- Mario Buono
- Roy Drissen
- Adriana Gambardella
- Amit Grover
- Alejandra Sanjuan-Pla
- Grigoris Tsolkas
- Chinnavuth Vatanashevanopakorn
- Agnes Zay
- Mancini Elena, Sanjuan-Pla Alejandra, Luciani Luisa, Moore Susan, Grover Amit, Zay Agnes, Rasmussen Kasper D, Luc Sidinh, Bilbao Daniel, O'Carroll Donal, Jacobsen Sten E, and Nerlov Claus (2012) FOG-1 and GATA-1 act sequentially to specify definitive megakaryocytic and erythroid progenitors. EMBO J, 31(2):351-65.
- Bereshchenko Oxana, Mancini Elena, Moore Susan, Bilbao Daniel, Mansson Robert, Luc Sidinh, Grover Amit, Jacobsen Sten EW, Bryder David, and Nerlov Claus (2009) Hematopoietic stem cell expansion precedes the generation of committed myeloid leukemia-initiating cells in C/EBPalpha mutant AML. Cancer Cell, 16(5):390-400.
- Lopez Rodolphe G, Garcia-Silva Susana, Moore Susan J, Bereshchenko Oksana, Martinez-Cruz Ana B, Ermakova Olga, Kurz Elke, Paramio Jesus M, and Nerlov Claus (2009) C/EBPalpha and beta couple interfollicular keratinocyte proliferation arrest to commitment and terminal differentiation. Nat Cell Biol, 11(10):1181-90.
- Ruffell Daniela, Mourkioti Foteini, Gambardella Adriana, Kirstetter Peggy, Lopez Rodolphe G, Rosenthal Nadia, and Nerlov Claus (2009) A CREB-C/EBPbeta cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair. Proc Natl Acad Sci U S A, 106(41):17475-80.
- Kirstetter Peggy, Schuster Mikkel B, Bereshchenko Oksana, Moore Susan, Dvinge Heidi, Kurz Elke, Theilgaard-Monch Kim, Mansson Robert, Pedersen Thomas A, Pabst Thomas, Schrock Evelin, Porse Bo T, Jacobsen Sten EW, Bertone Paul, Tenen Daniel G, and Nerlov Claus (2008) Modeling of C/EBPalpha mutant acute myeloid leukemia reveals a common expression signature of committed myeloid leukemia-initiating cells. Cancer Cell, 13(4):299-310.
The hematopoietic stem cell is capable of maintaining the output of >10 cellular lineage for the entire lifespan of the organism. This is made possible by the presence of structures (niches) dedicated to long-term maintenance of the multi-potent stem cell state, as well as mechanisms for the generation and subsequent lineage specification of stem cell progeny lacking long-term self-renewal capacity.
We use genetic methods, combined with genome-wide gene expression and chromatin profiling, to address the complexity of the hematopoietic stem cell population, the niches that maintain them, and the changes hematopoietic stem cells and niches undergo during aging. We investigate the regulators (transcription factors, signaling molecules) that control the lineage commitment of multi-potent hematopoietic progenitors, as well as the cellular pathways that they specify. Finally, we model how mutations affecting the normal transcriptional control of myelopoiesis result in acute myeloid leukemia, and address how the leukemic stem cells responsible for the disease are maintained.
The final goal is to understand the molecular basis for and spatial organization of normal, aging and malignant hematopoiesis, and to use this knowledge to devise cell based and molecular therapies that can be used to treat hematopoietic insufficiencies and malignancies.
Wild type bone marrow (left) and bone marrow cells transformed by different combinations of CEBPA mutations (Cancer Cell 16: 390-400 (2009))