老澳门六合彩图库

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Research Group Lab Hall
Pharmacology and Toxicology
Antje Schaefer, PhD

Antje Schaefer, PhD

Assistant Professor

Locations

  • Pharmacology & Toxicology
    Basic Science Building
    Office: BSB-B6815; Lab: BSB-B6710

Contact Information

Education

PhD, Structural Biochemistry, Max-Planck-Institute for Molecular Physiology, Germany

Biography

Dr. Antje Schaefer joined the Department of Pharmacology & Toxicology at the 老澳门六合彩图库 as an Assistant Professor in September 2024. Her research program focuses on the mechanisms that drive gastric and pancreatic cancer growth and therapy resistance, with the goal of defining novel, target-based therapeutic strategies for both lethal cancers. Visit for additional information.

Prior to joining 老澳门六合彩图库, Dr. Schaefer was a Research Assistant Professor with Dr. Channing Der at the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill (UNC). She identified that the two most common mutations in the RHOA GTPase in gastric cancer are oncogenic cancer drivers and defined novel therapeutic targets to improve treatment of gastric cancer patients. She also studied the role of RHO GTPase-dependent cell plasticity in driving therapy resistance in RAS-mutant pancreatic, colorectal and head-and-neck-cancers and determined new strategies for combination therapies.

Dr. Schaefer pursued her PhD in RHO and RAS GTPase structure and biochemistry in the lab of Dr. Alfred Wittinghofer at the Max-Planck-Institute for Molecular Physiology in Dortmund, Germany. As a graduate student, she was recognized as a Minerva FemmeNet Program member of the Max-Planck Society. Dr. Schaefer conducted her postdoctoral training with Dr. Peter Hordijk at the Sanquin Blood Institute, Academic Medical Center Amsterdam, The Netherlands. She identified that leukocytes are recruited by an RHO-dependent stiffness gradient across the surface of the endothelial cells to permissive sites where they migrate from the blood vessel into the tissue. For her work, Dr. Schaefer was awarded the Sanquin Science Award, a Sanquin Blood Foundation Research Grant and she was a finalist of the Young Investigator Award from the German Society of Microcirculation and Vascular Biology.

Research Experience

  • Carcinoma, Pancreatic Ductal
  • Cell Plasticity
  • Drug Screening Assays, Antitumor
  • Organoids
  • ras Proteins
  • rho GTP-Binding Proteins
  • Stomach Neoplasms

Research Interests

  • Gastric and pancreatic cancer
  • RHO and RAS GTPases
  • Cancer drug resistance mechanisms
  • Cell plasticity

RAS GTPases (e.g., KRAS) and the similar RHO (RAS homologous) GTPases (e.g., RHOA) are key signaling proteins that regulate a variety of different cellular functions and, when dysregulated, drive pathological processes including cancer as well as developmental and neurological disorders. Four decades ago, mutationally activated RAS genes encoding KRAS, HRAS and NRAS were discovered in cancer and now comprise one of the most frequently mutated oncogene family. By contrast, the cancer-associated functions of RHO GTPases such as RHOA are poorly understood. Only ten years ago, mutations in RHO GTPases and fusion genes of RHO-regulating protein were identified in tumor sequencing studies. Unexpectedly, the cancer-inducing genetic mechanisms (e.g., localization of the mutational hotspots) between RHO and RAS proteins are strikingly different - despite their high similarity in sequence and structure. Thus, extrapolations from the key cancer driver RAS are of limited value. Consequently, RHO-driven cancers such as gastric cancer as well as certain hematopoietic and lymphoid cancers are poorly defined and highly lethal due to the lack of effective therapies. In addition, RHO GTPases play also a critical, yet poorly understood role in the mechanisms that drive treatment resistance in RAS-mutant cancers and, thus, limiting therapy success in patients.

Our research program addresses the following current challenges in the research field:

  1. Dissect the molecular mechanisms by which aberrant RHOA function, induced either by RHOA mutations or RhoGAP fusion genes, drive gastric cancer growth and therapy resistance.
  2. Define the molecular mechanisms by which RHO GTPases modulate treatment resistance in KRAS-dependent pancreatic cancer.

Our overall goal is to discover novel therapeutic vulnerabilities in order to develop better, targeted therapies for these lethal cancers. Our lab uses a multidisciplinary approach including advanced microscopy, functional genomics and proteomics, cancer drug pharmacology, structural biochemistry, patient-derived cell lines and organoids, and mouse models.

