Sara Meyer Email & Phone Number
@jefferson.edu
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Sara Meyer is listed as Associate Professor at Thomas Jefferson University, based in Philadelphia, Pennsylvania, United States. AeroLeads shows a work email signal at jefferson.edu and a matched LinkedIn profile for Sara Meyer.
Sara Meyer previously worked as Assistant Professor at Thomas Jefferson University and Postdoctoral Fellow at Cincinnati Children'S Hospital Medical Center. Sara Meyer holds Doctor Of Philosophy - Phd, Cell/Cellular And Molecular Biology from University Of Cincinnati.
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About Sara Meyer
I have been working in academia for nearly two decades on translational cancer research, and I am currently Associate Professor of Pharmacology, Physiology & Cancer Biology. I have comprehensive expertise, technical, and analytical skill sets diversified across multiple disciplines with special emphasis in molecular and cell biology, epigenetics, non-coding RNA, clonal tumor architecture, cell surface receptor signaling, immuno-oncology, immunology, mouse models of development and tumorigenesis. I am the Principal Investigator (PI) of a 7-year $1.6 million NIH/NCI R37 MERIT Award, co-Director of the Sidney Kimmel Cancer Center (SKCC) Flow Cytometry and Human Immune Monitoring Shared Resource core facility, involved in clinical correlate studies for two clinical trials at Jefferson, and my research is partially supported by Pharmaceutical industry. The research focus of my laboratory is molecular and pathogenic mechanisms of epigenetic and immune signaling in the development, maintenance, and therapeutic responsiveness of human cancer, and in particular myeloid malignancies. Overall, my research program has led to identification of new therapeutically targetable pathways in epigenetic, innate immune signaling, and cell cycle control using human-mouse cross-species analyses of pre-clinical murine models.
Listed skills include Leukemia, Hematopoiesis, Cancer Cell Biology, Molecular Biology, and 13 others.
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Sara Meyer work experience
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Associate Professor
My lab studies the cellular and molecular mechanisms of high risk poor outcome subsets of epigenetic modifier mutant Acute Myeloid Leukemia (AML). We consider AML from the perspective of an immune cell and aim to see how far we can push the cells toward normal immune function. We also view our approach as a novel anti-AML option. In all our work tumor heterogeneity and cross-talk with the immune microenvironment are important aspects of all of our studies. To this end we use in vivo and single cell approaches.I am the Co-Director of the Sidney Kimmel Cancer Center Flow Cytometry and Human Immune Monitoring Shared Resource Facility. Co-Director of the Mechanisms of Health and Disease Seminar Series. Serve on numerous PhD qualifying exam committees, PhD thesis committees. I mentor PhD students in my lab for their thesis projects and I also mentor junior faculty at Jefferson and serve as a faculty member for the international European Society of Hematology and American Society of Hematology Translational Research in Training Scholar Award Program.Publications:https://www.ncbi.nlm.nih.gov/myncbi/1R_d5vxDT-HQM/bibliography/public/
Assistant Professor
My lab studies the cellular and molecular mechanisms of high risk poor outcome subsets of epigenetic modifier mutant Acute Myeloid Leukemia (AML). We consider AML from the perspective of an immune cell and aim to see how far we can push the cells toward normal immune function. We also view our approach as a novel anti-AML option. In all our work tumor heterogeneity and cross-talk with the immune microenvironment are important aspects of all of our studies. To this end we use in vivo and single cell approaches.Publications:https://www.ncbi.nlm.nih.gov/myncbi/1R_d5vxDT-HQM/bibliography/public/
Postdoctoral Fellow
