly understood. We have recently developed a Drosophila model of obesity;raising Drosophila on a diet high in carbohydrates led to metabolic dysfunction including hyperglycemia, insulin-resistance and accumulation of fat. Feeding a high dietary sucrose to Ras/Src co- activated Drosophila cancer model developed aggressive tumor with emergent metastasis in a diet-dependent manner. The goal of this Application is to further utilize Drosophila as a useful in situ model to explore mechanistic link between diet-induced obesity and tumor progression.

Public Health Relevance

Epidemiological studies have long shown that obesity and other metabolic dysfunctions increase the risk and severity of tumor progression. In this Application we use fruit flies to explore the mechanisms by which high dietary sugar enhances tumorigenesis.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA170495-03
Application #
8677826
Study Section
Special Emphasis Panel (ZCA1-SRLB-9 (M1))
Program Officer
Spalholz, Barbara A
Project Start
2012-08-20
Project End
2016-05-31
Budget Start
2014-06-01
Budget End
2015-05-31
Support Year
3
Fiscal Year
2014
Total Cost
$341,162
Indirect Cost
$139,887
Name
Icahn School of Medicine at Mount Sinai
Department
Biology
Type
Schools of Medicine
DUNS #
078861598
City
New York
State
NY
Country
United States
Zip Code
10029
Das, T K; Sangodkar, J; Negre, N et al. (2013) Sin3a acts through a multi-gene module to regulate invasion in Drosophila and human tumors. Oncogene 32:3184-97
Hirabayashi, Susumu; Baranski, Thomas J; Cagan, Ross L (2013) Transformed Drosophila cells evade diet-mediated insulin resistance through wingless signaling. Cell 154:664-75