Publications

  • (Zhang F, Sahu V, Peng K, Wang Y, Li T, Bala P, Aitymbayev D, Sahgal P, Schaefer A, Der CJ, Ryeom S, Yoon S, Sethi N, Bass AJ, Zhang H.) Gut. 2024 Jul 11;73(8):1280-1291 PMID: 38621923 PMCID: PMC11287566 04/16/2024

  • (Klomp JE, Diehl JN, Klomp JA, Edwards AC, Yang R, Morales AJ, Taylor KE, Drizyte-Miller K, Bryant KL, Schaefer A, Johnson JL, Huntsman EM, Yaron TM, Pierobon M, Baldelli E, Prevatte AW, Barker NK, Herring LE, Petricoin EF 3rd, Graves LM, Cantley LC, Cox AD, Der CJ, Stalnecker CA.) Science. 2024 Jun 07;384(6700):eadk0850 PMID: 38843329 PMCID: PMC11301400 06/06/2024

  • (Schaefer A, Hodge RG, Zhang H, Hobbs GA, Dilly J, Huynh MV, Goodwin CM, Zhang F, Diehl JN, Pierobon M, Baldelli E, Javaid S, Guthrie K, Rashid NU, Petricoin EF, Cox AD, Hahn WC, Aguirre AJ, Bass AJ, Der CJ.) Sci Signal. 2023 Dec 19;16(816):eadg5289 PMID: 38113333 PMCID: PMC10791543 12/19/2023

  • (Huynh MV, Hobbs GA, Schaefer A, Pierobon M, Carey LM, Diehl JN, DeLiberty JM, Thurman RD, Cooke AR, Goodwin CM, Cook JH, Lin L, Waters AM, Rashid NU, Petricoin EF 3rd, Campbell SL, Haigis KM, Simeone DM, Lyssiotis CA, Cox AD, Der CJ.) Sci Signal. 2022 Aug 09;15(746):eabn2694 PMID: 35944066 PMCID: PMC9534304 08/10/2022

  • (Schaefer A, Der CJ.) Trends Cancer. 2022 Aug;8(8):655-669 PMID: 35568648 05/15/2022

  • (Javaid S, Schaefer A, Goodwin CM, Nguyen VV, Massey FL, Pierobon M, Gambrell-Sanders D, Waters AM, Lambert KN, Diehl JN, Hobbs GA, Wood KC, Petricoin EF, Der CJ, Cox AD.) Mol Cancer Ther. 2022 May 04;21(5):762-774 PMID: 35247914 PMCID: PMC9081222 03/06/2022

  • (Cook DR, Kang M, Martin TD, Galanko JA, Loeza GH, Trembath DG, Justilien V, Pickering KA, Vincent DF, Jarosch A, Jurmeister P, Waters AM, Hibshman PS, Campbell AD, Ford CA, Keku TO, Yeh JJ, Lee MS, Cox AD, Fields AP, Sandler RS, Sansom OJ, Sers C, Schaefer A, Der CJ.) Cancer Res. 2022 Jan 01;82(1):90-104 PMID: 34737214 PMCID: PMC9056178 11/06/2021

  • (Waters AM, Khatib TO, Papke B, Goodwin CM, Hobbs GA, Diehl JN, Yang R, Edwards AC, Walsh KH, Sulahian R, McFarland JM, Kapner KS, Gilbert TSK, Stalnecker CA, Javaid S, Barkovskaya A, Grover KR, Hibshman PS, Blake DR, Schaefer A, Nowak KM, Klomp JE, Hayes TK, Kassner M, Tang N, Tanaseichuk O, Chen K, Zhou Y, Kalkat M, Herring LE, Graves LM, Penn LZ, Yin HH, Aguirre AJ, Hahn WC, Cox AD, Der CJ.) Cell Rep. 2021 Jun 29;35(13):109291 PMID: 34192548 PMCID: PMC8340308 07/01/2021

  • (Arrington ME, Temple B, Schaefer A, Campbell SL.) J Biol Chem. 2020 Aug 21;295(34):12130-12142 PMID: 32636302 PMCID: PMC7443499 07/09/2020

  • (Hodge RG, Schaefer A, Howard SV, Der CJ.) Crit Rev Biochem Mol Biol. 2020 Aug;55(4):386-407 PMID: 32838579 08/26/2020

  • (Ozkan-Dagliyan I, Diehl JN, George SD, Schaefer A, Papke B, Klotz-Noack K, Waters AM, Goodwin CM, Gautam P, Pierobon M, Peng S, Gilbert TSK, Lin KH, Dagliyan O, Wennerberg K, Petricoin EF 3rd, Tran NL, Bhagwat SV, Tiu RV, Peng SB, Herring LE, Graves LM, Sers C, Wood KC, Cox AD, Der CJ.) Cell Rep. 2020 Jun 16;31(11):107764 PMID: 32553168 PMCID: PMC7393480 06/20/2020

  • (Zhang H, Schaefer A, Wang Y, Hodge RG, Blake DR, Diehl JN, Papageorge AG, Stachler MD, Liao J, Zhou J, Wu Z, Akarca FG, de Klerk LK, Derks S, Pierobon M, Hoadley KA, Wang TC, Church G, Wong KK, Petricoin EF, Cox AD, Lowy DR, Der CJ, Bass AJ.) Cancer Discov. 2020 Feb;10(2):288-305 PMID: 31771969 PMCID: PMC7007383 11/28/2019

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