Publications by authors named "O Blau"
Background: Distinguishing donor- vs. recipient-derived myelodysplastic neoplasm (MDS) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is challenging and has direct therapeutical implications.
Methods: Here, we took a translational approach that we used in addition to conventional diagnostic techniques to resolve the origin of MDS in a 38-year-old patient with acquired aplastic anemia and evolving MDS after first allo-HSCT.
Multiple myeloma is an aggressive neoplasm of plasma cells. While numerous drugs have gained approval, the absence of established predictive markers for individual drug responses poses a challenge. In this study, we explored the microwell- and fluorescence-based Cellply CC-Array® technology for high-throughput analysis of in vitro drug responses as a potential predictive marker for patient treatment outcomes.
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- Acute myeloid leukemia (AML) often involves deletions of chromosome 7, which are linked to poor patient outcomes, but the full impact of other genetic changes related to this is not well understood.
- Researchers analyzed genetic alterations in 519 AML patients, using whole-exome sequencing and a specialized gene panel, finding that mutations in TP53, which occurred in 33% of cases, were among the most common.
- The study identified specific genes, like TP53 and PTPN11, that have a significant negative effect on overall and relapse-free survival, highlighting the complex relationship between chromosome 7 abnormalities and patient prognosis in AML.
Acute myeloid leukemia (AML) is a heterogeneous disease characterized by genomic aberrations in oncogenes, cytogenetic abnormalities, and an aberrant epigenetic landscape. Nearly 50% of AML cases will relapse with current treatment. A major source of therapy resistance is the interaction of mesenchymal stroma with leukemic cells resulting in therapeutic protection.
View Article and Find Full Text PDFAcute myeloid leukemia with complex karyotype (CK-AML) is associated with poor prognosis, which is only in part explained by underlying TP53 mutations. Especially in the presence of complex chromosomal rearrangements, such as chromothripsis, the outcome of CK-AML is dismal. However, this degree of complexity of genomic rearrangements contributes to the leukemogenic phenotype and treatment resistance of CK-AML remains largely unknown.
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