Pahl

Prof. Dr.
Heike Pahl
Department of Medicine IPhone: 0049-761-27063400
heike.pahl@uniklinik-freiburg.de
www.uniklinik-freiburg.de/medizin1/forschung
CV
- 1987 B.A. Wellesley College
- 1990 M.A. Harvard Medical School
- 1992 Ph.D. Harvard Medical School
- 1997 Habilitation, Medical School, University of Freiburg
- Since 2012 Full Professor (C3) of Molecular Hematology, Medical Center - University of Freiburg
Focus of research
- Molecular etiology of myeloid neoplasms
- Molecular and cellular biology of myeloid and erythroid differentiation
- Myeloid and erythroid transcription factors
Selected publications
- Jutzi JS, Basu T, Pellmann M, Kaiser S, Steinemann D, Sanders MA, Hinai AA, Zeilemaker A, Kovacs SB, Koellerer C, Ostendorp J, Aumann A, Wang W. Rafoux E, Cassinat B, Bullinger L, Schlegelberger B, Valk PJM, Pahl HL (2019) Altered NFE2 activity predisposes to leukemic transformation and myelosarcoma with AML-specific aberrations. Blood, 133:1766-1777.
- Peeken JC, Jutzi JS, Wehrle J, Koellerer C, Staehle F, Becker H, Schoenwandt E, Seeger TS, Schanne DH, Gothwal M, Ott CJ, Gründer A, Pahl HL (2018) Two novel epigenetic pathways regulate NFE2 overexpression in myeloproliferative neoplasms, Blood, 131:2065-2073.
- Jutzi JS, Bogeska R, Nikoloski G, Schmid CA, Seeger TS, Stegelmann F, Schwemmers S, Gründer A, Peeken J, Gothwal M, Wehrle J, Aumann K, Hamdi K, Dierks, C, Wang W, Döhner K, Jansen JH, Pahl HL. MPN patients harbor recurrent truncating mutations in transcription factor NF-E2, J. Ex. Med. 2013; 210:1003-1019.
- Kaufmann KB, Gründer A, Hadlich T, Wehrle J, Gothwal M, Bogeska R, Seeger TS, Kayser S, Pham KB, Jutzi JS, Ganzenmüller L, Steinemann D, Schlegelberger B, Wagner JM, Jung M, Will B, Steidl U, Aumann K, Werner M, Günther T, Schüle R, Rambaldi A, Pahl HL. A novel murine model of myeloproliferative disorders generated by overexpressionof the transcription factor NF-E2. J. Exp. Med. 2012; 209:35-50.
- Wang W, Schwemmers S, Hexner EO, Pahl HL. AML1 is overexpressed in patients with myeloproliferative neoplasms and mediates JAK2V617F-independent overexpression of NF-E2. Blood. 2010; 116:254-266.