Dr Med Vet, postdoc
henrik [dot] lilljebjorn [at] med [dot] lu [dot] se
Publikationer (hämtat ur Lunds universitets publikationsdatabas)
- Activation of human telomerase reverse transcriptase through gene fusion in clear cell sarcoma of the kidney.
- Ebf1 heterozygosity results in increased DNA damage in pro-B cells and their synergistic transformation by Pax5 haploinsufficiency.
- Intratumoral genome diversity parallels progression and predicts outcome in pediatric cancer.
- A novel SERPINE1-FOSB fusion gene results in transcriptional up-regulation of FOSB in pseudomyogenic haemangioendothelioma.
- Fusions involving protein kinase C and membrane-associated proteins in benign fibrous histiocytoma.
- GRM1 is upregulated through gene fusion and promoter swapping in chondromyxoid fibroma.
- Modeling chronic myeloid leukemia in immunodeficient mice reveals expansion of aberrant mast cells and accumulation of pre-B cells.
- RNA-seq identifies clinically relevant fusion genes in leukemia including a novel MEF2D/CSF1R fusion responsive to imatinib.
- Concomitant deletions of tumor suppressor genes MEN1 and AIP are essential for the pathogenesis of the brown fat tumor hibernoma.
- Genetic analysis of dasatinib-treated chronic myeloid leukemia rapidly developing into acute myeloid leukemia with monosomy 7 in Philadelphia-negative cells.
- Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia.
- Integrative analysis of gene expression and copy number alterations using canonical correlation analysis
- Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations.
- The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood acute lymphoblastic leukemias
- Combined high-resolution array-based comparative genomic hybridization and expression profiling of ETV6/RUNX1-positive acute lymphoblastic leukemias reveal a high incidence of cryptic Xq duplications and identify several putative target genes within the commonly gained region
- Fusion gene-mediated truncation of RUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndrome.