Katarzyna Ewa Rekiel

Ms. Katarzyna Ewa Rekiel

orcid

Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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NRNina Rembiałkowska
Nina Rembiałkowska
KRKatarzyna Ewa Rekiel
Katarzyna Ewa Rekiel
PUPiotr Kacper Urbanowicz
Piotr Kacper Urbanowicz
MMMateusz Bartosz Mamala
Mateusz Bartosz Mamala
KMKarolina Maria Marczuk
Karolina Maria Marczuk
Julita KulbackaJulita Kulbacka
Julita Kulbacka
Epigenetic modifications are heritable, reversible alterations that causally reshape chromatin architecture and thereby influence DNA repair without changing nucleotide sequence. DNA methylation, histone modifications and non-coding RNAs profoundly influence DNA repair mechanisms and genomic stability. Aberrant epigenetic patterns in cancer compromise DNA damage recognition and repair, therefore impairing homologous recombination (HR), non-homologous end joining (NHEJ), and base excision repair (BER) by suppressing key repair genes and lowering access to repair sites. Then it is dissected how loss-of-function mutations in Switch/Sucrose non-fermentable, imitation switch and CHD (Chromodomain helicase DNA-binding) chromatin-remodeling complexes impair nucleosome repositioning, preventing effective damage sensing and assembly of repair machinery. Non-coding RNAs contribute to epigenetic silencing at DNA break sites, exacerbating repair deficiencies. This review evaluates recent advances concerning epigenetic dysfunction and DNA repair impairment. It is also highlighted that nanoparticle-mediated delivery strategies are designed to overcome pharmacologic resistance. It is presented how epigenetic dysregulation of DNA repair can guide more effective and drug-resistant cancer therapies.

1 May 2025 in Cancers
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EBElżbieta Laura Bartoszewska
Elżbieta Laura Bartoszewska
MCMelania Czapla
Melania Czapla
KRKatarzyna Anna Rakoczy
Katarzyna Anna Rakoczy
MFMichał Filipski
Michał Filipski
KRKatarzyna Ewa Rekiel
Katarzyna Ewa Rekiel
CKChristopher Kobierzycki
Christopher Kobierzycki
Ion channels are proteins that regulate the flow of ions across cell membranes, playing a vital role in cervical cancer development and progression. These channels serve as both potential diagnostic markers and therapeutic targets, offering new opportunities for cancer treatment. Moreover, ion channels are crucial molecular indicators and possible therapeutic targets due to their role in the development of cervical cancer. Our review focuses on the various types of ion channels which are associated with cervical cancer (CCa), including sodium, calcium, and potassium channels. In our review, we clarify their diagnostic and prognostic value, as well as their relationship to the prognosis and stage of the disease. We also examine how ion channels contribute to the metastasis of cervical cancer, specifically in relation to their influence on cell motility, invasion, and interaction with the tumor microenvironment. By examining preclinical and clinical research involving ion channel blockers and modulators, we also highlight the therapeutic potential of targeting ion channels. We have demonstrated the available assays and imaging methods based on ion channel activity as examples of emerging diagnostic breakthroughs that show promise for enhancing the early detection of cervical cancer. Additionally, the possibility that ion channel modulator-based combination therapy could improve the efficacy of traditional treatments is investigated. To demonstrate the potential of ion channels in cervical cancer diagnosis and treatment, our review highlights the current challenges and the promising role in cervical cancer diagnostics and therapy.

4 September 2026 in International Journal of Innovative Technologies in Social Science
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PMPaulina Musiał
Paulina Musiał
SPSzymon Pieczara
Szymon Pieczara
ZSZofia Klara Stefanik
Zofia Klara Stefanik
EDEwa Drzazga-Wilk
Ewa Drzazga-Wilk
MSMikołaj Stańko
Mikołaj Stańko
KRKatarzyna Ewa Rekiel
Katarzyna Ewa Rekiel
Background: Head and neck squamous cell carcinoma (HNSCC) is the seventh most common malignancy worldwide and is associated with substantial morbidity and mortality. Although tobacco use, alcohol consumption, and human papillomavirus (HPV) infection remain the principal risk factors, growing evidence suggests that oral microbiome dysbiosis may contribute to tumor initiation, progression, and treatment response. Aim: This review summarizes current evidence linking oral microbiome dysbiosis with HNSCC, evaluates proposed biological mechanisms, and highlights major gaps requiring future investigation. Methods: A literature review was conducted by searching PubMed, Scopus, Web of Science, and Google Scholar for studies published through March 2026. Summary: Prospective cohort studies and case-control analyses have reported enrichment of periodontal-associated pathogens, including Fusobacterium nucleatum, Porphyromonas gingivalis, and Treponema denticola, in tumor tissues and saliva of patients with HNSCC, alongside depletion of commensal genera such as Streptococcus, Rothia, and Actinomyces. These organisms may influence carcinogenesis through NF-κB activation, Wnt/β-catenin signaling, epithelial–mesenchymal transition, apoptosis resistance, and immune modulation. Cancer therapies, particularly radiotherapy and chemotherapy, profoundly alter oral microbial communities and may worsen oral mucositis, candidiasis, and dental complications. Microbiome-targeted strategies, including probiotics, represent promising adjunctive approaches, although robust clinical validation is still required.

21 September 2026 in Viruses
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JGJulia Klaudia Gąsiorowska
Julia Klaudia Gąsiorowska
MHMaciej Mateusz Hanypsiak
Maciej Mateusz Hanypsiak
NJNatalia Jendrzejaczyk
Natalia Jendrzejaczyk
AAArtur Ams
Artur Ams
JFJan Rafał Falana
Jan Rafał Falana
PDPaweł Dąbrowski
Paweł Dąbrowski
Objective: This review aims to describe the macroscopic methods used to detect poliomyelitis in human skeletal remains and to highlight the limitations of current diagnostic frameworks. Materials: The reviewed materials consist of published paleopathological literature and case studies analyzing human skeletal remains for evidence of the disease. Methods: We evaluated existing studies that focus on the macroscopic analysis of secondary skeletal alterations caused by paralysis, such as unilateral limb atrophy, bone shortening, pronounced asymmetry, and compensatory hypertrophy. Results: Current diagnostic frameworks rely almost exclusively on macroscopic markers; notably, none of the reviewed studies utilized molecular or genetic techniques. Consequently, definitively confirmed cases of ancient poliomyelitis remain exceptionally rare. Conclusions: The paleopathological diagnosis of poliomyelitis currently suffers from a substantial methodological gap due to an overreliance on morphological assessments. Transcending these traditional techniques is essential to definitively confirm ancient cases. Significance: Analyzing skeletal evidence provides crucial insights into how this debilitating viral infection afflicted human populations in antiquity. It also underscores the importance of rigorous differential diagnosis to distinguish poliomyelitis from other paralytic etiologies, such as cerebral palsy.