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• Journal title: The Epigenetic Impact of on Cancer Prevention (Royston & Tollefsbol

2015)

• What diets can regulate epigenetic modifications?


• Diets can regulate epigenetic modifications. Cruciferous vegetables or
Brassicaceae have chemical components that exhibit anti-inflammatory
effects.
• These vegetables have important role for detoxification of certain carcinogenic
enzymes and are toxic to many types of cancer cells.
• Cruciferous vegetables such as kale, cabbage, Brussels sprouts, and broccoli
sprouts contain chemical components, such as sulforaphane (SFN) and indole-
3-carbinol (I3C), which have been studied to be regulators of microRNAs
(miRNAs) and inhibitors of histone deacetylases (HDACs) and DNA
methyltransferases (DNMTs).

• Outline on how the disease/conditions present clinically?


• Cancer is a group of diseases involving abnormal cell growth with
the potential to invade or spread to other parts of the body.
These contrast with benign, which do not spread.
• Abnormality resulting in the development of cancer is the
continual unregulated proliferation of cancer cells.
• Rather than responding appropriately to the signals that control
normal cell behavior, cancer cells grow and divide in an
uncontrolled manner, invading normal tissues and organs and
eventually spreading throughout the body.
• The generalized loss of growth control exhibited by cancer cells
is the net result of accumulated abnormalities in multiple cell
regulatory systems and is reflected in several aspects of cell
behavior that distinguish cancer cells from their normal
counterparts.

• Identify the underlying cause (SNP, autosomal, etc)


• The mis-regulation and overexpression of microRNAs (miRNAs) and histone
deacetylases (HDACs) and DNA methyltransferases (DNMTs) are responsible
for the uncontrolled cellular proliferation and viability of various types of
cancer cells.
• MicroRNAs (miRNAs) are important in the inhibition of translation and the
degradation of mRNA.
• miRNAs negatively regulate many genes, and their malfunction has been
linked to various pathways of cancer.
• One issue that arises with uncontrolled proliferation is the ability of cancer
cells to use these epigenetic traits in the continued growth and spread of
diseased cells.
• Outline of the dietary interaction that occurs
• The incorporation of miRNA regulators and DNMT/HDAC inhibitors as a
means to promote apoptosis and prevent uncontrolled cellular proliferation
through dietary consumption has proven to improve current cancer
remediation.
• Cruciferous vegetables
(CV) such as kale, cabbage,
Brussels sprouts, and
broccoli sprouts contain
chemical components
including sulforaphane
(SFN) and indole-3-
carbinol (I3C) which have
been revealed to be
potent inhibitors of HDACs
and DNMTs.

• Describe the overall impact the condition would have on the population and health
care management of the condition/related condition.
• Studies suggest that cruciferous vegetables are not only an important source
of nutrients but also important in the elimination of cancer as a life-
threatening disease and key instruments in advancing progress toward the
prevention of cancer.
• The ingestion of indoles and isothiocyanates shows tremendous results on
improving both hormone-based and non-hormone based chemotherapies,
which is another reason the epigenetic diet, or the control of epigenetic
modifiers through the consumption of dietary phytochemicals, is of extreme
interest.
• Evidence shows that individuals who consume a diet rich in Cruciferous
Vegetables have lower risks of developing cancer.
• Additionally, some studies have shown SFN and I3C to have an effect on
estrogen receptor (ER) in breast cancer cells.
These specific studies suggest that future research may lead to
breakthroughs in understanding better means to treat breast cancer and
enhance hormone-based therapies through the incorporation of broccoli and
other cruciferous vegetables into the human diet.

Reference:
Royston, K. J. & Tollefsbol, T. O. J. C. P. R. 2015. The Epigenetic Impact of Cruciferous
Vegetables on Cancer Prevention. 1(1): 46-51.

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