Victoria Seewaldt

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. ncbi request reprint The gift of being first-generation American
    Victoria L Seewaldt
    Division of Medical Oncology and Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Cancer Biol Ther 5:1042-5. 2006
  2. pmc Suppression of p53 function in normal human mammary epithelial cells increases sensitivity to extracellular matrix-induced apoptosis
    V L Seewaldt
    Division of Medical Oncology, Duke University, Durham, NC 27710, USA
    J Cell Biol 155:471-86. 2001
  3. pmc Evidence for phenotypic plasticity in aggressive triple-negative breast cancer: human biology is recapitulated by a novel model system
    Nicholas C D'Amato
    Department of Pharmacology and Cancer Biology, Duke University, Durham, North Carolina, USA
    PLoS ONE 7:e45684. 2012
  4. ncbi request reprint Human papillomavirus type 16 E6 inactivation of p53 in normal human mammary epithelial cells promotes tamoxifen-mediated apoptosis
    V L Seewaldt
    Division of Medical Oncology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Cancer Res 61:616-24. 2001
  5. ncbi request reprint Overweight and obese perimenopausal and postmenopausal women exhibit increased abnormal mammary epithelial cytology
    Victoria L Seewaldt
    Department of Medicine, Duke University Medical Center, Box 2628, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 16:613-6. 2007
  6. ncbi request reprint Images in clinical medicine. Rapid progression of basal-type breast cancer
    Victoria L Seewaldt
    Duke University, Durham, NC 27710, USA
    N Engl J Med 356:e12. 2007
  7. pmc Protein microarray analysis of mammary epithelial cells from obese and nonobese women at high risk for breast cancer: feasibility data
    Patrick G Pilie
    Duke University Medical Center, Box 2628, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 20:476-82. 2011
  8. pmc Optical redox ratio differentiates breast cancer cell lines based on estrogen receptor status
    Julie Hanson Ostrander
    Department of Medicine, Division of Medical Oncology, Duke University Medical Center and Department of Biomedical Engineering, Fitzpatrick Institute for Photonics, Duke University, Durham, NC 27710, USA
    Cancer Res 70:4759-66. 2010
  9. doi request reprint Uptake of 2-NBDG as a method to monitor therapy response in breast cancer cell lines
    Stacy R Millon
    Department of Biomedical Engineering, Duke University, Durham, NC 27708 0281, USA
    Breast Cancer Res Treat 126:55-62. 2011
  10. doi request reprint Breast self-examination: defining a cohort still in need
    Lee G Wilke
    Duke University, Department of Surgery, Durham, NC, USA
    Am J Surg 198:575-9. 2009

Research Grants

  1. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2007
  2. p53 loss in HMECs: a model of breast cancer prevention
    Victoria Seewaldt; Fiscal Year: 2007
  3. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2007
  4. p53 loss in HMECs: a model of breast cancer prevention
    Victoria Seewaldt; Fiscal Year: 2004
  5. Extracellular Matrix Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2004
  6. p53 loss in HMECs: a model of breast cancer prevention
    Victoria Seewaldt; Fiscal Year: 2003
  7. Molecular markers of breast cancer risk and prevention
    Victoria Seewaldt; Fiscal Year: 2009
  8. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria L Seewaldt; Fiscal Year: 2010
  9. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2009
  10. Molecular markers of breast cancer risk and prevention
    Victoria Seewaldt; Fiscal Year: 2007

