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Gliomas are the predominant cause of cancer-related deaths among the young population. Even after incorporation of IDH1/2 mutations and 1p19q codeletion there are doubts regarding adjuvant treatment in WHO G2/G3 gliomas. miRNA molecules control about 30% of all genes, also many oncogenes, tumor suppressor genes and genes responsible for the response to ionizing radiation and systemic treatment. Patients with brain gliomas exhibit miRNA disorders. We aimed to evaluate the expression of miR-200 family members in relation to selected clinico-pathological factors and their prognostic value. We enrolled 53 patients diagnosed with WHO G2/G3 brain gliomas treated between 2012–2016. RT-qPCR based expression of miR-200 family was assessed in tumor and surrounding non-cancerous tissue. An analysis of selected clinico-pathological features was carried out. A logistic regression model was prepared for the miRNA signature. The predictive potential of the signature was assessed using the ROC curve. A stepwise backward regression model was used to select variables with a significant predictive potential related to OS. It was shown that miR-200a-3p, miR-200a-5p, miR-200c-5p, miR-141-3p and miR-429 can be independent predictors of survival. Better 2- and 5-year OS was associated with higher expression of miR-200a-3p, miR141-3p and lower expression of miR-200a-5p, miR-200c-5p, miR-429. The strongest predictors of survival were miR-200a-5p, miR-200b-3p, miR-200c-5p, miR-141-3p, miR-429, tumor volume and CTV. Members of the miR-200 family exhibit prognostic value for 2- and 5-year OS. Presented predictive models of survival may be clinically useful for treatment optimization.

Mitochondria are organelles necessary for oxidative phosphorylation. The interest in the role of mitochondria in the process of carcinogenesis results from the fact that a respiratory deficit is found in dividing cells, especially in cells with accelerated proliferation. The study included tumor and blood material from 30 patients diagnosed with glioma grade II, III and IV according to WHO (World Health Organization). DNA was isolated from the collected material and next-generation sequencing was performed on the MiSeqFGx apparatus (Illumina). The study searched for a possible relationship between the occurrence of specific mitochondrial DNA polymorphisms in the respiratory complex I genes and brain gliomas of grade II, III and IV. The impact of missense changes on the biochemical properties, structure and functioning of the encoded protein, as well as their potential harmfulness, were assessed in silico along with their belonging to a given mitochondrial subgroup. The A3505G, C3992T, A4024G, T4216C, G5046A, G7444A, T11253C, G12406A and G13604C polymorphisms were assessed as deleterious changes in silico, indicating their association with carcinogenesis.

Mitochondrial DNA changes can contribute to both an increased and decreased likelihood of cancer. This process is complex and not fully understood. Polymorphisms and mutations, especially those of the missense type, can affect mitochondrial functions, particularly if the conservative domain of the protein is concerned. This study aimed to identify the possible relationships between brain gliomas and the occurrence of specific mitochondrial DNA polymorphisms and mutations in respiratory complexes III, IV and V. The investigated material included blood and tumour material collected from 30 Caucasian patients diagnosed with WHO grade II, III or IV glioma. The mitochondrial genetic variants were investigated across the mitochondrial genome using next-generation sequencing (MiSeq/FGx system—Illumina). The study investigated, in silico, the effects of missense mutations on the biochemical properties, structure and functioning of the encoded protein, as well as their potential harmfulness. The A14793G (MTCYB), A15758G, (MT-CYB), A15218G (MT-CYB), G7444A (MT-CO1) polymorphisms, and the T15663C (MT-CYB) and G8959A (ATP6) mutations were assessed in silico as harmful alterations that could be involved in oncogenesis. The G8959A (E145K) ATP6 missense mutation has not been described in the literature so far. In light of these results, further research into the role of mtDNA changes in brain tumours should be conducted.

The goal of the study was to explore the spectrum of pathogenic variants in the RPGR gene in a group of male Polish patients with a retinitis pigmentosa (RP) phenotype. A total of 45 male index patients, including twins, being members of 44 families, were screened for pathogenic variants in the RPGR gene via the direct sequencing of PCR-amplified genomic DNA and underwent a comprehensive ophthalmological examination in one center located in Poland. A total of two pathogenic and five likely pathogenic variants in eight patients (18%) were detected in the studied cohort. Of these, five variants were novel, and five disease-causing variants (71%) were identified within the ORF15 mutational hotspot of the RPGR gene. The median age of onset of the disease was 10 years (range 6–14 years), the median age during the examination was 30 years (range 20–47 years), and the median visual acuity was 0.4 (range 0.01–0.7). The majority of patients had middle constriction of the visual field and thinning of the central foveal thickness. Dizygotic twins bearing the same hemizygous mutation showed a different retinal phenotype in regard to the severity of the symptoms. This is the first RPGR mutation screening in Poland showing a prevalence of 18% of RPGR pathogenic mutations and likely pathogenic variants in the studied cohort of male patients with an RP phenotype.

The city of Warsaw, Poland, has endured significant damage throughout its history, particularly during World War II. The city was bombed in September 1939, and many buildings were blown up following the Warsaw Ghetto Uprising in May 1943. The Warsaw Uprising in August and September 1944 led to further destruction from artillery bombardments and fires. Even after the surrender and civilian evacuation in October 1944, additional demolitions occurred, leaving almost 90% of Warsaw in ruins. Despite ongoing efforts to rebuild the city, many landmarks could not be fully reconstructed. However, invaluable historical archives preserve remnants of Warsaw’s rich history. To reconstruct 3D models of pre-war buildings in Warsaw, a methodology was developed that integrates cartographic materials, spatial data, and results from tachymetric measurements. Historical maps, terrestrial and aerial photographs, and architectural blueprints from the National Archives in Warsaw were used to propose three distinct approaches to 3D modeling. Notable structures such as the Grand Synagogue, the Kamienica Theater building, and the Tłomackie buildings were selected for 3D modeling. These buildings either were destroyed or endured significant damage during the war. The 3D modeling process involved meticulous processing and calibrating of historical photographs alongside tachymetric surveying for accurate measurements. The proposed methodology showcases the feasibility of recreating 3D renderings of historical edifices, even those lost to time, utilizing archival cartographic data and spatial information from diverse sources. By leveraging cartographic heritage with digital advancements, a unique perspective on Warsaw’s narrative can be gained, enriching the understanding of its past for both residents and professionals such as historians, archivists, and cartographers.