الفهرس 
Cancer
Applications of KD in numerous diseaseOnly 14 pages are availabe for public view
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Abstract
Cancer is a process results from multiple factors such as genome mutations, infections, environmental agents. Genetic mutations involving genes of the DNA repair, cell cycle or cell death pathways were associated with malignancy. Otto Warburg found that the cancer cells used glycolytic pathway for production of ATP not oxidative phosphorylation for anerobic oxidation of glucose. He also discovered that there was increased glucose uptake in the cancerous cells more than normal cells. The Warburg effect and different metabolic alterations allowing cancer cell to increase its anabolism, which includes the synthesis of nucleotides, amino acids, and lipids, maintain cellular hemostasis and reprogram gene expression in a metabolism-dependent way to support their proliferation. Ehrlich‘s Ascites Carcinoma (EAC) is a murine mammary adenocarcinoma which is used for the study of tumor biology, and pathology. It was also used for development of immunomodulatory compounds. These cells have a higher capacity of metastasis, it also can be kept in vitro for controlled cell growth. The Ehrlich tumor was similar to many human carcinomas responsive to chemotherapy as it is undifferentiated tumor and has rapid growth potential. Using dietary interventions such as ketogenic diet in different types of cancer which provide diverse biological effects, protecting normal cells, even though sensitizing broad variety of tumor cells to cytotoxic therapeutics. A ketogenic diet which is rich in fats and low in carbohydrates can switch the metabolism from carbohydrate to fatty acid metabolism. So a high rate of fatty acid and ketone bodies formation will provide adequate level of ketone bodies in blood. Metabolic incapacity of cancer cells to metabolize ketone bodies due to impaired mitochondrial function and the reduced expression of ketolytic enzymes. So ketogenic diet would starve cancer cells that depend heavily on glycolysis. Furthermore, reduced blood glucose, insulin, and insulin-like growth factors levels could halt cancer cell proliferation The epigenetic outlook of a cell is determined by status of DNA methylation, histones covalent modifications, chromatin structure, noncoding RNAs and networking with each other. Histone acetylation is regulated by the opposing actions of histone acetyltransferase and Histone deacetylase (HDAC). Histone acetyltransferases mediate the acetylation of lysine residues associated with gene transcription, HDAC remove the acetyl group from the positively charged histone lysine residues, enabling the negatively charged DNA to bind to the nucleosome proteins. HDAC is critical regulator of gene expression that act as transcriptional repressors. Concerning the forkhead box class O (FOXO) family is a ubiquitously expressed transcription factor that plays important role in higher organisms. FOXO family has been shown to regulate developmental processes and energy metabolism as well as a variety of cellular processes including apoptosis, proliferation, cell cycle progression and DNA damage. All these functions are mediated by the specific activation of a coordinated transcriptional program. The deregulation of FOXO functions will cause uncontrolled cell proliferation and accumulation of DNA damage, which results in carcinogenesis. Necroptosis is a programmed lytic cell death pathway. Its molecular players contribute to embryonic and postnatal development, tissue homeostasis and in development of various kinds of pathological conditions. Moreover, because excessive inflammation it can promote cancer cell growth and metastasis. RIPK3 has been implicated in regulation of apoptosis, and cytokine production. RIPK3 expression has been shown to be lost in several cancer cell lines and cancer types. Concerning pyroptosis is a highly inflammatory form of lytic programmed cell death. Which is characterized by gasdermin D (GSDMD)-mediated membrane pore formation, cell swelling and rapid lysis, followed by the massive release of pro-inflammatory mediators such as interleukin-1β and interleukin-18. Gasdermin D (GSDMD) is an effector molecule for pyroptosis down stream of canonical and noncanonical inflammasome signaling pathways.