Walther, Zenta - Yale University - Biological & Biomedical Sciences

个人简介

Dr. Walther is a physician-scientist with clinical expertise in gastrointestinal and liver pathology, the molecular diagnostics of surgical pathology specimens, and molecular oncology of solid tumors. As Clinical Director of the YNHH Tumor Profiling Laboratory, she focuses on molecular and genomic analyses of solid tumor specimens, to enable the identification of therapeutic targets within individual patients' cancers, and thus to promote precision medicine in oncology. MD Cornell University (1995) PhD Rockefeller University (1994) BS Yale University (1986) Fellow Yale University School of Medicine Fellow Yale University School of Medicine Resident Yale University School of Medicine Board Certification AB of Pathology, Anatomic Pathology (2001) Board Certification AB of Pathology, Molecular Genetic Pathology (2011)

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Acquired Resistance of EGFR-Mutant Lung Adenocarcinomas to Afatinib plus Cetuximab Is Associated with Activation of mTORC1. Pirazzoli V, Nebhan C, Song X, Wurtz A, Walther Z, Cai G, Zhao Z, Jia P, de Stanchina E, Shapiro EM, Gale M, Yin R, Horn L, Carbone DP, Stephens PJ, Miller V, Gettinger S, Pao W, Politi K. Acquired resistance of EGFR-mutant lung adenocarcinomas to afatinib plus cetuximab is associated with activation of mTORC1. Cell Rep. 2014 May 22;7(4):999-1008. Reduced NF1 Expression Confers Resistance to EGFR Inhibition in Lung Cancer. de Bruin EC, Cowell C, Warne PH, Jiang M, Saunders RE, Melnick MA, Gettinger S, Walther Z, Wurtz A, Heynen GJ, Heideman DA, Gómez-Román J, García-Castaño A, Gong Y, Ladanyi M, Varmus H, Bernards R, Smit EF, Politi K, Downward J. Reduced NF1 expression confers resistance to EGFR inhibition in lung cancer. Cancer Discov. 2014 May;4(5):606-19. MyD88 signaling in colonic mononuclear phagocytes drives colitis in IL-10 deficient mice. Hoshi N, Schenten D, Nish SA, Walther Z, Gagliani N, Flavell RA, Reizis B, Shen Z, Fox JG, Iwasaki A, Medzhitov R. MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice. Nat Commun. 2012;3:1120. Mitochondrial genome instability and ROS enhance intestinal tumorigenesis in APC(Min/+) mice. Woo DK, Green PD, Santos JH, D'Souza AD, Walther Z, Martin WD, Christian BE, Chandel NS, Shadel GS. Mitochondrial genome instability and ROS enhance intestinal tumorigenesis in APC(Min/+) mice. Am J Pathol. 2012 Jan;180(1):24-31. Molecular Tumor Profiling for Prediction of Response to Anti-Cancer Therapies. Walther, Z., and J. Sklar. 2011. Molecular Tumor Profiling for Prediction of Response to Anti-Cancer Therapies. Cancer J. 17:71-79. Molecular pathology of hepatic neoplasms: classification and clinical significance. Walther, Z. and D.J. Jain. 2011. Molecular pathology of hepatic neoplasms: classification and clinical significance. Pathol. Res. Int. Apr 7:403929. CASK deletion in intestinal epithelia causes mislocalization of LIN7C and the DLG1/Scrib polarity complex without affecting cell polarity. Lozovatsky, L., Abayasekara, N., Piawah, S., and Walther, Z. 2009. CASK deletion in intestinal epithelia causes mislocalization of LIN7C and the DLG1/Scrib polarity complex without affecting cell polarity. Mol. Biol. Cell 20:4489-4499. A PDZ-binding motif controls basolateral targeting of syndecan-1 along the biosynthetic pathway in polarized epithelial cells. Maday, S., Anderson, E., Chang, H.C., Shorter, J., Satoh, A., Sfakianos, J., Folsch, H., Anderson, J.M., Walther, Z., and Mellman, I. 2008. A PDZ-binding motif controls basolateral targeting of syndecan-1 along the biosynthetic pathway in polarized epithelial cells. Traffic 9:1915-24. COX-2 and Angiogenesis in Gastric Cancer. Walther, Z. 2003. COX-2 and Angiogenesis in Gastric Cancer. J Clin Gastroenterol 37(1):4-6. hCASK and hDlg associate in epithelia, and their src homology 3 and guanylate kinase domains participate in both intramolecular and intermolecular interactions. Nix, S.L., Chishti, A.H., Anderson, J.M., and Walther, Z. 2000. hCASK and hDlg associate in epithelia, and their src homology 3 and guanylate kinase domains participate in both intramolecular and intermolecular interactions. J. Biol. Chem. 275:41192-41200.