PRELUDIUM 24 Grants for PhD Candidates at the International Doctoral School
We have learned the names of the PRELUDIUM 24 competition winners funded by the National Science Centre. Among the awarded researchers are three doctoral candidates from the International Doctoral School.
We extend our heartfelt congratulations and wish them continued success on their scientific paths!
The PRELUDIUM competitions are well-known NCN programmes among researchers in Poland, enabling the implementation of basic research in Polish institutions. PRELUDIUM grants allow researchers at a very early stage of their careers – still before completing their PhD – to gain their first experience in carrying out research projects lasting up to three years.
| Panel | Project title | Principal Investigator | Name of entity | Granted funds |
|---|---|---|---|---|
| NZ2 | Profiling circulating serum miRNAs as potential biomarkers for patients with syndromic mitochondrial diabetes mellitus | mgr Sebastian Kacper Skoczylas | Medical University of Lodz | 209 644,00 PLN |
| NZ4 | The role of IFN-γ in inducing phenotype alterations and disulfidptosis in drug-naïve and BRAFV600/MEK inhibitor-resistant melanoma cells | mgr Piotr Wawrzyniak | Medical University of Lodz | 209 962,00 PLN |
| NZ7 | The JAK/STAT pathway as a molecular contributor to the development of endometriosis: therapeutic potential of JAK inhibition | lek. Aleksander Radosław Rycerz | Medical University of Lodz | 209 800,00 PLN |
Sebastian Skoczylas, MSc
Project Supervisor: prof. Agnieszka Zmysłowska
Department of Clinical Genetics
Project’s title: Profiling circulating serum miRNAs as potential biomarkers for patients with syndromic mitochondrial diabetes mellitus
Mitochondrial diabetes mellitus is a monogenic form of diabetes caused by mutations in mitochondrial DNA (mtDNA), most commonly the m.3243A>G mutation. These defects impair beta cell function and can lead to insulin resistance. They are also frequently associated with multisystem syndromes, such as mitochondrial diabetes with deafness (MIDD) and mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS). These syndromes can present with symptoms including hearing loss, muscle weakness, neurological impairment and cardiac issues. Despite genetic confirmation, predicting the disease’s phenotype or progression remains difficult, and current blood-based biomarkers are unreliable. There is therefore a need for new, non-invasive tools with which to assess disease severity and progression. Circulating microRNAs have emerged as potential indicators of mitochondrial dysfunction and have already been validated as diagnostic and prognostic markers in cancer, cardiovascular diseases and neurological diseases. Our project aims to identify serum microRNA (miRNA) signatures specific to individuals with m.3243A>G-associated diabetes and compare them with age- and sex-matched non-diabetic controls. Using NGS, we will generate a comprehensive miRNA profile and correlate expression patterns with clinical severity, glucose metabolism and metabolic parameters. This work could help define novel miRNA biomarkers for diagnosis and prognosis, improving our understanding of the pathogenesis of mitochondrial diabetes.
Piotr Wawrzyniak, MSc
Project Supervisor: dr hab. prof. Mariusz Hartman
Department of Molecular Biology of Cancer
Project’s title: The role of IFN-γ in inducing phenotype alterations and disulfidptosis in drug-naïve and BRAFV600/MEK inhibitor-resistant melanoma cells
The response to immunotherapy with immune checkpoint inhibitors depends on the tumor microenvironment, and one of its key components is interferon-gamma (IFN-γ) secreted by immune cells. As a pro-inflammatory cytokine, IFN-γ enhances the immune response by increasing antigen presentation and recruiting effector immune cells to the tumor site. However, melanoma can respond to signals from the microenvironment and adapt to unfavorable conditions due to its high phenotypic plasticity.
The aim of the project is to evaluate phenotypic changes induced by short-term and long-term exposure of melanoma cells to IFN-γ and to determine whether these changes increase their sensitivity to disulfidptosis, a recently described form of non-apoptotic cell death that occurs under conditions of glucose starvation in cells with high expression of SLC7A11, a component of the cystine–glutamate transporter xCT. The studies will be conducted using cell lines that are therapy-naïve or resistant to targeted therapy using BRAFV600 and/or MEK1/2 inhibitors. Melanoma cell lines will be subjected to short-term exposure to IFN-γ to mimic patients’ responses to immunotherapy, while long-term exposure to IFN-γ will be used as a model of resistance to immunotherapy with immune checkpoint inhibitors.
Aleksander Rycerz, MD
Project Supervisor: prof. Wojciech Fendler
Department of Biostatistics and Translational Medicine
The study aims to understand how activation of the JAK/STAT signaling pathway contributes to the development and progression of endometrial lesions. In addition, the effectiveness of JAK inhibitors in the non-hormonal treatment of endometriosis will be evaluated. The project will analyze changes in the expression of JAK/STAT pathway proteins in tissues from women with endometriosis. In parallel, in vitro studies will be conducted using endometriosis cell lines to assess the effects of JAK inhibitors on cell proliferation. The obtained results will enable the identification of new molecular therapeutic targets, which are particularly important for patients who do not respond to currently available treatment methods or who require non-hormonal therapy.