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Dietary epigenetics in cancer and aging,easy fast ways to lose weight without exercise,healthy baking recipes south africa - Review

Epigenetics refers to the study of changes in the regulation of gene activity and expression that are not dependent on gene DNA sequence. A weblog on the sciences and practices of living healthily very long – perhaps hundreds of years. Certain plant polyphenols not only exercise general positive health effects but also inhibit oncogenic transformation or the proliferation of cancer cells. In normal cells, the stress generated by normal dietary intake of CFPs is within the hormetic range of response.
For the same reasons related to both non-hormetic oxidative stress and histone acetylation, cancer cells in an acetylated state are more likely to experience damage to their DNA repair machinery. However, in cancer cells which are relatively deregulated to start with, the stress created by ingestion of CFPs can be beyond the hormetic range, with the result being damage or death to the cancer cell. Histone deacetylase inhibition (HDACi) is an important emerging approach to cancer therapy. Background: Histone deacetylase inhibitors (HDACis) re-express silenced tumor suppressor genes and are currently undergoing clinical trials.
Very specifically, CFPs can inhibit cancers via damage to their DNA repair machinery inflicted due to the HDAC activity of the polyphenols. In the last few years there has been increasing focus on the roles of mRNAs in epigenetic regulation(ref)(ref) The operation of this knockout punch is illustrated in this diagram. Finally, the sixth knockout punch – CFPs inhibit DNA methyltransferases (DNMT) in cancer cells, thus blocking the methylation and inactivation of tumor suppressor genes in cancers. Extensive research during the last half century has identified various molecular targets that can potentially be used not only for the prevention of cancer but also for treatment. Epigenetic alterations have been identified as promising new targets for cancer prevention strategies as they occur early during carcinogenesis and represent potentially initiating events for cancer development. These medicines have been looked at in terms of their detailed chemical structures, their proteomic properties, the molecular biological pathways through which they work, their gene activation and epigenetic properties, their pharmacological properties, etc, This work has generally been of high quality and has resulted in thousands or tens of thousands of research reports, many of them published in highly respected Western journals. We hypothesize that during carcinogenesis, certain pathways or biological gene sets are commonly dysregulated via DNA methylation across cancer types. While many substances are HDAC inhibitors including a number of CFPs, the drug panobinostat is being particularly studied and experimentally used in the cancer research community.
Histone acetyltransferases (HATs) and histone deacetylases (HDACs) are two opposing classes of enzymes, which tightly control the equilibrium of histone acetylation. Acetylation and deacetylation are catalyzed by specific enzymes, histone acetyltransferases (HATs) and histone deacetylases (HDACs), respectively. Unsurprisingly, HDAC expression is frequently altered in hematologic and solid tumor malignancies.
This provides an avenue for therapeutic intervention, since cancer cells are more susceptible than normal cells to DNA damaging agents. Pre-miRNA is exported from nucleus to the cytoplasm and further processed by Dicer into miRNA duplex.
Indeed, gene expression is modulated by the acetylation status of histones and transcription factors.
THE INTENTION OF THOSE DISCUSSIONS IS TO CONVEY CURRENT RESEARCH FINDINGS AND OPINIONS, NOT TO GIVE MEDICAL ADVICE.
I have been at this part-time for well over a decade, and in 2007 this became my mainline activity. An imbalance in the equilibrium of histone acetylation has been associated with carcinogenesis and cancer progression.


