Curriculum Vitae. Priv.-Doz. Dr. med. Cyrus Khandanpour

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1 Academic activity since graduation: Research: Curriculum Vitae Priv.-Doz. Dr. med. Cyrus Khandanpour 1/2017- present Venia legendi for internal medicine (Privatdozent, corresponding roughly to associate professor) 3/2012-present Principal Investigator, Department of Hematology, West German Cancer Center, University Clinic of Essen Field of study: Experimental therapy for leukemia and lymphoma 5/ /2010 Post-Doc, Institute de recherches cliniques de Montréal, IRCM Research Unit: Hematopoiesis & Cancer Supervisor: Prof. Tarik Möröy, PhD Field of study: Oncology, molecular biology 1/2005-4/2006 Post-Doc, Institut für Zellbiologie (Tumorforschung) University of Duisburg Essen, Medical Faculty, Germany Supervisor: Prof. Tarik Möröy, PhD Field of study: Oncology, molecular biology Clinical 09/2015-current Board certified in Internal Medicine, Hematology and Oncology Training in palliative care 1/2011-9/2015 Residency Internal Medicine and Fellow Hematology/Oncology, West German Cancer Center, University Hospital of Essen, Germany 7/ /2004 Residency Internal Medicine Department of Internal Medicine, University Hospital of Essen, Germany

2 Doctoral Degree: Doktor der Medizin 11/2005 Supervisor: Prof. Herbert Peter Jennissen, MD, Institut für Medical Degree 3. Staatsexamen und Approbation (equivalent to MD) Physiologische Chemie University of Duisburg-Essen, Medical Faculty, Essen, Germany Field of study: Protein-Protein interaction 5/2003 Medical Faculty, University of Duisburg-Essen, Essen, Germany and Leicester University, Leicester, Great Britain

3 Fellowships and Prizes awarded 09/2015 Abstract achievement award, Haematological malignancies meeting of the American Society of Hematology (ASH), Chicago, Illinois, USA 02/2013 Leukemia Clinical Research award of the German Society of Haematology and Oncology 10/2011 Translational Research Haematology Training fellowship of the American Society of Hematology (ASH) and the European Hematology Association (EHA). Awarded 10/211, however because of medical emergency, participation had to be cancelled. 12/2011 German Cancer fund for cancer research (Max Eder group) 10/2011 Abstract achievement award American Society of Hematology (ASH 2011) 01/2011 Starting Grant for young investigators, University Clinic of Essen 05/2010 Poster award for best poster presentation at the Cole Foundation Science day 07/ /2010 Postdoctoral fellowship from the Cole Foundation for the project: Role of Gfi1 in the development of leukemia 06/2009 Roger Boucher award for best poster at the Journée de la recherché at the Institute de recherches cliniques de Montréal (IRCM). 06/2008 Boehringer Ingelheim award for best oral presentation at the Journée de la recherché at the Institute de recherches cliniques de Montréal (IRCM).

4 List of 10 most important original works 1. Al-Matary, Y. S., Botezatu, L., Opalka, B., Hones, J. M., Lams, R. F., Thivakaran, A., Schutte, J., Koster, R., Lennartz, K., Schroeder, T., Haas, R., Duhrsen, U., and Khandanpour, C. (2016) Acute myeloid leukemia cells polarize macrophages towards a leukemia supporting state in a Growth factor independence 1 dependent manner. Haematologica 101, Opening a new field of interaction between macrophages and AML cells, showing that AML cells instruct macrophages to begin supporting leukemic cells instead of targeting them. (Independent of my Post-Doc or MD supervisor). 2. Botezatu, L., Michel, L. C., Helness, A., Vadnais, C., Makishima, H., Hones, J. M., Robert, F., Vassen, L., Thivakaran, A., Al-Matary, Y., Lams, R. F., Schutte, J., Giebel, B., Gorgens, A., Heuser, M., Medyouf, H., Maciejewski, J., Duhrsen, U., Moroy, T., and Khandanpour, C. (2016) Epigenetic therapy as a novel approach for GFI136N-associated murine/human AML. Exp Hematol 44, e714. Showing a new approach to treating leukemia by targeting the fact that the presence of a mutated form of GFI1 (called GFI1-36N) leads to epigenetic changes which in turn is one factor promoting AML. Use of HATis impede growth of these leukemic cells. 3. Botezatu, L., Michel, L. C., Makishima, H., Schroeder, T., Germing, U., Haas, R., van der Reijden, B., Marneth, A. E., Bergevoet, S. M., Jansen, J. H., Przychodzen, B., Wlodarski, M., Niemeyer, C., Platzbecker, U., Ehninger, G., Unnikrishnan, A., Beck, D., Pimanda, J., Hellstrom-Lindberg, E., Malcovati, L., Boultwood, J., Pellagatti, A., Papaemmanuil, E., Le Coutre, P., Kaeda, J., Opalka, B., Moroy, T., Duhrsen, U., Maciejewski, J., and Khandanpour, C. (2016) GFI1(36N) as a therapeutic and prognostic marker for myelodysplastic syndrome. Exp Hematol 44, e591 A mutated form of GFI1 is a novel independent prognostic marker for a preleukemic disease called myelodysplastic syndrome, thus enabling a better tailored therapy for MDS. 4. Hones, J. M., Botezatu, L., Helness, A., Vadnais, C., Vassen, L., Robert, F., Hergenhan, S. M., Thivakaran, A., Schutte, J., Al-Matary, Y. S., Lams, R. F., Fraszscak, J., Makishima, H., Radivoyevitch, T., Przychodzen, B., da Conceicao Castro, S. V., Gorgens, A., Giebel, B., Klein-Hitpass, L., Lennartz, K., Heuser, M., Thiede, C., Ehninger, G., Duhrsen, U., Maciejewski, J. P., Moroy, T., and Khandanpour, C. (2016) GFI1 as a novel prognostic and therapeutic factor for AML/MDS. Leukemia 30, Low level of Gfi1, in contrast to complete absence of Gfi1, promotes AML and MDS by repressing genes involved in leukemia. We also examined a first appoach to exploiting this finding on a therapeutic level. 5. Monteferrario, D., Bolar, N. A., Marneth, A. E., Hebeda, K. M., Bergevoet, S. M., Veenstra, H., Laros-van Gorkom, B. A., MacKenzie, M. A., Khandanpour, C., Botezatu, L., Fransen, E., Van Camp, G., Duijnhouwer, A. L., Salemink, S., Willemsen, B., Huls, G., Preijers, F., Van Heerde, W., Jansen, J. H., Kempers, M. J., Loeys, B. L., Van Laer, L., and Van der Reijden, B. A. (2014) A dominant-negative GFI1B mutation in the gray platelet syndrome. N Engl J Med 370,

