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Journal of Food Science and Nutrition | Volume 2
December 09-10, 2019 | Dubai, UAE
Nutrition, Food Science and Technology
8th International Conference on
J Food Sci Nutr, Volume:2
Our research has demonstrated that advanced glycation
end products (AGEs) derived from diet can directly
impact both pubertal developmental programs and neoplastic
growth to increase cancer risk and progression. Most people
are unaware of what AGEs are or the damage they can cause,
but we are exposed to them every day through the lives we
lead and the foods that we eat. The Western diet together
with more sedentary habits means that lifestyle-associated
AGEs are accumulating in our bodies at a faster rate than
ever before. Changes in the AGE equilibrium due to lifestyle
cause protein dysfunction, reduced genetic fidelity, and
aberrant cell signaling activation which we believe contribute
to cancer outcomes. Disparity populations defined by AGE-
associated risk factors such as diet, smoking, drinking and
physical inactivity often bear a greater cancer burden when
compared to the general population (reviewed by the PI,
Cancer Research 2015). Lifestyle associated AGEs therefore
may represent a unifying biological consequence of the
social, demographic and environmental risk factors that
contribute to increased cancer incidence and mortality. Early
life exposures during mammary development influence the
breast microenvironment to increase breast cancer risk. We
show that due to an innate ability to influence the cellular
matrix, dietary AGEs disrupt mammary development during
puberty and accelerate tumor growth and progression.
Critically, dietary-AGE mediated effects on pubertal
development and tumor growth were dependent upon the
stromal activation of the receptor for AGE (RAGE). Our studies
show that dietary-AGE activation of RAGE alters cytokine
profiles and increases immune cell recruitment to produce
an activated stroma. An activated stroma was characterized
by the increased recruitment and activation of fibroblasts and
macrophages. stromal cells adopt distinct metabolic patterns
which function to maintain the energy requirements needed
for cell differentiation and functionality. Pathway analysis
of expression data from excised tumors shows that AGE
consumptionsignificantlyimpactsenergymetabolismthrough
the aberrant expression of MYC regulated transcriptional
targets. Our combined data show that AGEs contained in
the foods we eat can impact cancer risk and progression.
Due to their links with lifestyle, both pharmacological and/
or interventional strategies aimed at reducing the AGE
accumulation pool may be viewed as universal health care
preventive and/or therapeutic initiatives. This may be an
attractive option for populations where lifestyle change is
not feasible due to poverty, inability, illness, treatment side
effects, time, apathy and/or depression.
Speaker Biography
Turner has accumulated over 20 years of basic and translational cancer
research experience in the UK, Europe and USA and has a track record of
success. Through peer reviewed publications, multiple intercontinental
collaborations,andnumerousscientificmeetingsaroundtheworldhiswork
is internationally recognized. His research program has been dedicated to
defining the biological mechanisms involved in promoting cancer with
a emphasis on the effects of lifestyle and diet. In order to be successful
in his chosen field he has established working collaborations with a
multidisciplinary team of investigators including clinicians, epidemiologists
as well as behavioral and population scientists in order to fully comprehend
the translational link between lifestyle, cancer and cancer disparity. He
continues to show a strong commitment to community outreach and has
developed bridges with numerous community leaders and has presented
at many community events.
e:
David P Turner
Medical University of South Carolina, USA
Advanced glycation end products: A tumor promoting
consequence of Nutrition