Genomes and Genes
George S Watts
Affiliation: University of Arizona
- The acetyltransferase p300/CBP-associated factor is a p53 target gene in breast tumor cellsGeorge S Watts
Bone Marrow Transplant Program, Arizona Cancer Center and Department of Pharmacology and Toxicology, University of Arizona, Tucson, AZ 85724, USA
Neoplasia 6:187-94. 2004..Taken together, the results show that PCAF expression can be induced by wild-type p53...
- Maintenance of mitochondrial genomic integrity in the absence of manganese superoxide dismutase in mouse liver hepatocytesANTHONY R CYR
Free Radical and Radiation Biology Program, Department of Radiation Oncology, Carver College of Medicine and The Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, IA 52242, USA
Redox Biol 1:172-7. 2013..Taken together, these results suggest that murine hepatocytes have a large reserve capacity to cope with the presence of additional mitochondrial reactive oxygen species. ..
- DNA methylation changes in ovarian cancer are cumulative with disease progression and identify tumor stageGeorge S Watts
Department of Medical Pharmacology, College of Medicine, University of Arizona, Tucson AZ 85724 USA
BMC Med Genomics 1:47. 2008..Hypermethylation of promoter CpG islands with associated loss of gene expression, and hypomethylation of CpG-rich repetitive elements that may destabilize the genome are common events in most, if not all, epithelial cancers...
- Performance evaluation of commercial short-oligonucleotide microarrays and the impact of noise in making cross-platform correlationsRichard Shippy
GE Heathcare formerly Amersham Biosciences Chandler, Arizona 85248, USA
BMC Genomics 5:61. 2004..To address this issue we conducted a thorough evaluation of two commercial microarray platforms to determine an appropriate methodology for making cross-platform correlations...
- Identification of Fn14/TWEAK receptor as a potential therapeutic target in esophageal adenocarcinomaGeorge S Watts
Arizona Cancer Center, University of Arizona, Tucson, AZ, USA
Int J Cancer 121:2132-9. 2007..Fn14's potential as a therapeutic target was further supported by immunohistochemistry on a tissue microarray of patient samples that showed that Fn14 protein expression increased with disease progression in EAC...
- cDNA microarray analysis of multidrug resistance: doxorubicin selection produces multiple defects in apoptosis signaling pathwaysG S Watts
Arizona Cancer Center, University of Arizona, Tucson, 85724, USA
J Pharmacol Exp Ther 299:434-41. 2001..We conclude that doxorubicin selection led to changes in gene expression that reduce the apoptotic response to death-inducing stimuli and thus contribute to the multidrug resistance phenotype...
- Different mutant/wild-type p53 combinations cause a spectrum of increased invasive potential in nonmalignant immortalized human mammary epithelial cellsDamian J Junk
Cancer Biology Graduate Interdisciplinary Program, The University of Arizona, Tucson, AZ 85724, USA
Neoplasia 10:450-61. 2008..These changes may constitute novel biomarkers or reveal novel treatment modalities that could inhibit progression from primary to metastatic breast disease...
- Pharmacogenomics of the polyamine analog 3,8,13,18-tetraaza-10,11-[(E)-1,2-cyclopropyl]eicosane tetrahydrochloride, CGC-11093, in the colon adenocarcinoma cell line HCT1161Natalia A Ignatenko
Department of Cell Biology and Anatomy, Arizona Cancer Center, The University of Arizona, 1515 N Campbell Avenue, Tucson, Arizona 85724, USA
Technol Cancer Res Treat 5:553-64. 2006....
- Agglomerative epigenetic aberrations are a common event in human breast cancerPetr Novak
Arizona Cancer Center, University of Arizona, Tucson, Arizona 85724, USA
Cancer Res 68:8616-25. 2008..Taken together, our results suggest that agglomerative epigenetic aberrations are frequent events in human breast cancer...
- Mutant p53 and aberrant cytosine methylation cooperate to silence gene expressionMarc M Oshiro
Bone Marrow Transplant Program, Arizona Cancer Center and Department of Pharmacology and Toxicology, The University of Arizona, Tucson, AZ 85724, USA
Oncogene 22:3624-34. 2003..These results suggest that cancer treatments that target both genetic and epigenetic facets of gene regulation may be a useful strategy towards the therapeutic transcriptional reprogramming of cancer cells...
- Epigenetic inactivation of the HOXA gene cluster in breast cancerPetr Novak
Arizona Cancer Center, Department of Pharmacology and Toxicology, Arizona Respiratory Center, University of Arizona, Tucson, Arizona, USA
Cancer Res 66:10664-70. 2006....
- Expression of bile acid transporting proteins in Barrett's esophagus and esophageal adenocarcinomaKaterina Dvorak
Department of Cell Biology and Anatomy, The University of Arizona, Tucson, Arizona 85724, USA
Am J Gastroenterol 104:302-9. 2009..Our major goal was to evaluate the expression of bile acid transporters in normal squamous epithelium, BE with different grades of dysplasia, and esophageal adenocarcinoma (EAC)...
- The decreased expression of Beclin-1 correlates with progression to esophageal adenocarcinoma: the role of deoxycholic acidHeather B Roesly
Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ 85724, USA
Am J Physiol Gastrointest Liver Physiol 302:G864-72. 2012..In summary, these data suggest that autophagy is initially activated in response to bile acids, but chronic exposure to bile acids leads to decreased Beclin-1 expression and autophagy resistance...
- Low-level arsenite induced gene expression in HEK293 cellsXing Hui Zheng
Department of Pharmacology and Toxicology, University of Arizona, 1723 E Mabel Street, Tucson, AZ 85724, USA
Toxicology 187:39-48. 2003..These findings imply that arsenite induces complex cellular injury and the cellular adaptation to As(III) is associated with alterations in the expression of many genes...
- The chemopreventive agent alpha-difluoromethylornithine blocks Ki-ras-dependent tumor formation and specific gene expression in Caco-2 cellsNatalia A Ignatenko
Department of Cell Biology and Anatomy, Arizona Cancer Center, The University of Arizona, Tucson, Arizona, USA
Mol Carcinog 39:221-33. 2004..DFMO reversed these increases. The results indicated that the Ki-ras oncogene caused changes in experimental cell migration and cell-cell communication genes and that some of these changes could be reversed by DFMO...
- The matrix protein CCN1/CYR61 is required for α(V)β5-mediated cancer cell migrationJana Jandova
Department of Medicine, Dermatology Division, University of Arizona, Tucson, AZ 85724, USA
Cell Biochem Funct 30:687-95. 2012..These results represent an advance to the understanding of the role of CYR61 and α(V)β5 integrin as proteins that cooperate to mediate cancer cell migration...
- Development and molecular characterization of HCT-116 cell lines resistant to the tumor promoter and multiple stress-inducer, deoxycholateCara L Crowley-Weber
Department of Microbiology and Immunology, College of Medicine, University of Arizona, Tucson 85724 5049, USA
Carcinogenesis 23:2063-80. 2002..These analyses provide the rationale for the development of hypothesis-driven intermediate biomarkers to assess colon cancer risk on an individual basis...