Andreas Reinisch
Medical University of Graz, Stanford Medicine
Research areas: Medicine · Hematology · Hematopoietic Stem Cell Transplantation · Acute Myeloid Leukemia Research · Mesenchymal stem cell research
0000-0001-9333-7689
About
I am a hematology fellow and independent principal investigator at the Division of Hematology, Department of Internal Medicine, at the Medical University of Graz in Austria. After completing my medical studies in 2006, I undertook a PhD studying mesenchymal stromal cell biology at the Division of Hematology, Medical University of Graz, which was awarded in 2010. While training as a clinical fellow for two years I was awarded an Erwin Schroedinger Overseas Research fellowship from the Austrian Research Fund that allowed me to conduct my postdoctoral studies in the lab of Professor Ravindra Majeti at the Hematology Department, Stanford School of Medicine, and Stanford Cancer Institute. There I was focusing on (1) in vivo leukemia models and (2) identification of novel interactions of leukemia stem cells as well as hematopoietic stem and progenitor cells with their physiological microenvironment, the bone marrow niche. In collaboration with the lab of Matthew Porteus (Stanford Medicine, Dept. of Pediatrics) I improved CRISPR/Cas9 genome engineering tools to be applicable for manipulation of primary human hematopoietic stem and progenitor cells (HSPCs). I have acquired a depth of experience in human hematopoietic stem and progenitor cell biology, in vitro and in vivo leukemia models, molecular and phenotypic characterization of rare hematopoietic cell populations, and genetic manipulation of human primary hematopoietic cells.
During my time at Stanford, I have developed a unique xenotransplantation niche model that allows for the first time to study human normal and malignant hematopoietic cells in their physiological human habitat. My work has been selected for oral presentation at international meetings and has been published in Nature Medicine (2016), Nature Protocols (2017), and Blood (2015). Additionally, I have developed innovative technologies for the culture and genetic manipulation of primary HSPCs and leukemia patient samples as well as BM stromal elements using novel CRISPR/Cas9 based methods (Nature 2016, Elife 2017). During my scientific carrier, I authored and co-authored more than 40 peer-reviewed papers, 1 review, 1 preview, and 3 book chapters in the fields of stem and progenitor cell biology, hematopoiesis, leukemia, and genome engineering.
At the Medical University of Graz, I am currently a member of the PhD Faculty for Molecular Medicine and lead a research lab focusing on investigating the genetic and molecular events leading to leukemia with a particular emphasis on the contribution of the bone marrow microenvironment (aka niche). In our research, we try to reconstruct leukemogenic events in normal hematopoietic stem and progenitor cells using CRISPR/Cas9 technology to elucidate how they give rise to leukemic stem cell development and eventually cause frank leukemia. Finally, my research aims to investigate how the bone marrow niche interacts with normal and malignant hematopoietic cells and how niche cells contribute to leukemogenesis or vice versa may get altered by leukemia.
Employment
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Medical University of Graz Attending physician2021 - Present
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Medical University of Graz Clinical Fellow2017 - 2021
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Stanford Medicine Postdoctoral Research Fellow2012 - 2017
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Medical University of Graz Clinical Fellow2011 - 2012
Education
- 2007 - 2011
- 2000 - 2006
Projects & Funding
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CRISPR/Cas9 genome engineering to dissect MPN pathogenesis FWF Austrian Science Fund2020 - 2023
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Identifying the hematopoietic and leukemic stem cell niches FWF Austrian Science Fund2020 - Present
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Clonal evolution of acute myeloid leukemia genomes FWF Austrian Science Fund2012 - 2014
Publications (58)
- Self-organized hemanoids derived from human iPSCs create a niche that produces definitive extraembryonic hematopoiesis Save
- Ultraprecision therapy for type 1 vs type 2 CALR+ MPN by dual epitope targeting that restores ruxolitinib sensitivity Save
- Triazoles Versus Echinocandins for the First-Line Treatment of Invasive Pulmonary Aspergillosis: A Propensity Score–Weighted Multicenter Study Save
- Engineered cytokine-expressing MSCs support ex vivo culture of human HSPCs and AML cells Save
- Pulmonary Coinfection of Pneumocystis jirovecii and Aspergillus Species Save
- RUNX1 loss renders hematopoietic and leukemic cells dependent on IL-3 and sensitive to JAK inhibition Save
- Data from The Cell Type–Specific 5hmC Landscape and Dynamics of Healthy Human Hematopoiesis and TET2-Mutant Preleukemia Save
- Data from The Cell Type–Specific 5hmC Landscape and Dynamics of Healthy Human Hematopoiesis and TET2-Mutant Preleukemia Save
- Supplementary Figure from The Cell Type–Specific 5hmC Landscape and Dynamics of Healthy Human Hematopoiesis and TET2-Mutant Preleukemia Save
- Supplementary Figure from The Cell Type–Specific 5hmC Landscape and Dynamics of Healthy Human Hematopoiesis and TET2-Mutant Preleukemia Save
- Supplementary Table from The Cell Type–Specific 5hmC Landscape and Dynamics of Healthy Human Hematopoiesis and TET2-Mutant Preleukemia Save
- Supplementary Table from The Cell Type–Specific 5hmC Landscape and Dynamics of Healthy Human Hematopoiesis and TET2-Mutant Preleukemia Save
- The Cell Type–Specific 5hmC Landscape and Dynamics of Healthy Human Hematopoiesis and TET2-Mutant Preleukemia Save
- Targeted regulation of transcription in primary cells using CRISPRa and CRISPRi Save
- EZH2 inactivation in RAS-driven myeloid neoplasms hyperactivates RAS-signaling and increases MEK inhibitor sensitivity. Save
- Micro-RNA-125a mediates the effects of hypomethylating agents in chronic myelomonocytic leukemia. Save
- CD34 expression does not correlate with immunophenotypic stem cell or progenitor content in human cord blood products. Save
- Sensitive and broadly applicable residual disease detection in acute myeloid leukemia using flow cytometry-based leukemic cell enrichment followed by mutational profiling. Save
- TP53 mutated AML subclones exhibit engraftment in a humanized bone marrow ossicle mouse model Save
- A Dysregulated DNA Methylation Landscape Linked to Gene Expression in MLL-Rearranged AML. Save