Affiliation: University of Miami
- Androgen deprivation-induced senescence promotes outgrowth of androgen-refractory prostate cancer cellsDominick G A Burton
Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, United States of America
PLoS ONE 8:e68003. 2013..Thus our study demonstrates that ADIS promotes outgrowth of androgen-refractory PC cells and is consequently a suboptimal tumor-suppressor response to AD. ..
- Human Mut T Homolog 1 (MTH1): a roadblock for the tumor-suppressive effects of oncogenic RAS-induced ROSPriyamvada Rai
Department of Medicine, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA
Small Gtpases 3:120-5. 2012..Accordingly, targeting MTH1 in RAS-transformed tumor cells will not only induce proliferative defects but also potentially enhance therapeutic cytotoxicity by shifting cellular response away from pro-survival mechanisms...
- Creation and validation of a ligation-independent cloning (LIC) retroviral vector for stable gene transduction in mammalian cellsAsmita Patel
Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33136, USA
BMC Biotechnol 12:3. 2012..However, the relatively small number of feasible restriction enzyme sequences in their cloning sites can hinder successful generation of overexpression constructs if these sequences are also present in the target cDNA insert...
- NF-kappaB activation enhances cell death by antimitotic drugs in human prostate cancer cellsRicardo Parrondo
Geriatric Research, Education, and Clinical Center and Research Service, Bruce W, Carter Veterans Affairs Medical Center, Miami, FL 33125, USA
Mol Cancer 9:182. 2010..In prostate cancer, it is not clear in the different cell types (androgen-dependent and castration-resistant) if activation or inhibition of NF-kappaB is required for stimulation of apoptosis by chemotherapy...
- Oxidation in the nucleotide pool, the DNA damage response and cellular senescence: Defective bricks build a defective housePriyamvada Rai
Division of Gerontology and Geriatric Medicine, Department of Medicine, Rosenstiel Medical Sciences Building, Rm 7094 Locator Code D 503, 1600 NW 10th Ave, Miller School of Medicine, University of Miami, Miami, FL 33136, United States
Mutat Res 703:71-81. 2010..This review will explore the role of oxidation in the nucleotide pool as a major effector of oxidative stress-induced genotoxic damage and DDR in the context of cellular senescence and tumorigenic transformation...
- Enhanced elimination of oxidized guanine nucleotides inhibits oncogenic RAS-induced DNA damage and premature senescenceP Rai
Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Miami, Miller School of Medicine, Miami, FL 33136, USA
Oncogene 30:1489-96. 2011..These results indicate that the guanine nucleotide pool is a critical target for intracellular ROS produced by oncogenic RAS and that RAS-transformed cells require robust MTH1 expression to proliferate...
- MutT Homolog 1 (MTH1) maintains multiple KRAS-driven pro-malignant pathwaysA Patel
Department of Medicine, University of Miami Leonard M Miller School of Medicine, Miami, FL, USA
Oncogene 34:2586-96. 2015..Accordingly, our results indicate MTH1 is a novel and critical component of oncogenic KRAS-associated malignancy and its inhibition is likely to yield significant tumor-suppressive outcomes in KRAS-driven tumors. ..