Publications by authors named "M Jarosova"

Despite significant improvement in the survival of pediatric patients with cancer, treatment outcomes for high-risk, relapsed, and refractory cancers remain unsatisfactory. Moreover, prolonged survival is frequently associated with long-term adverse effects due to intensive multimodal treatments. Accelerating the progress of pediatric oncology requires both therapeutic advances and strategies to mitigate the long-term cytotoxic side effects, potentially through targeting specific molecular drivers of pediatric malignancies.

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We performed retrospective analysis of relapsed/refractory multiple myeloma (RRMM) patients previously exposed to daratumumab treated with ixazomib, lenalidomide, dexamethasone (IRd) regimen in real clinical practice. Our aim was to evaluate efficacy of IRd in these patients and select a subset of patients that would benefit from this treatment the most. In total, we analyzed 43 daratumumab-exposed RRMM patients treated in our center.

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Article Synopsis
  • Multiple myeloma (MM) is a complex blood cancer characterized by the expansion of abnormal plasma cells in the bone marrow, resulting in symptoms like bone damage, low blood cell counts, and kidney issues.
  • Despite improved treatments, the disease often relapses, and its development is linked to genomic instability, particularly a phenomenon called chromothripsis, which causes major chromosome shattering and rearrangement.
  • This review aims to summarize key chromosomal abnormalities in MM, with an emphasis on how chromothripsis contributes to the disease's complexity and opens up potential avenues for better diagnostics and understanding of its underlying mechanisms.
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Several in vitro models have been developed to mimic chronic lymphocytic leukemia (CLL) proliferation in immune niches; however, they typically do not induce robust proliferation. We prepared a novel model based on mimicking T-cell signals in vitro and in patient-derived xenografts (PDXs). Six supportive cell lines were prepared by engineering HS5 stromal cells with stable expression of human CD40L, IL4, IL21, and their combinations.

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