Open Access. Powered by Scholars. Published by Universities.®
- Institution
- Publication
- Publication Type
Articles 1 - 2 of 2
Full-Text Articles in Life Sciences
Role Of Hypoxia And Glycolysis In The Development Of Multi-Drug Resistance In Human Tumor Cells And The Establishment Of An Orthotopic Multi-Drug Resistant Tumor Model In Nude Mice Using Hypoxic Pre-Conditioning, Lara Milane, Zhenfeng Duan, Mansoor M. Amiji
Role Of Hypoxia And Glycolysis In The Development Of Multi-Drug Resistance In Human Tumor Cells And The Establishment Of An Orthotopic Multi-Drug Resistant Tumor Model In Nude Mice Using Hypoxic Pre-Conditioning, Lara Milane, Zhenfeng Duan, Mansoor M. Amiji
Mansoor M. Amiji
Background The development of multi-drug resistant (MDR) cancer is a significant challenge in the clinical treatment of recurrent disease. Hypoxia is an environmental selection pressure that contributes to the development of MDR. Many cancer cells, including MDR cells, resort to glycolysis for energy acquisition. This study aimed to explore the relationship between hypoxia, glycolysis, and MDR in a panel of human breast and ovarian cancer cells. A second aim of this study was to develop an orthotopic animal model of MDR breast cancer. Methods Nucleic and basal protein was extracted from a panel of human breast and ovarian cancer cells; …
Variations In Mre11/Rad50/Nbs1 Status And Dna Damage-Induced S-Phase Arrest In The Cell Lines Of The Nci60 Panel, Kristen M. K. Garner, Alan Eastman
Variations In Mre11/Rad50/Nbs1 Status And Dna Damage-Induced S-Phase Arrest In The Cell Lines Of The Nci60 Panel, Kristen M. K. Garner, Alan Eastman
Dartmouth Scholarship
The Mre11/Rad50/Nbs1 (MRN) complex is a regulator of cell cycle checkpoints and DNA repair. Defects in MRN can lead to defective S-phase arrest when cells are damaged. Such defects may elicit sensitivity to selected drugs providing a chemical synthetic lethal interaction that could be used to target therapy to tumors with these defects. The goal of this study was to identify these defects in the NCI60 panel of cell lines and identify compounds that might elicit selective cytotoxicity.