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.

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.

Breast cancer remains the primary cause of cancer-related mortality for women globally; therefore, further breakthroughs in treatment approaches are crucial. Palbociclib, ribociclib, and abemaciclib are among the Cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors that have become an innovative family of targeted therapy for hormone receptor-positive, Human Epidermal Growth factor receptor 2 (HR+/HER2-) breast cancer. These inhibitors work by preventing the action of CDK4/6, which are crucial in the regulation of the cell cycle. Leading cancer cells to cell cycle arrest and undergo apoptosis. When these inhibitors are used with endocrine medicines like letrozole and fulvestrant, clinical trials lead positive impact in progression-free survival and, in a few cases, complete survival. However, despite their effectiveness, resistance mechanisms are primary and current acquired problems, requiring combined approaches with additional targeted medicines and continuous investigation into innovative therapeutic plans. To maintain patient compliance and quality of life, common side effects such as tiredness, gastrointestinal problems, and neutropenia need to be effectively managed. There is hopefulness for wider oncological applications as next-generation CDK inhibitor development and adaptive clinical trials continue to test their potential beyond breast cancer. CDK4/6 inhibitors continue to be a key part of breast cancer treatment as cancer biology advances, marking a major advancement towards more potent and customized cancer medicines. This review aims to provide current evidence on CDK4/6 inhibitors in HR+/HER2- breast cancer, highlighting their mechanisms, interaction with endocrine resistance, combination strategies, and emerging biomarkers guiding personalized therapy.

Combined chemotherapy and photothermal therapy (PTT) represents a promising approach for enhancing cancer treatment efficacy. This study aimed to develop arsenic trioxide (ATO) and poly(cyclopentadithiophene-alt-benzothiadiazole) (PCPDTBT)-loaded nanoparticles (ATO/PCPDTBT@NPs) to evaluate their synergistic efficacy in inhibiting lung cancer growth and metastasis.

Progesterone (P4) is believed to inhibit breast cancer growth, but its role in counteracting estrogen (E2)-driven progression remains unclear. This study aimed to investigate the inhibitory effect of P4 on E2-induced cell proliferation, migration, and invasion in Estrogen receptor (ER)+/progesterone receptor (PR)+ breast cancer cells by examining its regulatory role in the epithelial-mesenchymal transition (EMT).

Breast cancer metastasis remains the leading cause of mortality and frequently targets the bone. Breast cancer cells release soluble factors and extracellular vesicles that disrupt bone marrow (BM)/bone homeostasis, promoting osteoclastogenesis and the accumulation of senescent cells. In line with updated cancer hallmarks, senescent mesenchymal stem/ stromal cells (MSCs), osteoblasts, and osteocytes contribute to remodeling of the BM microenvironment, thereby favoring pre-metastatic niche (PMN) formation and subsequent bone metastasis. We previously demonstrated that untreated stage III-B breast cancer patients (BCPs) exhibit increased oxidative stress and elevated reactive oxygen species (ROS) levels, accompanied by senescent and functionally impaired BM-MSCs-key regulators of BM/bone homeostasis. In the present study, we sought to identify the molecular targets affected by oxidative stress that drive MSC senescence in these patients.

Mucoepidermoid carcinoma (MEC) of the larynx is an extremely rare malignancy, accounting for less than 1% of primary laryngeal tumors. The optimal role of adjuvant therapy, particularly radiotherapy (RT), remains unclear due to limited evidence. This systematic review aimed to evaluate oncologic outcomes and the impact of adjuvant treatment in patients with early- and advanced-stage laryngeal MEC.

MicroRNAs (miRNAs) are small, non-coding RNAs that play a key role in the development of chemoresistance in various cancer types, including colorectal cancer (CRC). In this study, we aimed to study the underlying mechanisms of miRNA in chemotherapy-resistant CRC.