Stem cell origin of death-from-cancer phenotypes of human prostate and breast cancers.

@article{citeulike:2072545, abstract = {In clinical terms, all human cancers diagnosed in individuals can be divided in two major categories: malignant tumors that will be cured with the existing cancer therapies and tumors that have therapy-resistant phenotypes and will return after initial treatment as incurable metastatic disease. These tumors manifesting clinically lethal death-from-cancer phenotypes represent the most formidable challenge of experimental, translational, and clinical cancer research. Clinical genomics data demonstrate that gene expression signatures associated with the "stemness" state of a cell are informative as molecular predictors of cancer therapy outcome and can help to identify cancer patients with therapy-resistant tumors. Here, we present experimental and clinical evidence in support of the BMI1 pathway rule indicating a genetic link between the stemness state and therapy-resistant death-from-cancer phenotypes. Our analysis demonstrates that therapy-resistant and therapy-responsive cancer phenotypes manifest distinct patterns of association with stemness/differentiation pathways, suggesting that therapy-resistant and therapy-responsive tumors develop within genetically distinct stemness/differentiation programs. These differences can be exploited for development of prognostic and therapy selection genetic tests utilizing a microarray-based cancer therapy outcome predictor algorithm. One of the major regulatory pathways manifesting distinct patterns of association with therapy-resistant and therapy-responsive cancer phenotypes is the Polycomb group proteins chromatin silencing pathway.}, address = {Translational \& Functional Genomics Laboratory, Ordway Cancer Center, Ordway Research Institute, Albany, NY 12208, USA. gglinsky@ordwayresearch.org}, author = {Glinsky, G. V. }, citeulike-article-id = {2072545}, issn = {1550-8943}, journal = {Stem Cell Rev}, keywords = {breast\_cancer, stem\_cell}, month = {January}, number = {1}, pages = {79--93}, posted-at = {2007-12-07 11:09:55}, priority = {3}, title = {Stem cell origin of death-from-cancer phenotypes of human prostate and breast cancers.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/17873385}, volume = {3}, year = {2007} }

TY - JOUR ID - citeulike:2072545 L3 - citeulike-article-id:2072545 TI - Stem cell origin of death-from-cancer phenotypes of human prostate and breast cancers. JF - Stem Cell Rev VL - 3 IS - 1 SP - 79 EP - 93 AD - Translational & Functional Genomics Laboratory, Ordway Cancer Center, Ordway Research Institute, Albany, NY 12208, USA. gglinsky@ordwayresearch.org SN - 1550-8943 N2 - In clinical terms, all human cancers diagnosed in individuals can be divided in two major categories: malignant tumors that will be cured with the existing cancer therapies and tumors that have therapy-resistant phenotypes and will return after initial treatment as incurable metastatic disease. These tumors manifesting clinically lethal death-from-cancer phenotypes represent the most formidable challenge of experimental, translational, and clinical cancer research. Clinical genomics data demonstrate that gene expression signatures associated with the "stemness" state of a cell are informative as molecular predictors of cancer therapy outcome and can help to identify cancer patients with therapy-resistant tumors. Here, we present experimental and clinical evidence in support of the BMI1 pathway rule indicating a genetic link between the stemness state and therapy-resistant death-from-cancer phenotypes. Our analysis demonstrates that therapy-resistant and therapy-responsive cancer phenotypes manifest distinct patterns of association with stemness/differentiation pathways, suggesting that therapy-resistant and therapy-responsive tumors develop within genetically distinct stemness/differentiation programs. These differences can be exploited for development of prognostic and therapy selection genetic tests utilizing a microarray-based cancer therapy outcome predictor algorithm. One of the major regulatory pathways manifesting distinct patterns of association with therapy-resistant and therapy-responsive cancer phenotypes is the Polycomb group proteins chromatin silencing pathway. KW - breast_cancer KW - stem_cell AU - Glinsky, GV PY - 2007/01// UR - http://view.ncbi.nlm.nih.gov/pubmed/17873385 ER -