Background/Objectives: Rapid cellular proliferation, a hallmark of malignancy, requires sustained and elevated protein synthesis, which in turn requires efficient ribosome biogenesis. The aim of this study was to evaluate the expression levels of TP53, C-MYC, FBL, and NCL in pre-B ALL and neuroblastoma tissues compared to healthy bone marrow samples—factors that may carry prognostic significance in pediatric malignancies. Materials and methods: The cohort included 45 pre-B ALL patients, 19 neuroblastoma patients, and 12 healthy bone marrow donors as controls. Total RNA was extracted from bone marrow or tumor samples and cDNA synthesis was performed with the Bio-Rad iScript kit. Quantitative PCR was conducted using SYBR Green chemistry, with GAPDH as the reference gene. Primers targeted TP53, C-MYC, FBL, and NCL, and gene expression was calculated using the 2^−ΔCt method. Results: The expression of C-MYC and FBL was found to be significantly decreased in patients with pre-B ALL in comparison to the healthy control group. NCL expression was highest in healthy donors, intermediate in pre-B ALL, and lowest in neuroblastoma. In addition to intergroup comparisons, correlations between gene expression levels were assessed within each diagnostic group. In the pre-B ALL group, a positive correlation was observed between TP53 and C-MYC expression, as well as between TP53 and both FBL and NCL. Furthermore, a significant positive correlation was found between FBL and NCL. In the neuroblastoma group, a statistically significant positive correlation was identified between C-MYC and FBL expression. In the control group, TP53 expression was positively correlated with NCL, and FBL expression showed a significant positive correlation with NCL. Conclusions: This study suggests the altered expression of ribosome biogenesis-related genes in pediatric pre-B acute lymphoblastic leukemia and neuroblastoma. The reported dysregulation suggests a disease-associated disruption in nucleolar function and translational regulation and may contribute to oncogenesis through altered ribosomal assembly, protein synthesis, or proliferative signaling.

The bone tissue destruction during drilling is still one of the crucial problems in implantology. In this study, the influence of drilling speed, coolant presence, and its temperature on bone tissue was tested using swine rib as a biological model of human jaws. The same method of drilling (with or without coolant) was used in all tested samples. The microscopic investigation estimated the size of the destruction zone and morphology of bone tissue surrounding the drilling canal. The achieved results were statistically elaborated. The study proved that the optimal drilling speed was ca. 1200 rpm, but the temperature of the used coolant had no significant influence on provoked bone destruction. Simultaneously, the drilling system without coolant compared to this with coolant has statistical importance on drilling results. Further in vivo studies will verify the obtained results.

Ribosomes are central to cellular growth and proteome maintenance, and cancer cells frequently depend on increased ribosome biogenesis and altered translation to sustain proliferation, stress tolerance, and metabolic rewiring. Paradoxically, inherited “ribosomopathies” caused by germline defects in ribosomal proteins or ribosome biogenesis factors present with tissue hypoplasia and bone marrow failure early in life, yet confer substantially increased lifetime risk of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), and selected solid tumors. In parallel, somatic alterations affecting ribosomal proteins and ribosome regulatory pathways recur across malignancies, including hematologic cancers such as T-cell acute lymphoblastic leukemia (T-ALL), and in pediatric solid tumors. Mechanistically, oncogenic ribosome disturbances can reprogram translation toward specific mRNA subsets, alter translational fidelity, trigger nucleolar/ribosomal stress signaling via the 5S ribonucleoprotein (5S RNP)–MDM2–p53 axis, and enable selection for compensatory or cooperating lesions (notably TP53 pathway alterations). Clinically, these insights support diagnostics and surveillance of inherited ribosome-related cancer predisposition syndromes, therapeutic targeting of ribosome biogenesis and translational control, including RNA polymerase I inhibition, and the eIF4 translation-initiation machinery. Here, we present current evidence linking constitutional and acquired ribosomal dysfunction to leukemogenesis and tumorigenesis, highlight disease- and context-specific mechanisms, and outline priorities for translational research and precision therapy.