Cancer cells exhibit distinctive metabolisms unlike normal cells, not only energy production dependent on aerobic glycolysis, but also dysregulated cell signaling and mechanism , increased fatty acid synthesis and glutaminolysis are obviously observed. (Y Zhao et al. 2013) Simultaneously, intrinsic and extrinsic molecular mechanisms were modified, to modify cellular metabolisms to meet the demand for nutrients in the rapid growth of cancer cells, usually carbohydrates, proteins, lipids and nucleic acids. are the essential sources that cancer cells need to support their growth and division. Previous studies have highlighted cancer metabolic phenotypes for which the Warberg effect appears to be an important feature. Cancer cells would switch ATP production from oxidative phosphorylation to glycolysis, even under anaerobic conditions. This effect is regulated by the PI3K pathway, hypoxia-inducible factor (HIF), p53, and AMP-activated kinase (AMPK)-liver kinase B1 (LKB1). However, adaptation to a new microenvironment such as the cellular remodeling process to reach the cancer cell requires both macromolecular synthesis and maintenance of redox balance. In the rapid proliferation stage, NADPH and a high level of reactive oxygen species (ROS) are the key molecules that distinguish cancer cells from normal cells. Importantly, genetic alterations affecting metabolic change typically find oncogenes and tumor suppressor gene mutations that influence intracellular metabolism. signaling pathways. These changes can alter metabolism and redesign the process facilitating rapid growth and survival of cancer cells via the RAS and mTORC1 pathways. (Rob A. Cairns. et al. 2001 and Chi V Dang. 2012)Lipids, proteins...... middle of paper ...... complex mechanisms of each type of cancer, there may be differences in details and you may need to know more. It would be useful to adopt the comprehensible approach of studies on melanoma modalities to the ASS negative cancer type which has a high cancer prevalence in Thailand, HCC and cholangiocarcinoma (CCA). Beyond the complex mechanisms of cancer cells, ADI treatment interestingly combines with other chemotherapy to improve the results of treatment aimed at destroying cancer synergistically. This is an interesting point to make since the cancer itself has changed to avoid the effects of the drug over time. Thus forcing the cancer to shift towards apoptosis and reducing the resistance that might arise later. A thorough study of these detailed mechanisms should have been conducted to provide a solution for successful cancer treatment..