Collaborators

Detail Information

Publications27

  1. ncbi request reprint The gift of being first-generation American
    Victoria L Seewaldt
    Division of Medical Oncology and Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Cancer Biol Ther 5:1042-5. 2006
  2. pmc Suppression of p53 function in normal human mammary epithelial cells increases sensitivity to extracellular matrix-induced apoptosis
    V L Seewaldt
    Division of Medical Oncology, Duke University, Durham, NC 27710, USA
    J Cell Biol 155:471-86. 2001
    ....
  3. pmc Evidence for phenotypic plasticity in aggressive triple-negative breast cancer: human biology is recapitulated by a novel model system
    Nicholas C D'Amato
    Department of Pharmacology and Cancer Biology, Duke University, Durham, North Carolina, USA
    PLoS ONE 7:e45684. 2012
    ..The DKAT model provides a novel model to study the molecular mechanisms regulating phenotypic plasticity and the aggressive biology of triple-negative breast cancers...
  4. ncbi request reprint Human papillomavirus type 16 E6 inactivation of p53 in normal human mammary epithelial cells promotes tamoxifen-mediated apoptosis
    V L Seewaldt
    Division of Medical Oncology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Cancer Res 61:616-24. 2001
    ..Observations in our model system predict a critical role for the early institution of tamoxifen chemoprevention...
  5. ncbi request reprint Overweight and obese perimenopausal and postmenopausal women exhibit increased abnormal mammary epithelial cytology
    Victoria L Seewaldt
    Department of Medicine, Duke University Medical Center, Box 2628, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 16:613-6. 2007
    ..Further research is needed to confirm these findings and to determine if this potential biomarker is responsive to changes in body weight resulting from diet and/or exercise interventions...
  6. ncbi request reprint Images in clinical medicine. Rapid progression of basal-type breast cancer
    Victoria L Seewaldt
    Duke University, Durham, NC 27710, USA
    N Engl J Med 356:e12. 2007
  7. pmc Protein microarray analysis of mammary epithelial cells from obese and nonobese women at high risk for breast cancer: feasibility data
    Patrick G Pilie
    Duke University Medical Center, Box 2628, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 20:476-82. 2011
    ....
  8. pmc Optical redox ratio differentiates breast cancer cell lines based on estrogen receptor status
    Julie Hanson Ostrander
    Department of Medicine, Division of Medical Oncology, Duke University Medical Center and Department of Biomedical Engineering, Fitzpatrick Institute for Photonics, Duke University, Durham, NC 27710, USA
    Cancer Res 70:4759-66. 2010
    ..This source of optical contrast could be a potentially useful tool for drug screening in preclinical models...
  9. doi request reprint Uptake of 2-NBDG as a method to monitor therapy response in breast cancer cell lines
    Stacy R Millon
    Department of Biomedical Engineering, Duke University, Durham, NC 27708 0281, USA
    Breast Cancer Res Treat 126:55-62. 2011
    ..Results indicate that 2-NBDG uptake can be used to measure changes in glycolysis and has potential for use in early drug development...
  10. doi request reprint Breast self-examination: defining a cohort still in need
    Lee G Wilke
    Duke University, Department of Surgery, Durham, NC, USA
    Am J Surg 198:575-9. 2009
    ..The value of breast self-examination (BSE) to detect early breast cancer is controversial...
  11. pmc ESR1 promoter hypermethylation does not predict atypia in RPFNA nor persistent atypia after 12 months tamoxifen chemoprevention
    Joseph C Baker
    Duke University Medical Center, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 17:1884-90. 2008
    ..Currently, we lack biomarkers to predict whether high-risk women with mammary atypia will respond to tamoxifen chemoprevention...
  12. pmc Obesity promotes breast cancer by CCL2-mediated macrophage recruitment and angiogenesis
    Lisa M Arendt
    Authors Affiliations Developmental, Molecular, and Chemical Biology Department, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine Molecular Oncology Research Institute and Medical Oncology and Department of Pathology, Tufts Medical Center, Boston, Massachusetts and Departments of Medicine, Duke University, Durham, North Carolina
    Cancer Res 73:6080-93. 2013
    ..These findings provide a mechanistic role for adipocytes and macrophages before carcinogenesis that may be critical for prevention and treatment of obesity-related cancer...
  13. ncbi request reprint Hypermethylation of the breast cancer-associated gene 1 promoter does not predict cytologic atypia or correlate with surrogate end points of breast cancer risk
    Gregory R Bean
    Duke University Medical Center, Box 2628, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 16:50-6. 2007
    ....
  14. ncbi request reprint Tamoxifen and tamoxifen ethyl bromide induce apoptosis in acutely damaged mammary epithelial cells through modulation of AKT activity
    Eric C Dietze
    Division of Medical Oncology, Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Oncogene 23:3851-62. 2004
    ....
  15. pmc Reproducibility of random periareolar fine needle aspiration in a multi-institutional Cancer and Leukemia Group B (CALGB) cross-sectional study
    Catherine Ibarra-Drendall
    Duke University Medical Center, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 18:1379-85. 2009
    ..To address these key limitations, the Cancer and Leukemia Group B (CALGB) Prevention Group tested the reproducibility of RPFNA in a multi-institutional cross-sectional study...
  16. pmc CpG island tumor suppressor promoter methylation in non-BRCA-associated early mammary carcinogenesis
    Shauna N Vasilatos
    Department of Medicine, Duke University Medical Center, Box 2628, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 18:901-14. 2009
    ..Only 5% of all breast cancers are the result of BRCA1/2 mutations. Methylation silencing of tumor suppressor genes is well described in sporadic breast cancer; however, its role in familial breast cancer is not known...
  17. ncbi request reprint Morphologically normal-appearing mammary epithelial cells obtained from high-risk women exhibit methylation silencing of INK4a/ARF
    Gregory R Bean
    Duke University Medical Center, Durham, NC 27710, USA
    Clin Cancer Res 13:6834-41. 2007
    ..These data suggest that cells that lack p16(INK4a) activity would be at high risk for breast cancer development and may exhibit an increased frequency of DNA methylation events in early cancer...
  18. ncbi request reprint Atypia in random periareolar fine-needle aspiration affects the decision of women at high risk to take tamoxifen for breast cancer chemoprevention
    Vanessa K Goldenberg
    Duke University Medical Center, Durham, North Carolina, USA
    Cancer Epidemiol Biomarkers Prev 16:1032-4. 2007
    ..Further research is needed to determine the mechanisms through which RPFNA results affect the decision to use tamoxifen, or any other breast cancer chemopreventive agent...
  19. ncbi request reprint Retinoic acid receptor-beta2 promoter methylation in random periareolar fine needle aspiration
    Gregory R Bean
    Division of Medical Oncology, Duke University Medical Center, Durham, NC 27710, USA
    Cancer Epidemiol Biomarkers Prev 14:790-8. 2005
    ..Results from this study indicate that the RARbeta2 P2 promoter is frequently methylated (69%) in primary breast cancers and shows a positive association with increasing cytologic abnormality in RPFNA...
  20. ncbi request reprint CREB-binding protein regulates apoptosis and growth of HMECs grown in reconstituted ECM via laminin-5
    Eric C Dietze
    Division of Medical Oncology, Duke University, Durham, NC 27710, USA
    J Cell Sci 118:5005-22. 2005
    ..Results in these studies may provide insight into early events in basal-type mammary carcinogenesis...
  21. ncbi request reprint Interferon-regulatory factor-1 is critical for tamoxifen-mediated apoptosis in human mammary epithelial cells
    Michelle L Bowie
    Division of Medical Oncology, Duke University, Durham, NC 27710, USA
    Oncogene 23:8743-55. 2004
    ..These data indicate that Tam induces apoptosis in HMEC-E6 cells through a novel IRF-1-mediated signaling pathway that results in activated caspase-1 and -3...
  22. ncbi request reprint Retinoids and retinoic acid receptors regulate growth arrest and apoptosis in human mammary epithelial cells and modulate expression of CBP/p300
    Eric C Dietze
    Division of Medical Oncology and Transplantation, Duke University Medical Center, Durham, North Carolina, 27710, USA
    Microsc Res Tech 59:23-40. 2002
    ..Since CBP and p300 are normally present in limiting amounts, their regulation by ATRA and RARs may be an important element in the control of transcriptional activation of genes regulating growth arrest and apoptosis...
  23. ncbi request reprint CBP/p300 induction is required for retinoic acid sensitivity in human mammary cells
    Eric C Dietze
    Division of Medical Oncology and Transplantation, Duke University Medical Center, Box 2628, Durham, NC 27710, USA
    Biochem Biophys Res Commun 302:841-8. 2003
    ..Thus, in human mammary epithelial cells, CBP/p300 were both modulated by an ATRA signaling pathway and were required for a normal response to ATRA...
  24. ncbi request reprint Retinoic acid receptor beta2 inhibition of metastasis in mouse mammary gland xenografts
    Piper M Treuting
    Department of Pathology, University of Washington, Seattle 98195, USA
    Breast Cancer Res Treat 72:79-88. 2002
    ..000001). Our findings suggest that RARbeta2 may play a role in inhibiting the metastatic cascade in a mouse mammary gland xenograft tumor model and is a potential candidate for therapeutic intervention in human breast cancer...
  25. ncbi request reprint Long-term raloxifene in a woman at high risk for breast cancer
    Gregory R Bean
    N Engl J Med 355:1620-2. 2006
  26. ncbi request reprint Delayed-type hypersensitivity reaction with iscador M given in combination with cytotoxic chemotherapy
    Heather S Shaw
    J Clin Oncol 22:4432-4. 2004
  27. ncbi request reprint Tumor progression and metastasis from genetic to microenvironmental determinants: a workshop of the tumor progression and metastasis NIH study section in honor of Dr. Martin L. Padarathsingh, May 31, 2006, Georgetown, Washington, DC
    YVES A DE CLERCK
    University of Southern California Keck School of Medicine, Los Angeles, California 90027, USA
    Cancer Biol Ther 5:1588-99. 2006

Research Grants22

  1. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2007
    ..Significance: Completions of these aims will provide insight into early events in ER(-) mammary carcinogenesis and provide novel targets for breast cancer chemoprevention. ..
  2. p53 loss in HMECs: a model of breast cancer prevention
    Victoria Seewaldt; Fiscal Year: 2007
    ..abstract_text> ..
  3. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2007
    ..Significance: Completions of these aims will provide insight into early events in ER(-) mammary carcinogenesis and provide novel targets for breast cancer chemoprevention. ..
  4. p53 loss in HMECs: a model of breast cancer prevention
    Victoria Seewaldt; Fiscal Year: 2004
    ..abstract_text> ..
  5. Extracellular Matrix Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2004
    ....
  6. p53 loss in HMECs: a model of breast cancer prevention
    Victoria Seewaldt; Fiscal Year: 2003
    ..abstract_text> ..
  7. Molecular markers of breast cancer risk and prevention
    Victoria Seewaldt; Fiscal Year: 2009
    ....
  8. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria L Seewaldt; Fiscal Year: 2010
    ..Significance: Completions of these aims will provide insight into early events in ER(-) mammary carcinogenesis and provide novel targets for breast cancer chemoprevention. ..
  9. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2009
    ..Significance: Completions of these aims will provide insight into early events in ER(-) mammary carcinogenesis and provide novel targets for breast cancer chemoprevention. ..
  10. Molecular markers of breast cancer risk and prevention
    Victoria Seewaldt; Fiscal Year: 2007
    ....
  11. Extracellular Matrix Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2001
    ....
  12. ECM-Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2006
    ..Significance: Completions of these aims will provide insight into early events in ER(-) mammary carcinogenesis and provide novel targets for breast cancer chemoprevention. ..
  13. Molecular markers of breast cancer risk and prevention
    Victoria Seewaldt; Fiscal Year: 2006
    ....
  14. p53 loss in HMECs: a model of breast cancer prevention
    Victoria Seewaldt; Fiscal Year: 2006
    ..abstract_text> ..
  15. p53 loss in HMECs: a model of breast cancer prevention
    Victoria Seewaldt; Fiscal Year: 2005
    ..abstract_text> ..
  16. Extracellular Matrix Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2005
    ....
  17. Extracellular Matrix Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2003
    ....
  18. Extracellular Matrix Mediated Apoptosis in p53 (-) HMECs
    Victoria Seewaldt; Fiscal Year: 2002
    ....
  19. Molecular markers of breast cancer risk and prevention
    Victoria L Seewaldt; Fiscal Year: 2010
    ....