Two HDAC inhibitors (vorinostat and romidepsin) have been approved by the US FDA for the treatment of cutaneous T-cell lymphoma. Epigenetic gene expression regulation is a complex process and several key enzymes play crucial roles.
However, there is growing evidence that the epigenetic mechanisms that impact DNA methylation and histone status also contribute to genomic instability. Acetylation of histone lysine residues modulates histone-DNA and histone-protein interactions as well as chromatin remodeling.
In this review, we present evidence that numerous agents identified from fruits and vegetables can interfere with several cell-signaling pathways. During carcinogenesis, major cellular functions and pathways, including drug metabolism, cell cycle regulation, potential to repair DNA damage or to induce apoptosis, response to inflammatory stimuli, cell signalling, and cell growth control and differentiation become deregulated. RESULTS: We developed a web-based gene set enrichment application called LRpath with clustering functionality that allows for identification and comparison of pathway signatures across multiple studies.
So far, a number of structurally distinct classes of compounds have been identified as HDAC inhibitors including the short-chain fatty acids, hydroxamates, cyclic tetrapeptides and benzamides.
As single agents, treatment with HDAC inhibitors has demonstrated limited clinical benefit for patients with solid tumors, prompting the investigation of novel treatment combinations with other cancer therapeutics. Here we provide evidence that several DNA repair genes are downregulated by HDAC inhibition and provide a mechanism involving the E2F1 transcription factor in the process. 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. Thus, hyperacetylation of histones is associated with a relaxed state of chromatin and active gene expression (Minucci and Pelicci 2006). I was founding dean of a graduate school and a university professor at the State University of New York, a senior consultant working in a variety of fields at Arthur D.
The agents include curcumin (turmeric), resveratrol (red grapes, peanuts and berries), genistein (soybean), diallyl sulfide (allium), S-allyl cysteine (allium), allicin (garlic), lycopene (tomato), capsaicin (red chilli), diosgenin (fenugreek), 6-gingerol (ginger), ellagic acid (pomegranate), ursolic acid (apple, pears, prunes), silymarin (milk thistle), anethol (anise, camphor, and fennel), catechins (green tea), eugenol (cloves), indole-3-carbinol (cruciferous vegetables), limonene (citrus fruits), beta carotene (carrots), and dietary fiber. This article summarizes recent advances in in vitro and in vivo research on the anti-cancer effects and related mechanisms of some promising natural products.
Here, we employed LRpath analysis to unravel the commonly altered pathways and other gene sets across ten cancer studies employing DNA methylation data profiled with the Illumina HumanMethylation27 BeadChip.
These compounds lead to an accumulation of acetylated histone proteins both in tumor cells and in normal tissues.
They also modulate expression of several other genes related to cell cycle, apoptosis, and angiogenesis. In this article, the rationales and clinical progress of several combinations with HDAC inhibitors are presented, including DNA-damaging chemotherapeutic agents, radiotherapy, hormonal therapies, DNA methyltransferase inhibitors and various small-molecule inhibitors. Histone acetylases (HAT) and histone deacetylases (HDAC) are responsible for the acetylation and de-acetylation of lysine residues within histone tails, respectively.
Many HDACs overexpressed in cancer cells have been implicated in protecting such cells from genotoxic insults.
Little, Inc., Chief Scientist and C00 of Mirror Systems, a software company, and an international Internet consultant.
For instance, the cell-signaling pathways inhibited by curcumin alone include NF-kappaB, AP-1, STAT3, Akt, Bcl-2, Bcl-X(L), caspases, PARP, IKK, EGFR, HER2, JNK, MAPK, COX2, and 5-LOX. Chemopreventive agents that target the epigenome include micronutrients (folate, retinoic acid, and selenium compounds), butyrate, polyphenols from green tea, apples, coffee, black raspberries, and other dietary sources, genistein and soy isoflavones, curcumin, resveratrol, dihydrocoumarin, nordihydroguaiaretic acid (NDGA), lycopene, anacardic acid, garcinol, constituents of Allium species and cruciferous vegetables, including indol-3-carbinol (I3C), diindolylmethane (DIM), sulforaphane, phenylethyl isothiocyanate (PEITC), phenylhexyl isothiocyanate (PHI), diallyldisulfide (DADS) and its metabolite allyl mercaptan (AM), cambinol, and relatively unexplored modulators of histone lysine methylation (chaetocin, polyamine analogs). In eukaryotic cells NF-kB is an important regulator of genes that control cell proliferation and cell survival.


We observed a surprising level of concordance in differential methylation across multiple cancer types. Several HDAC inhibitors are currently in clinical trials both for solid and hematologic malignancies.
Because of these histone modifications, conformational changes in chromatin structure lead to changes in DNA accessibility for transcription regulators and polymerases. 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. The active principle identified in fruit and vegetables and the molecular targets modulated may be the basis for how these dietary agents not only prevent but also treat cancer and other diseases. So far, data are still mainly derived from in vitro investigations, and results of animal models or human intervention studies are limited that demonstrate the functional relevance of epigenetic mechanisms for health promoting or cancer preventive efficacy of natural products.
NF-kB regulates anti-apoptotic genes that protect healthy cells from cell death and activates the expression of genes that keep cells proliferating. Prostate cancer cells demonstrated a decreased DNA repair capacity and an increased sensitization to chemical- and radio-DNA damaging agents upon HDAC inhibition. This review summarizes how dietary phytochemicals that affect the epigenome also can trigger DNA damage and repair mechanisms. Interestingly, the transactivation function of other transcription factors, such as p53 and FOXO proteins, is also positively regulated by acetylation.
Commonly hypermethylated groups included homeobox and other DNA-binding genes, nervous system and embryonic development, and voltage-gated potassium channels. Based on our AFA data, we hypothesized that the E2F transcription factors may play a role in the downregulation of key repair genes upon HDAC inhibition in prostate cancer cells. 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.
Moreover, the acetylation of factors involved in maturation, stability and translation of messenger RNA can have an impact on their function. Several well-known cancer-related pathways were significantly affected, while others were depleted in differential methylation. Downregulation of the repair genes is on account of a decrease in amount and promoter recruitment of the E2F1 transcription factor. I have published something like 200 books and papers as well as over 430 substantive.entries in this blog, and have enjoyed various periods of notoriety. It is likely that NF-kB expression is central to a programmed set of changes which we call aging. One study(ref1) confirms that that in multiple mammalian tissues (including skin fibroblasts, kidney, cortex, kidney medulla, abdominal muscle, skeletal muscle, and brain), aging involves continuing changes in expression of hundreds of genes.
Indeed, the acetylation of p53, p73, Smad7 (mothers against decapentaplegic homolog 7) and c-myc prevents their ubiquitination and thus their degradation. And, further, NF-kB signaling appears to be a major regulator of gene expression related to the aging progress.
In fact, by inhibiting NF-kB cell signaling the researchers were able to cause the epidermal tissue of old mice to revert to the state of very young mouse tissue, both in observable characteristics and in genetic expression profile.



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