Unction is necessary to support 3-Methyladenine 3-MA cell proliferation and Rentabilit t. Many genes of this network as potential therapeutic targets and targets are used for combination therapy, as shown by the effect of the synthetic lethality t depletion RNAi. Note that we explore not 2/3 of the shRNA library since starting chips contains bar code could lt Only 000 B52 probes annotated to the library, the 000 shRNA contains B74 Lt This led to many potential candidate genes are not detected in the position. Moreover, the selection of stable cell lines over a period of two weeks, some of the targets selected Hlt have, and they would be missing from the list of genes neratinib sensitization. Our lethality t ynthetic identified several hemosensitizer Genes. Our results suggest that breast cancer cells is a massive growth and survival requirements, where inactivation of these genes by RNAi in combination with neratinib, but not of a leads to chemosensitization of these cells have. Targeting such key vulnerabilities is an interesting approach to selective cancer therapy. Our study also shows that highly parallel dropout synthetic lethal screens using RNAi library covering the entire human genome annotations can call a big number of genes or e t Dliche chemosensitizer that a potential new drug targets to identify repr presents. The functional genetic approach demonstrated here is a quick, alternative and complementary Efforts to re sequencingbased Ans tze Such as the Cancer Genome Atlas and anything similar efforts that focus on k Rperliche JNK Signaling Ver offers Changes in the cancer genome. In addition to the physical mapping of the genomes of cancer, then put Using functional genomics, genome-wide RNAi screens to identify genetic dependence Dependencies of cancer cells. Identified in fact, among the many genes and verified in this screen as potential target molecules, are only some of them oncogene or tumor suppressor genes are known, suggesting that there is a much broader group of not the oncogene or tumor suppressor genes as a target in the treatment of cancer is used.
The concept of addiction ononcogene To completely Requests reference requests getting dependence Dependence of mutated cancer cells on the function of various gene networks that are not in cancer or oncogene for their survival and growth described previously proposed.53, 54 have been in this new area has the potential new reveal insights into the mechanisms of tumor formation and provides new M therapeutic opportunities for cancer that are not discovered by studying the genetic changes Ver in tumors can k. RNAi-chemosensitization screens provide information about m Possible targets that the selectivity of t could improve drugsfor of cancer cells from normal cells more, and as a result lead to improved therapeutic window. In addition, these displays the M Possibility, protein targets for drug-combination Maraviroc strategies and identify new mechanisms of drug sensitivity and resistance. Several recent reports have is the use of RNAi screens chemosensitization approach using standard chemotherapy drugs.39, 55 58, therefore, an expected result of our RNAi screens to identify gene products chemosensitizer, the objectives of the currently available compounds are shown the k nnte be used for the novel combination.