A5066074522- Acute Myeloid Leukemia Research
- Chronic Myeloid Leukemia Treatments
- Histone Deacetylase Inhibitors Research
- Chronic Lymphocytic Leukemia Research
- Retinoids in leukemia and cellular processes
- Acute Lymphoblastic Leukemia research
- Immune Cell Function and Interaction
- CAR-T cell therapy research
- Multiple Myeloma Research and Treatments
- Microtubule and mitosis dynamics
- T-cell and B-cell Immunology
- Vascular Tumors and Angiosarcomas
- Cancer Treatment and Pharmacology
- Lung Cancer Treatments and Mutations
- Blood disorders and treatments
- Angiogenesis and VEGF in Cancer
- Protein Degradation and Inhibitors
- T-cell and Retrovirus Studies
- Cancer therapeutics and mechanisms
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Eosinophilic Disorders and Syndromes
- HER2/EGFR in Cancer Research
University Medical Center Freiburg
2014-2025
University of Freiburg
2018-2025
Technical University of Munich
2010-2013
Klinikum rechts der Isar
2010-2013
LMU Klinikum
2013
Abstract Background HMAs have finally become the mainstay for AML and MDS patients (pts) ineligible more intensive therapy, due to their favorable safety profile activity also in adverse-genetic disease. Given these advantages over standard, induction chemotherapy („7+3“) we others demonstrated good feasibility of as bridge-to-transplant (Lübbert et al., J. Clin. Onc. 2013). In EORTC AML21 randomized phase III trial compared 10-day decitabine (DAC) monotherapy (300 pts) vs. 7+3 pts...
Abstract FLT3-ITD is the most predominant mutation in AML being expressed about one-third of patients and associated with a poor prognosis. Efforts to better understand downstream signaling possibly improve therapy response are needed. We have previously described FLT3-ITD-dependent phosphorylation CSF2RB, common receptor beta chain IL-3, IL-5, GM-CSF, therefore examined its significance for oncogenic transformation. discovered that directly binds CSF2RB cell lines blasts isolated from...
ABL tyrosine kinase inhibitors (TKI) like Imatinib, Dasatinib and Nilotinib are the gold standard in conventional treatment of CML. However, emergence resistance remains a major problem. Alternative therapeutic strategies TKI-resistant CML urgently needed. We asked whether dual inhibition BCR-ABL Aurora kinases A-C could overcome mediated by mutations. therefore tested PHA-739358 R763/AS703569 Ba/F3- cells ectopically expressing wild type (wt) or mutants. show that both compounds exhibited...
Patients relapsing with FLT3-ITD driven acute myeloid leukemia (FLT3-ITD+ AML) after allogeneic hematopoietic cell transplantation (allo-HCT) have an unfavourable prognosis. Recent studies shown that a combination of sorafenib and Donor Lymphocyte Infusions (DLI) evoked better response in these relapsed patients compared to chemotherapy alone. We found synergised T cells improved survival three murine models (BaF3-FLT3/ITD, MLLPTD/FLT3ITD, Flt3-ITD transduced BM) one humanised FLT3-ITD+ AML...
12024 Background: VEGF and Ang-2 inhibitors have demonstrated clinical activity in various tumor types. Given the overlap of VEGF/VEGFR2 Ang-2/Tie-2 signaling pathways there is a rationale for dual inhibition. BI 836880 humanized bispecific nanobody (engineered antibody fragment variable domains) that inhibits Ang2 has preclinical cancer models. Methods: Pts with solid tumors refractory after standard therapies/for whom no established treatment options were available received q3w (IV;...
In chronic phase myeloid leukemia (CML), the BCR-ABL kinase inhibitor imatinib leads to complete cytogenetic responses in majority of cases. Resistance towards is associated with domain mutations, leading structural changes that prevent from binding.1 In cases failure treatment, second generation inhibitors such as dasatinib or nilotinib have demonstrated activity CML.2 Both drugs are capable suppressing imatinib-resistant, mutant forms BCR-ABL.3 Most mutations gene mediating resistance...
Abstract DNA-hypomethylating agents are the backbone for non-intensive combination treatments of AML/MDS. In elderly AML patients, a DEC+ATRA resulted in an improved response rate and survival compared to DEC without ATRA, also those with prior hematologic disorder; additional valproic acid did not play significant role (Lübbert et al., JCO 2020). To evaluate whether patients oligoblastic benefit from this combination, DECIDER cohort 20-30% bone marrow blasts were analyzed clinical outcome...