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| 1 | Staged Management of Giant Abdominal Wall Defects: Acute and Long-Term Results显示文摘 | T. Wright Jernigan Timothy C. Fabian Martin A. Croce Natalie Moore F. Elizabeth Pritchard Gayle Minard Tiffany K. Bee | 2003 | Annals of Surgery2003，，3： | 1 |
| 2 | A comparison of stages IB1 and IB2 cervical cancers treated with radical hysterectomy. Is size the real difference?显示文摘 | Teresa L. Rutledge Scott A. Kamelle Todd D. Tillmanns Natalie S. Gould Jason D. Wright David E. Cohn Thomas J. Herzog Janet S. Rader Michael A. Gold Gary A. Johnson Joan L. Walker Robert S. Mannel D. Scott McMeekin | 2004 | Gynecologic Oncology2004，，1： | 1 |
| 3 | EGFR signaling promotes resistance to CHK1 inhibitor prexasertib in triple negative breast cancer显示文摘Aim:Innate resistance to the CHK1 inhibitor prexasertib has been described,but resistance mechanisms are not understood.We aimed to determine the role epidermal growth factor receptor(EGFR)plays in innate resistance to prexasertib in triple negative breast cancer(TNBC).Methods:Using a panel of pre-clinical TNBC cell lines,we measured the sensitivity to prexasertib.We examined the effect activation of EGFR had on prexasertib sensitivity.We measured the synergy of dual blockade of EGFR with erlotinib and CHK1 with prexasertib in TNBC cell lines and xenografts.Results:EGFR overexpression and activation increased resistance to CHK1 inhibition by prexasertib.EGFR promoted the phosphorylation of BCL2-associated agonist of cell death(BAD),inactivating its pro-apoptotic functions.Inhibition of EGFR reversed BAD phosphorylation,increasing sensitivity to prexasertib.Conclusion:The use of prexasertib as a monotherapy in TNBC has been limited due to modest clinical responses.We demonstrated that EGFR activation contributes to innate resistance to prexasertib in TNBC and potentially other cancers.EGFR expression status should be considered in clinical trials examining prexasertib’s use as a monotherapy or combination therapy. | Kevin J.Lee Griffin Wright Hannah Bryant Leigh Ann Wiggins Michele Schuler Natalie R.Gassman | 2020 | Cancer Drug Resistance2020，3，4： | 1 |
| 4 | Prevalence and risk factors for hepatitis C virus infection at an Urban veterans administration medical center显示文摘 | Megan E. Briggs Christiane Baker Robert Hall J.Michael Gaziano David Gagnon Natalie Bzowej Teresa L. Wright | 2001 | Hepatology2001，，6： | 1 |
| 5 | Health Emergency and Disaster Risk Management: Five Years into Implementation of the Sendai Framework显示文摘The Sendai Framework for Disaster Risk Reduction 2015–2030 recognizes health at the heart of disaster risk management(DRM)at the global policy level.Five years on,it has catalyzed the rapid development of the field of Health Emergency and Disaster Risk Management(Health EDRM)by providing a mandate for building partnerships as well as enhancing scientific research.Key milestones achieved include publication of the World Health Organization’s Health EDRM Framework,development of the WHO Thematic Platform for Health EDRM and the WHO Health EDRM Research Network,and further application of health information principles to DRM.Furthermore,health actors at all levels have continued to engage in the Sendai Framework processes and have had a key role in its implementation and proposed monitoring.There have been significant gains made through the partnership of health and DRM,but the relationship has not been without its challenges.Many national,regional,and global initiatives continue to operate with a lack of consistency and of linkages to respond to the Sendai Framework’s call for embedding health resilience in DRM,and conversely,embedding DRM in health resilience.Overcoming this hurdle is important,and doing so will be a key marker of success of the next 10 years of partnership under the Sendai Framework. | Natalie Wright Lucy Fagan Jostacio MLapitan Ryoma Kayano Jonathan Abrahams Qudsia Huda Virginia Murray | 2020 | International Journal of Disaster Risk Science2020，11，2： | 1 |
| 6 | HIV-1infection of human macrophages directly induces Viperin which inhibits viral production显示文摘 | Najla Nasr Susan Maddocks Stuart G Turville Andrew N Harman Natalie Woolger Karla J Helbig John Wilkinson Chris R Bye Thomas K Wright Dharshini Rambukwelle Heather Donaghy Michael R Beard Anthony L Cunningham | 2012 | Blood2012，120，4： | 1 |
| 7 | EGFR signaling promotes resistance to CHK1 inhibitor prexasertib in triple negative breast cancer显示文摘Aim:Innate resistance to the CHK1 inhibitor prexasertib has been described,but resistance mechanisms are not understood.We aimed to determine the role epidermal growth factor receptor(EGFR)plays in innate resistance to prexasertib in triple negative breast cancer(TNBC).Methods:Using a panel of pre-clinical TNBC cell lines,we measured the sensitivity to prexasertib.We examined the effect activation of EGFR had on prexasertib sensitivity.We measured the synergy of dual blockade of EGFR with erlotinib and CHK1 with prexasertib in TNBC cell lines and xenografts.Results:EGFR overexpression and activation increased resistance to CHK1 inhibition by prexasertib.EGFR promoted the phosphorylation of BCL2-associated agonist of cell death(BAD),inactivating its pro-apoptotic functions.Inhibition of EGFR reversed BAD phosphorylation,increasing sensitivity to prexasertib.Conclusion:The use of prexasertib as a monotherapy in TNBC has been limited due to modest clinical responses.We demonstrated that EGFR activation contributes to innate resistance to prexasertib in TNBC and potentially other cancers.EGFR expression status should be considered in clinical trials examining prexasertib’s use as a monotherapy or combination therapy. | Kevin J.Lee Griffin Wright Hannah Bryant Leigh Ann Wiggins Michele Schuler Natalie R.Gassman | 2021 | Cancer Drug Resistance2021，4，4： | 0 |
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