# Consequences of Glucose Enriched Diet on Oncologic Patients
###### Abstract  
Malignant tumors demonstrate increased rates of glucose utilization and uptake. Therefore, clinical trials are being used to evaluate a variety of inhibitors of glycolytic metabolism. Antibodycolytic drugs have been proven to promote chemotherapy and radio-induced cell death. Glucose influences the levels and activation of pro-apoptotic BH3-only proteins, such as Puma, Bad, Noxa, and Bim, and the family of anti-apoptotic proteins Bcl-2; synergistic effects are probably the result of the regulation of the apoptotic machinery. Antibodycolytic medicines and glucose deprivation induce tumor cell death by caspase-8-mediated or mitochondrial apoptosis or even necrosis. The last is known to activate the effector caspases, principally through the cleavage of the Bcl-2 family member Bid and the consequent activation of the mitochondrial pathway. Modifications to the host's diet can modify the availability of nutrients in the tumor microenvironment, which could offer a feasible technique to restrict growth. Dietary alterations can reduce particular nutritional requirements of the tumor that target the metabolic vulnerabilities or boost the cytotoxicity of anticancer medications. According to recent studies, increasing the amount of key minerals in the diet can affect how well cancer therapies can function. The research reveals that the eating habits and nutritional state of a patient should be regarded during cancer research and therapy. apoptosis; Bcl2 proteins; cancer; glucose; nutrition; Warburg effect +
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cell in each phase of the cycle are described, indicating some of the checkpoints of the cell cycle: G1 that blocks the beginning, S that reduces the replication rate, the checkpoint of the G2-M transition that arrests the cycle in this transition, and the internal mitotic control. The myriad ways that cancer cells diverge from normal cells allow them to expand and flourish unchecked. Unlike normal cells, which evolve into a range of diverse cell types with unique activities, cancer cells are less specialized [11]. When the mechanisms that govern apoptosis fail, both by excess and by default, the balance is upset and numerous diseases can emerge. Resistance to apoptosis is one of the traits that contribute to the creation of a tumor [12] and can also be the cause of various autoimmune disorders. In the opposite case, an excess of apoptosis could be related to neurodegenerative disorders [13]. Cancer is a hereditary disease that can be caused by alterations in proto-oncogenes and tumor suppressor genes, which are genes that regulate the way our cells divide, grow, and work. The genetic alterations that generate cancer can be inherited from parents. They can also develop during a person's life due to mistakes that may happen due to DNA damage caused by environmental exposures, such as chemicals in cigarette smoke and radiation, such as ultraviolet rays from the sun, or as cells divide [11]. The genetic alterations caused by cancer involve three primary categories of genes: DNA repair genes, tumor suppressor genes, and proto-oncogenes [11]. Proto-oncogenes are involved in proper cell division and proliferation. However, when these genes are more active than normal or are modified in a certain way, they can become cancer-causing genes (or oncogenes), allowing cells to survive and thrive when they should not. Tumor suppressor genes are connected to the control of cell division and proliferation. Cells with defective tumor suppressor genes can divide abundantly. DNA repair genes are involved in the repair of damaged DNA. Mutated cells in these genes are likely to produce additional mutations in other genes. Together, these alterations can cause cells to become malignant. Cancer cells also tend to avoid the immune system. Although damaged or abnormal cells are generally cleared from the body by the immune system, certain cancer cells can remain \"hidden\". Cancer cells have the ability to fool the immune system into helping them stay alive and develop [11].