Cancer cell: using inflammation to invade the host Export

@article{citeulike:1231772, abstract = {Background 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. Presentation of the hypothesis 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. Testing the hypothesis 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. Implication of the hypothesis 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.}, author = {Arias, Jose-Ignacio and Aller, Maria-Angeles and Arias, Jaime}, citeulike-article-id = {1231772}, citeulike-linkout-0 = {http://dx.doi.org/10.1186/1476-4598-6-29}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17437633}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17437633}, doi = {10.1186/1476-4598-6-29}, issn = {1476-4598}, journal = {Molecular Cancer}, keywords = {background, cancer, cell, host, inflammation, invasion, superlist, thelist}, month = {April}, pages = {29+}, posted-at = {2008-11-29 03:31:20}, priority = {2}, title = {Cancer cell: using inflammation to invade the host}, url = {http://dx.doi.org/10.1186/1476-4598-6-29}, volume = {6}, year = {2007} }

TY - JOUR ID - citeulike:1231772 L3 - citeulike-article-id:1231772 N2 - Background 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. Presentation of the hypothesis 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. Testing the hypothesis 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. Implication of the hypothesis 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. JF - Molecular Cancer SN - 1476-4598 TI - Cancer cell: using inflammation to invade the host VL - 6 SP - 29 KW - background KW - cancer KW - cell KW - host KW - inflammation KW - invasion KW - superlist KW - thelist AU - Arias, Jose-Ignacio AU - Aller, Maria-Angeles AU - Arias, Jaime PY - 2007/04/16/ UR - http://dx.doi.org/10.1186/1476-4598-6-29 ER -