Histone modification is an important mechanism of epigenetic regulation. New histone modifications play key roles in the regulation of gene expression and in the development and progression of various diseases. In addition to histone modifications, epigenetic regulation includes classic pathways such as DNA methylation, chromatin remodeling complexes and non‑coding RNAs, which interact with each other and jointly shape the occurrence and development of gastric cancer (GC). The present study systematically elaborated on the role of histone modification in GC and introduced several main types of histone modification, including acetylation, methylation, citrullination, ubiquitination and lactylation, focusing on histone lactylation modification and exploring its biochemical basis, interaction with other modifications and functions such as metabolic reprogramming, cell proliferation, migration and immune escape, covering non‑tumor and other cancer fields. On this basis, the specific application of histone modification (acetylation, methylation and other modifications) in GC is further explained and the effects of histone lactylation on metabolic reprogramming, proliferation, migration and immune escape of GC are analyzed in detail. Finally, the clinical significance of histone lactylation modifications in the diagnosis and prognosis of GC, biomarkers, therapeutic targets and drug resistance mechanisms provides a reference for an in‑depth understanding of the role of histone modifications, especially lactylation modifications, in the development of GC and clinical transformation applications.

Lung cancer is an aggressive malignancy associated with a rapid progression and poor prognosis, for which immunotherapy only exhibits modest efficacy in most patients. In lung cancer, high lactate is associated with a low immunotherapy response and shortened survival; however, causal lactylation‑related genes remain to be elucidated. In the present study, candidate genes were screened using Mendelian randomization (MR) analysis, with expression quantitative trait loci data and genome‑wide association study summary statistics used as analytical resources. A total of 46 lactylation‑related genes were included in the MR analysis, and multiple testing correction was performed using the false discovery rate (FDR) and Bonferroni methods to control the false‑positive risk. MR identified three core genes [platelet‑type phosphofructokinase; SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4; and stathmin 1 (STMN1)]. Among these genes, only STMN1 was significantly associated with increased lung cancer risk (inverse variance weighting original P=0.005, FDR‑corrected P=0.014995, Bonferroni‑corrected P=0.014995, odds ratio=1.741, 95% confidence interval: 1.182‑2.564), with robust results confirmed by heterogeneity/pleiotropy/sensitivity analyses. Subsequently, transcriptomic analysis was conducted to assess STMN1 expression in lung cancer tissues and its association with patient survival. In vitro (cell proliferation, migration, invasion and apoptosis assays) and in vivo experiments (murine tumor models) were also conducted to explore the function of STMN1. STMN1 exhibited upregulation in lung cancer tissues, and was associated with a shorter survival, reduced antitumor immune cell infiltration and an immunosuppressive tumor microenvironment (TME) phenotype. STMN1 knockdown inhibited lung cancer malignancy both in vitro and in vivo, and modulated key markers, whereas its overexpression exhibited the opposite effects. Additionally, STMN1 promoted global histone lactylation and histone H3 lysine 18 lactylation in lung cancer cells, establishing a direct functional link between STMN1 and the lactylation pathway. In conclusion, STMN1 is a lactylation‑related causal oncogene in lung cancer, driving progression via malignant phenotypes, and its high expression is associated with an immunosuppressive TME that may synergistically facilitate tumor progression. Therefore, STMN1 may be considered a novel target for lung cancer therapy.

Metastasis of hepatocellular carcinoma (HCC) is a key factor contributing to poor patient prognosis, with extracellular vesicles (EVs) and circulating tumor cells (CTCs) playing a marked synergistic role in this process. Current research suggests that EVs, acting as essential mediators of intercellular communication, facilitate CTC‑driven HCC recurrence and metastasis by transporting bioactive molecules, including nucleic acids, proteins and lipids. CTCs are regarded as the initiators of tumor metastasis, while the bioactive cargo carried by EVs functions as critical factors that promote their outgrowth. EVs not only remodel the microenvironment of target organs by forming a 'pre‑metastatic niche', but also establish a permissive microenvironment for CTC colonization. This tripartite interplay establishes a cascade model that enhances metastatic dissemination. The present manuscript reviewed the recent advancements and clinical value in understanding the roles of EVs and CTCs in HCC metastasis and recurrence, as well as the mechanisms by which EVs mediate CTC‑driven liver cancer spread, aiming to promote further in‑depth research into HCC metastasis mechanisms.

