Current projects

• GACHR 24-1173OS (2024-2026):

The role of the damaged DNA response in protecting against malignant progression of preleukemic conditions.

Cell cycle regulation in MPNs and MDS is influenced by the interplay between cellular DNA damage response (DDR) and inflammatory signaling. Based on our results, we have conceptualized biological mechanisms by which polycythemia vera (PV) and low-risk MDS (LR-MDS) progenitors are protected from malignant transformation. The research will contribute to the understanding of progression and therapeutic options in PV and LR-MDS.

• AZV NU23-10-00160 (2023-2026):

VEXAS syndrome; characterization and clinical implications of different genetic variants of UBA1 in patients with rheumatic and hematological diseases.

VEXAS is a disease caused by somatic mutations in the UBA1 gene in hematopoietic progenitor cells. These mutations cause activation of inflammatory pathways that are clinically manifested in elderly patients with systemic inflammation and the possibility of progression to myelodysplastic, myeloproliferative or lymphoproliferative disease.

• AZV NU23-03-00401 (2023-2025):

Advanced genomic characterization of secondary myeloid malignancies: implications for diagnosis and prognostication.

Therapy-related myeloid neoplasms (t-MNs) are secondary malignancies that arise after chemotherapy and/or radiation therapy for a previous cancer. In this project, we focus on advanced genomic and transcriptomic analysis of t-MNs.

• GAČR 23-05462S (2023-2025):

Inhibition of FLT3 with novel dual inhibitors as a potential approach to treat acute myeloid leukemia with MLL gene rearrangements.

FLT3 inhibitors with high selectivity for AML with MLL rearrangement and oncogenic FLT3 have been developed at Palacký University in Olomouc. These inhibitors have several other targets besides FLT3 and this project will elucidate the importance of dual inhibition of FLT3/CDK9 and FLT3/SFK as a basis for a possible therapeutic strategy.

• AZV NU21-03-0056 (2021-2024):

Study of the molecular pathogenesis of bone marrow failure and identification of clinically relevant biomarkers in the hypoplastic form of myelodysplastic syndrome and acquired aplastic anemia.

We are performing detailed genome-wide analyses of hMDS and acquired AA to characterize the molecular pathogenesis of KD decline and define clinically relevant biomarkers to facilitate differential diagnosis, predict progression, and evaluate the impact of immunosuppressive therapy on the development of the pathological clone.

• AZV NU20-03-00412 (2020-2023):

Role of transposable elements and PIWI-interacting RNAs in myelodysplastic syndrome and their potential clinical applications.

The aim of this project is to analyze TE and piRNA transcription using next-generation sequencing and to characterize their role in MDS. In addition to studying the involvement of these molecules in the pathogenesis of MDS, their use as potential molecular markers of disease progression will be tested.

• GACR GA20-19162S (2020-2022):

Circular RNAs and their relationship to RNA splicing in the pathogenesis of myelodysplastic syndrome.

In this project, we use next-generation sequencing, integrative data analysis and functional studies to identify and characterize the role of circRNAs in the pathogenesis of MDS. We are investigating the relationship between circRNAs and splicing mutations in MDS.

• AZV NV18-03-00227 (2018-2022):

Identification and monitoring of prognostic and predictive molecular markers of progression in low-risk myelodysplastic syndrome patients.

In the present project, we are looking for genomic alterations that predict disease progression.

• AZV 17-31398A (2017-2020):

Long non-coding RNAs in myelodysplastic syndrome: clinical significance and implications for pathogenesis.

This project performed genome-wide examination of lncRNAs levels in MDS patients and comparison of expression profiles between different patient groups to find lncRNAs with significantly different levels and potential use in MDS diagnosis.