-Interrogation of the miRNA regulated cancer transcriptome in AML.Publications:Meyer SE, Qin T, Muench DE, Masuda K, Venkatasubramanian M, Orr E, Elisabeth Paietta, Tallman MS, Fernandez H, Melnick A, Le Beau MM, Kogan S, Salomonis N, and Figueroa ME, Grimes HL. Dnmt3a haploinsufficiency transforms Flt3-ITD myeloproliferative disease into a rapid, spontaneous, and fully-penetrant acute myeloid leukemia. Cancer Discov. Published OnlineFrist March 25, 2016; doi:10.1158/2159-8290.CD-16-0008.Grimes HL and Meyer SE. A 2-way miRror of red blood cells and leukemia. Blood. 2015 Feb 19;125(8):1202-3.Raines AM*, Adam M*, Magella B, Meyer SE, Grimes HL, Dey SK, Potter SS. Recombineering based dissection of flanking and paralogous Hox gene functions in reproductive tracts. Development. 2013 Jul;140(14):2942-52.Meyer SE and Grimes HL. MicroRNA in Myelopiesis and Myeloid Disorders Chater 21 Section 3. MicroRNA in Medicine. 2012.Khandanpour C, Krongold J, Schütte J, Bouwman F, Vassen L, Gaudreau MC, Chen R, Calero-Nieto FJ, Diamanti E, Hannah R, Meyer SE, Grimes HL, van der Reijden BA, Jansen JH, Patel CV, Peeters JK, Löwenberg B, Dührsen U, Göttgens B, Möröy T. The human GFI136N variant induces epigenetic changes at the Hoxa9 locus and accelerates K-RAS driven myeloproliferative disorder in mice. Blood. 2012 Nov 8;120(19):4006-17.Stoffers SL, Meyer SE, Grimes HL. MicroRNAs in the Midst of Myeloid Signal Transduction. J Cell Physiol. 2012 Jan;227(2):525-33.Meyer SE*, Hasenstein JR*, Baktula A*, Velu CS, Xu Y, Wan H, Whitsett JA, Gilks CB, Grimes HL. Kruppel-Like Factor 5 is not required for K-RasG12D lung tumorigenesis, but represses ABCG2 expression and is associated with good prognosis. Am J Pathol. 2010. Sep; 177(3):1503-13.
Graduate Student
-Receptor tyrosine kinase, Ron, signaling in normal development and tumor formation.Publications:Jiang P, Hu Q, Meyer S, Waltz S, Khan S, Ito M, Roeder R, Zhang X. Key Roles for MED1 LxxLL Motifs in Pubertal Mammary Gland Development and Luminal-Cell Differentiation. Proc Natl Acad Sci. 2010, 107:6765-6770.Meyer SE, Peace BP, Bahassi EM, Robbins SB, Yin M, Stambrook PJ, Zinser GZ, Waltz SE. Chek2*1100delC mutation increases susceptibility to Ron-induced mammary tumorigenesis in mice. Canc Letters 2010.Meyer SE, Waltz SE, Goss KH. The Ron receptor tyrosine kinase is not required for intestinal adenoma formation in ApcMin/+ mice. Mol Carcinog. 2009 Nov;48(11):995-1004.Meyer SE*, Zinser GZ*, Stuart WD, Pathrose P, Waltz SE. The Ron receptor tyrosine kinase negatively regulates mammary gland branching morphogenesis. Dev Biol. 2009 Sep 1;333(1):173-85.Funding:National Cancer Institute (NCI) T32 CA 59268 Training Grant
Sara Meyer education
Doctor Of Philosophy - Phd, Cell/Cellular And Molecular Biology
Bs, Molecular And Cellular Biology
Frequently asked questions about Sara Meyer
Quick answers generated from the profile data available on this page.
What company does Sara Meyer work for?
Sara Meyer works for Thomas Jefferson University.
What is Sara Meyer's role at Thomas Jefferson University?
Sara Meyer is listed as Associate Professor at Thomas Jefferson University.
What is Sara Meyer's email address?
AeroLeads has found 1 work email signal at @jefferson.edu for Sara Meyer at Thomas Jefferson University.
Where is Sara Meyer based?
Sara Meyer is based in Philadelphia, Pennsylvania, United States while working with Thomas Jefferson University.
What companies has Sara Meyer worked for?
Sara Meyer has worked for Thomas Jefferson University, Cincinnati Children'S Hospital Medical Center, and University Of Cincinnati.
How can I contact Sara Meyer?
You can use AeroLeads to view verified contact signals for Sara Meyer at Thomas Jefferson University, including work email, phone, and LinkedIn data when available.
What schools did Sara Meyer attend?
Sara Meyer holds Doctor Of Philosophy - Phd, Cell/Cellular And Molecular Biology from University Of Cincinnati.
What skills is Sara Meyer known for?
Sara Meyer is listed with skills including Leukemia, Hematopoiesis, Cancer Cell Biology, Molecular Biology, Rna, Cell, Cell Signaling, and Cancer Research.
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