Objective To investigate the concordance of programmed death ligand-1 (PD-L1) expression between primary non-small cell lung cancer (NSCLC) and paired brain metastasis, analyze its relationship with clinicopathological characteristics, and evaluate the feasibility of using primary tumor PD-L1 status to predict brain metastasis status. Methods Thirty-two paired primary NSCLC and brain metastasis samples, pathologically diagnosed between January 1, 2017 and July 1, 2022, were collected. PD-L1 expression was detected by immunohistochemistry and interpreted using the Tumor Proportion Score (TPS), with cut-off values set at 1% and 50%. The Chi-square test was used to analyze the relationship between PD-L1 expression and clinicopathological features. Paired Chi-square and Kappa consistency tests were employed to assess the concordance of PD-L1 expression between primary and metastatic sites. Results PD-L1 expression showed no significant correlation with patient gender, age, treatment history, or histologic type. At the 1% cut-off, the overall PD-L1 expression showed moderate concordance between primary and metastatic sites (Kappa=0.624). Subgroup analysis revealed high concordance in untreated patients (Kappa=0.761, P=0.001), whereas the treated group showed weak concordance without statistical significance (Kappa=0.324, P=0.205). At the 50% cut-off, both the treatment group and the untreated group showed weak concordance without statistical significance. Although the chemotherapy subgroup showed perfect agreement (Kappa=1.000) at the 50% cut-off, the high-expression concordance rate was only 20.00%, indicating limited clinical reference value. Conclusion The strong concordance of PD-L1 expression in the untreated group patients supports the use of primary tumor PD-L1 status to guide clinical decision-making when brain metastasis tissue is unavailable. Treatment status (mainly including chemotherapy) may be an important factor affecting the consistency of high PD-L1 expression between primary NSCLC and brain metastasis.

Olfactory meningiomas are common neoplasms accounting for 4.5-18% of all intracranial meningiomas. Currently, transcranial (pterional, unilateral subfrontal, bilateral subfrontal, interhemispheric and through the frontal sinus) and endoscopic endonasal approaches are actively used.

Endocrine inactive pituitary microadenomas are ones of the most common incidental findings in neuroimaging. Their prevalence is up to tens of cases per 100.000. According to current data, the vast majority of microadenomas remain stable over long-term follow-up, and the risk of progression, hypopituitarism, or the need for surgical intervention is extremely low. Clinical factors such as baseline adenoma size, gender and age have not proven predictive value for the risk of microadenoma growth. Current recommendations for follow-up vary significantly. There is evidence of safety of less aggressive strategies (delaying the first MRI for up to 3 years without clinical manifestations and no routine hormonal screening in patients with stable course). This approach combines clinical effectiveness and cost-effectiveness. Thus, current data allow us to consider endocrine inactive pituitary microadenomas as lesions with favorable prognosis. Revising international guidelines in favor of more rational and personalized surveillance strategies appears to be a justified and necessary step to optimize clinical practice.

Dopamine agonists are an effective and safe treatment for prolactinomas. However, analysis of recent data has shown that dopamine agonists, including cabergoline, can cause tumor fibrosis and complicate subsequent surgery.

Background. Diffuse brainstem tumors account for 10-20% of all brain tumors in children. These neoplasms are the leading cause of death in pediatric neuro-oncology. There are no effective treatments for this disease. Overall survival rarely exceeds 1.5-2 years.

Glioblastoma or grade IV glioma is characterized by extremely poor prognosis. Resistance to radio- / chemotherapy and recurrences are associated with tumor stem cells. Transmembrane protein CD133 is considered a potential marker of tumor stem cells. To overcome the limitations of detecting cellular CD133 by antibodies, potential of aptamers (nucleic acid-based molecular recognition elements) is being explored. To obtain reproducible results, it is necessary to study the interaction of fluorescent aptamers to CD133 with standard cell lines and cell cultures derived from patient tumors using various methods.

Bladder cancer (BCa) progression is closely linked to the immune microenvironment. However, the key molecules that regulate this microenvironment and their specific mechanisms remain poorly understood. This study aims to identify a key molecule and elucidate its mechanisms, providing a theoretical basis for identifying novel therapeutic targets.

