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• W2104939102 startingPage "29" @default.
• W2104939102 abstract "Inflammation is increasingly recognized as an important component of tumorigenesis, although the mechanisms involved are not fully characterized. The invasive capacity of cancers is reflected in the classic metastatic cascade: tumor (T), node (N) and metastasis (M). However, this staging system for cancer would also have a tumoral biological significance. To integrate the mechanisms that control the inflammatory response in the actual staging system of cancer. It is considered that in both processes of inflammation and cancer, three successive phenotypes are presented that represent the expression of trophic functional systems of increasing metabolic complexity for using oxygen. While a malignant tumor develops it express phenotypes that also share the inflammatory response such as: an ischemic phenotype (anoxic-hypoxic), a leukocytic phenotype with anaerobic glycolysis and migration, and an angiogenic phenotype with hyperactivity of glycolytic enzymes, tumor proliferation and metastasis, and cachexia of the host. The increasing metabolic complexity of the tumor cell to use oxygen allows for it to be released, migrate and proliferate, thus creating structures of growing complexity. One aim of cancer gene therapy could be the induction of oxidative phosphorylation, the last metabolic step required by inflammation in order to differentiate the tissue that it produces." @default.
• W2104939102 created "2016-06-24" @default.
• W2104939102 creator A5011871761 @default.
• W2104939102 creator A5034104118 @default.
• W2104939102 creator A5048651154 @default.
• W2104939102 date "2007-01-01" @default.
• W2104939102 modified "2023-10-17" @default.
• W2104939102 title "Cancer cell: using inflammation to invade the host" @default.
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• W2104939102 doi "https://doi.org/10.1186/1476-4598-6-29" @default.
• W2104939102 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1855932" @default.
• W2104939102 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17437633" @default.

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