Sergio Martinez Hoyer Project

Currently, we are working on two projects:

1. Role of innate lymphoid cells in bone marrow fibrosis. Specific genetic alterations in the hematopoietic stem cell compartment can lead to the development of scar tissue in the bone marrow, which then loses its ability to support normal hematopoiesis. Previous work has demonstrated a role for innate lymphocytes in the development of fibrosis in different organs. I am exploring the contribution of innate lymphoid cells to the formation of fibrotic tissue in a mouse model of bone marrow fibrosis.
    
2. Identification of novel therapeutic targets in drug resistant myelodysplastic syndromes. My previous work on resistant MDS described the molecular mechanisms by which malignant cells escape the activity of lenalidomide in the bone marrow. Proof of principle experiments revealed that it should be possible to overcome drug resistance in mutated cells. Using a functional genomics approach on cell lines and primary tissue, we aim to identify novel therapeutic targets that effectively eliminate relapsed malignant cells.

Recent publications

A clinical transcriptome approach to patient stratification and therapy selection in acute myeloid leukemia.
Docking TR, Parker JDK, Jädersten M, Duns G, Chang L, Jiang J, Pilsworth JA, Swanson LA, Chan SK, Chiu R, Nip KM, Mar S, Mo A, Wang X, Martinez-Høyer S, Stubbins RJ, Mungall KL, Mungall AJ, Moore RA, Jones SJM, Birol İ, Marra MA, Hogge D, Karsan A.
Nat Commun. 2021 Apr 30;12(1):2474. 

Mechanisms of lenalidomide sensitivity and resistance.
Martinez-Høyer S, Karsan A.
Exp Hematol. 2020 Nov;91:22-31. 

Loss of lenalidomide-induced megakaryocytic differentiation leads to therapy resistance in del(5q) myelodysplastic syndrome.
Martinez-Høyer S, Deng Y, Parker J, Jiang J, Mo A, Docking TR, Gharaee N, Li J, Umlandt P, Fuller M, Jädersten M, Kulasekararaj A, Malcovati L, List AF, Hellström-Lindberg E, Platzbecker U, Karsan A.
Nat Cell Biol. 2020 May;22(5):526-533.