5 We provided the mouse model for a mutated form of Gfi1b, which is responsible for a new type of thrombopenia disease in humans. 6. Khandanpour, C., Phelan, J. D., Vassen, L., Schutte, J., Chen, R., Horman, S. R., Gaudreau, M. C., Krongold, J., Zhu, J., Paul, W. E., Duhrsen, U., Gottgens, B., Grimes, H. L., and Moroy, T. (2013) Growth factor independence 1 antagonizes a p53-induced DNA damage response pathway in lymphoblastic leukemia. Cancer Cell 23, Leukemic cells require expression of Gfi1 to counteract p53 activation and that loss of Gfi1 eradicates leukemic cells and at the same time spares normal cells. 7. Khandanpour, C., Krongold, J., Schutte, J., Bouwman, F., Vassen, L., Gaudreau, M. C., Chen, R., Calero-Nieto, F. J., Diamanti, E., Hannah, R., Meyer, S. E., Grimes, H. L., van der Reijden, B. A., Jansen, J. H., Patel, C. V., Peeters, J. K., Lowenberg, B., Duhrsen, U., Gottgens, B., and Moroy, T. (2012) The human GFI136N variant induces epigenetic changes at the Hoxa9 locus and accelerates K-RAS driven myeloproliferative disorder in mice. Blood 120, I generated a new mouse model to study the function of a mutated form of Gfi1, called GFI1-36N. I found that this mutated form of Gfi1 promotes AML development. We hereby presented a innovative model of how GFI136N affects AML development. 8. Khandanpour, C., Kosan, C., Gaudreau, M. C., Duhrsen, U., Hebert, J., Zeng, H., and Moroy, T. (2011) Growth factor independence 1 protects hematopoietic stem cells against apoptosis but also prevents the development of a myeloproliferative-like disease. Stem Cells 29, I explored the function of Gfi1 in stem cells and found that Gfi1 is necessary for protecting stem cells against apoptosis in a stress situation. This work presents one model explaining how the loss of Gfi1 crutially affects the function of stem cells. 9. Khandanpour, C., Sharif-Askari, E., Vassen, L., Gaudreau, M. C., Zhu, J., Paul, W. E., Okayama, T., Kosan, C., and Moroy, T. (2010) Evidence that growth factor independence 1b regulates dormancy and peripheral blood mobilization of hematopoietic stem cells. Blood 116, Gfi1b critically restrictsthe expansion of hematopetic stem cells. Loss of Gfi1b leads to a massive expansion of functional stem cells. This finding can be of utmost importance in understanding the role of Gfi1b in AML development. 10. Khandanpour, C., Thiede, C., Valk, P. J., Sharif-Askari, E., Nuckel, H., Lohmann, D., Horsthemke, B., Siffert, W., Neubauer, A., Grzeschik, K. H., Bloomfield, C. D., Marcucci, G., Maharry, K., Slovak, M. L., van der Reijden, B. A., Jansen, J. H., Schackert, H. K., Afshar, K., Schnittger, S., Peeters, J. K., Kroschinsky, F., Ehninger, G., Lowenberg, B., Duhrsen, U., and Moroy, T. (2010) A variant allele of Growth Factor Independence 1 (GFI1) is associated with acute myeloid leukemia. Blood 115, A single nucleotide polymorphism of Gfi1 predisposes patients to AML. At the time of publication, this was the biggest study to examine the interaction between GFI1 and AML. This SNP is also one of the most common SNPs affacting the development of AML.