CLINICAL EPIGENETICS, 2011
Finally, by virtue of their genetic and epigenetic mechanisms, cancer chemopreventive agents are being redefined as chemo- or radio-sensitizers.
A sustained DNA damage response coupled with insufficient repair may be a pivotal mechanism for apoptosis induction in cancer cells exposed to dietary phytochemicals.
A study reviews how dietary phytochemicals that affect the epigenome also can trigger DNA damage and repair mechanisms. Where such data is available, examples are cited from studies in vitro and in vivo of polyphenols, organosulfur/organoselenium compounds, indoles, sesquiterpene lactones, and miscellaneous agents such as anacardic acid.
• Indoles from cruciferous foods
• Sesquiterpene lactones from artichokes, garlic and other bitter plants
• organosulfur/organoselenium compounds from garlic and onions
• Polyphenols from colorful veggies and fruits
• Anacardic acids from cashew nuts, cashew apples, and cashew nutshell oil, but also in mangoes and Pelargonium geraniums

Genomic instability is a common feature of cancer etiology. This provides an avenue for therapeutic intervention, since cancer cells are more susceptible than normal cells to DNA damaging agents.
However, there is growing evidence that the epigenetic mechanisms that impact DNA methylation and histone status also contribute to genomic instability. The DNA damage response, for example, is modulated by the acetylation status of histone and non-histone proteins, and by the opposing activities of histone acetyltransferase and histone deacetylase (HDAC) enzymes.
Many HDACs overexpressed in cancer cells have been implicated in protecting such cells from genotoxic insults. Thus, HDAC inhibitors, in addition to unsilencing tumor suppressor genes, also can silence DNA repair pathways, inactivate non-histone proteins that are required for DNA stability, and induce reactive oxygen species and DNA double-strand breaks.

Content Type Journal ArticleCategory ReviewPages 1-23DOI 10.1186/1868-7083-3-4Authors Praveen Rajendran, Cancer Chemoprotection Program, Linus Pauling Institute, 307 Linus Pauling Science Center, Oregon State University, Corvallis, OR 97331, USAEmily Ho, Cancer Chemoprotection Program, Linus Pauling Institute, 307 Linus Pauling Science Center, Oregon State University, Corvallis, OR 97331, USADavid E Williams, Cancer Chemoprotection Program, Linus Pauling Institute, 307 Linus Pauling Science Center, Oregon State University, Corvallis, OR 97331, USARoderick H Dashwood, Cancer Chemoprotection Program, Linus Pauling Institute, 307 Linus Pauling Science Center, Oregon State University, Corvallis, OR 97331, USA Journal Clinical EpigeneticsOnline ISSN 1868-7083Print ISSN 1868-7075 Journal Volume Volume 3 Journal Issue Volume 3, Number 1

Apoptosis Definition
Apoptosis (pron.: /ˌæpəˈtoʊsɪs/ also pron.: /ˌeɪpɔːpˈtoʊsɪs/)[2][3] is the process of programmed cell death (PCD) that may occur in multicellular organisms.[4] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation. (See also apoptotic DNA fragmentation.)
Research in and around apoptosis has increased substantially since the early 1990s. In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in an extensive variety of diseases. Excessive apoptosis causes atrophy, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer.
In contrast to necrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis generally confers advantages during an organism’s life cycle. For example, the differentiation of fingers and toes in a developing human embryo occurs because cells between the fingers apoptose; the result is that the digits are separate. Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytic cells are able to engulf and quickly remove before the contents of the cell can spill out onto surrounding cells and cause damage.[5]
Between 50 and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day.[6]
Anacardic acids are chemical compounds found in the shell of the cashew nut (Anacardium occidentale). The exact mixture depends on the species of the plant.[2] of which the 15 carbon unsaturated side chain found in the cashew plant is very lethal to Gram positive bacteria.
Primarily used for tooth abscesses, it is also active against acne, some insects, tuberculosis, and MRSA. It is primarily found in foods such as cashew nuts, cashew apples, and cashew nutshell oil, but also in mangoes and Pelargonium geraniums.[3]