George S Watts

Summary

Affiliation: University of Arizona
Country: USA

Publications

  1. pmc The acetyltransferase p300/CBP-associated factor is a p53 target gene in breast tumor cells
    George 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
  2. pmc Performance evaluation of commercial short-oligonucleotide microarrays and the impact of noise in making cross-platform correlations
    Richard Shippy
    GE Heathcare formerly Amersham Biosciences Chandler, Arizona 85248, USA
    BMC Genomics 5:61. 2004
  3. ncbi request reprint cDNA microarray analysis of multidrug resistance: doxorubicin selection produces multiple defects in apoptosis signaling pathways
    G S Watts
    Arizona Cancer Center, University of Arizona, Tucson, 85724, USA
    J Pharmacol Exp Ther 299:434-41. 2001
  4. ncbi request reprint Identification of Fn14/TWEAK receptor as a potential therapeutic target in esophageal adenocarcinoma
    George S Watts
    Arizona Cancer Center, University of Arizona, Tucson, AZ, USA
    Int J Cancer 121:2132-9. 2007
  5. pmc Different mutant/wild-type p53 combinations cause a spectrum of increased invasive potential in nonmalignant immortalized human mammary epithelial cells
    Damian J Junk
    Cancer Biology Graduate Interdisciplinary Program, The University of Arizona, Tucson, AZ 85724, USA
    Neoplasia 10:450-61. 2008
  6. ncbi request reprint 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 HCT1161
    Natalia 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
  7. pmc Agglomerative epigenetic aberrations are a common event in human breast cancer
    Petr Novak
    Arizona Cancer Center, University of Arizona, Tucson, Arizona 85724, USA
    Cancer Res 68:8616-25. 2008
  8. ncbi request reprint Mutant p53 and aberrant cytosine methylation cooperate to silence gene expression
    Marc 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
  9. ncbi request reprint Epigenetic inactivation of the HOXA gene cluster in breast cancer
    Petr Novak
    Arizona Cancer Center, Department of Pharmacology and Toxicology, Arizona Respiratory Center, University of Arizona, Tucson, Arizona, USA
    Cancer Res 66:10664-70. 2006
  10. doi request reprint Expression of bile acid transporting proteins in Barrett's esophagus and esophageal adenocarcinoma
    Katerina Dvorak
    Department of Cell Biology and Anatomy, The University of Arizona, Tucson, Arizona 85724, USA
    Am J Gastroenterol 104:302-9. 2009

Collaborators

Detail Information

Publications15

  1. pmc The acetyltransferase p300/CBP-associated factor is a p53 target gene in breast tumor cells
    George 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...
  2. pmc Performance evaluation of commercial short-oligonucleotide microarrays and the impact of noise in making cross-platform correlations
    Richard 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...
  3. ncbi request reprint cDNA microarray analysis of multidrug resistance: doxorubicin selection produces multiple defects in apoptosis signaling pathways
    G 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...
  4. ncbi request reprint Identification of Fn14/TWEAK receptor as a potential therapeutic target in esophageal adenocarcinoma
    George 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...
  5. pmc Different mutant/wild-type p53 combinations cause a spectrum of increased invasive potential in nonmalignant immortalized human mammary epithelial cells
    Damian 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...
  6. ncbi request reprint 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 HCT1161
    Natalia 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
    ....
  7. pmc Agglomerative epigenetic aberrations are a common event in human breast cancer
    Petr 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...
  8. ncbi request reprint Mutant p53 and aberrant cytosine methylation cooperate to silence gene expression
    Marc 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...
  9. ncbi request reprint Epigenetic inactivation of the HOXA gene cluster in breast cancer
    Petr Novak
    Arizona Cancer Center, Department of Pharmacology and Toxicology, Arizona Respiratory Center, University of Arizona, Tucson, Arizona, USA
    Cancer Res 66:10664-70. 2006
    ....
  10. doi request reprint Expression of bile acid transporting proteins in Barrett's esophagus and esophageal adenocarcinoma
    Katerina 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)...
  11. pmc The decreased expression of Beclin-1 correlates with progression to esophageal adenocarcinoma: the role of deoxycholic acid
    Heather 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...
  12. ncbi request reprint Low-level arsenite induced gene expression in HEK293 cells
    Xing 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...
  13. ncbi request reprint The chemopreventive agent alpha-difluoromethylornithine blocks Ki-ras-dependent tumor formation and specific gene expression in Caco-2 cells
    Natalia 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...
  14. pmc The matrix protein CCN1/CYR61 is required for α(V)β5-mediated cancer cell migration
    Jana 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...
  15. ncbi request reprint Development and molecular characterization of HCT-116 cell lines resistant to the tumor promoter and multiple stress-inducer, deoxycholate
    Cara 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...