ADP-ribosyltransferases (ARTs) regulate key processes in cancer, including DNA repair, transcription, immune responses, and treatment resistance. The clostridial toxin-like ADP-ribosyltransferase (ARTC) family and the diphtheria toxin-like ADP-ribosyltransferase (ARTD) family play a crucial role in genomic stability by modification of proteins either with mono(ADP-ribosyl)ation (MARylation) or poly(ADP-ribosyl)ation (PARylation). These ARTs are promising therapeutic targets and could serve as biomarkers in cancer management. This review explores the roles of these enzymes and current knowledge on specific inhibitors. A literature search was conducted in PubMed and Google Scholar to identify studies published between 1992 and 2025 on ADP-ribosyltransferases and their roles in cancer. Among ARTC family, ART1 and ART3 modulate the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway, influencing angiogenesis, tumor growth, and immune evasion via cluster of differentiation 8+ (CD8+) T-cell apoptosis. Within the ARTD family, poly(ADP-ribose)polymerase (PARP)1 and PARP2 are activated by DNA single-strand breaks and are clinically validated targets in cancers with homologous recombination deficiency, such as breast cancer susceptibility genes 1/2 (BRCA1/2)-mutated breast cancer. Their inhibition exemplifies synthetic lethality and has shown clinical efficacy. Four PARP inhibitors, olaparib, niraparib, rucaparib, are approved by the Food and Drug Administration (FDA) approved. Despite these advances, selective inhibitors for ARTs remain underexplored. Ongoing research focuses on overcoming PARP inhibitor resistance, improving biomarker-driven patient selection, and expanding therapeutic strategies that target ART-related pathways.

The progression of prostate cancer cells to metastasis is supported by their tumor microenvironment. Within this microenvironment, infiltrating immune cells, such as B cells, can be either anti-tumorigenic or pro-tumorigenic. Our preliminary data showed that a higher density of the infiltrating B cells was found near prostate cancer cells in human cancer tissues, as compared to the benign prostate tissue regions, thus suggesting that infiltrating B cells would promote the progression of prostate cancer cells. In this study, we aim to investigate the role of infiltrating B cells in enhancing the migratory ability of human prostate cancer cells.

Long non-coding RNAs have been found to play a pivotal role in breast cancer, yet the majority of these lncRNAs remain to be thoroughly investigated. This study aimed to explore the role of differentially expressed long non-coding RNAs (lncRNAs) in breast cancer stemness and drug sensitivity.

The management of renal neoplasms in adolescent patients poses unique clinical challenges due to their transitional position between paediatric and adult populations. This age group exhibits marked heterogeneity in tumour histology, ranging from entities commonly observed in paediatric oncology to tumours typical of adult age, as well as rare histological subtypes that exceptionally affect the kidney. Given the substantial differences in clinical protocols between paediatric and adult populations, rigorous multidisciplinary evaluation is essential to determine optimal diagnostic and therapeutic strategies for adolescent patients.

Glioblastoma (GB) therapy is challenged by tumor heterogeneity and multidrug resistance (MDR), highlighting the need for effective therapies. This study aimed to explore the combined anticancer effects of Sunitinib (SNB) and Fenofibrate (FEN) on U87 cells.

Lung adenocarcinoma (LUAD), the most prevalent histological subtype of lung cancer, remains a leading cause of cancer-related mortality due to late diagnosis, metastasis, and therapy resistance. The aim of the study is to investigate the role of Kinetochore Scaffold 1 (KNL1) in promoting LUAD progression and its underlying molecular regulatory mechanisms.

Tumor recurrence is a major determinant of poor prognosis in hepatocellular carcinoma (HCC), yet its cellular and molecular basis remains incompletely understood. This study aimed to identify recurrence-associated genes at single-cell resolution and to develop a prognostic model for predicting survival outcomes and immunotherapy responsiveness in HCC.

Decisions regarding CT after nCCRT for locally advanced rectal cancer (LARC) are challenging due to limited evidence guiding treatment. This study aimed to (i) evaluate the predictive performance of machine learning (ML) models in patients treated with neoadjuvant concurrent chemoradiotherapy (nCCRT) alone vs. those receiving nCCRT plus chemotherapy (CT), (ii) identify features associated with treatment improvement, and (iii) derive ML-based thresholds for treatment response.

Hepatocellular carcinoma (HCC) has limited systemic options with substantial toxicity. G-quadruplex (G4) structures in oncogene promoters are attractive but challenging drug targets. This study aimed to determine whether glutamic acid-chelated cobalt (GACC) is a G4-active scaffold with anti-HCC efficacy and favorable in vivo safety, and whether an AI-guided phenotypic response surface (PRS) can optimize less toxic combinations.

-Synovial sarcoma is a rare soft tissue sarcoma. Treatment of synovial sarcoma includes surgery, radiation, pazopanib, and chemotherapy. Targeted therapies, such as B-Raf proto-oncogene, serine/threonine kinase (BRAF) inhibitors, are emerging as a potential treatment option. We describe the sixth case of a BRAFV600E synovial sarcoma, the first extra-thoracic case. This case is the first to show a complete pathological response to BRAF & mitogen-activated protein kinase kinase (MEK) inhibitors.