Schiff bases, formed through the condensation of carbonyl compounds with primary amines, serve as valuable precursors for the development of anticancer nanomaterials. Their incorporation into metal-based nanoparticles, polymeric systems, and liposomal carriers has expanded the possibilities for targeted and effective cancer therapy. Current evidence indicates that Schiff base nanoparticles offer notable benefits over conventional therapies, particularly in improving drug efficacy and reducing systemic toxicity. This review outlines the synthesis of Schiff bases along with the methods used to develop their nanoparticles. The discussion also covers commonly used preparation methods, approaches for physicochemical characterization, and the major biological pathways through which these nanoparticles influence cancer cell survival. Despite the progress made, a number of issues still require attention, including the need for more precise nanoparticle designs, better understanding of long-term interactions in biological environments, and clearer links between laboratory findings and clinical translation. This review summarises the current progress and highlights the potential and the limitations of Schiff base functionalized nanoparticles as future anticancer agents.

To determine whether adolescent and young adults (AYA) with Hodgkin lymphoma (HL) who are treated by oncologists with "AYA expertise" improve outcomes.

All AYA aged 15-21 years diagnosed with HL in Ontario, Canada between 1992 and 2012 were identified, and clinical data abstracted as part of the IMPACT cohort. Linked administrative data were used to identify primary oncologists, defined as "AYA experts" if at diagnosis, ≥ 15% of the oncologist's previous 2 years of chemotherapy billings were for patients aged 15-29 years. Associations between seeing an AYA expert and outcomes were analysed.

Among 863 AYA with HL, 225 unique primary oncologists were identified. A total of 112 (13.0%) AYA had a primary oncologist with AYA expertise. Older patients [adjusted OR (aOR): 0.8 per year, 95% CI: 0.7-1.0; p = 0.04] and those seen in adult community hospitals [vs. regional cancer centre, aOR: 0.1, 95% CI: 0.02-0.4; p = 0.001] were less likely to see an AYA expert. Only 56 (6.4%) AYA received a fertility consult within 30 days of HL diagnosis; most occurred in the later study period (2006-2012). Seeing an AYA expert was associated with increased odds of fertility consultation (aOR: 2.1, 95% CI: 1.0-4.3; p = 0.04). Among the full cohort, there was no association between AYA expert care and event-free survival (EFS), overall survival (OS), or subsequent live birth.

A volume-based definition of AYA expertise was associated with receipt of fertility consults, but not with EFS or OS for AYA with HL. If validated in other populations and settings, seeing a volume-defined AYA expert could serve as a quality metric in AYA cancer care.

Renal cell carcinoma (RCC) presents a significant global health challenge, with a substantial proportion of patients diagnosed with advanced or metastatic disease due to the limitations of current diagnostic imaging and the lack of validated non-invasive biomarkers. These conventional methods, including computed tomography and magnetic resonance imaging, often lack the sensitivity and specificity to differentiate benign from malignant small renal masses reliably or to detect minimal residual disease (MRD) post-treatment. This review explores the transformative potential of liquid biopsy, explicitly focusing on circulating tumour DNA (ctDNA) fragmentomics and epigenetic signatures, to overcome these clinical hurdles. This review also explores how the analysis of ctDNA fragmentation patterns-such as size distribution, end motifs, and nucleosome footprints-provides a mutation-independent method to enhance RCC detection, even in low-shedding tumours. Concurrently, RCC-specific epigenetic alterations, particularly DNA methylation profiles, offer particular biomarkers for early detection, tumour classification, and prognostication. This Review examines evidence that integrating these multi-analyte approaches-combining fragmentomic and epigenetic data-synergistically improves diagnostic accuracy, enables sensitive MRD assessment, and allows precision monitoring of treatment response and tumour evolution. Despite existing technical and biological challenges, the convergence of ctDNA fragmentomics and epigenetic profiling heralds a new era for the non-invasive, dynamic, and personalised management of RCC, promising to improve patient outcomes through earlier intervention and tailored therapeutic strategies.

Acute myeloid leukemia (AML) with plasmacytoid dendritic cell differentiation (pDC-AML) is a newly described subtype of leukemia with features resembling blastic plasmacytoid dendritic cell neoplasm (BPDCN).

Herein, we present a case of pDC-AML in which bone marrow findings were best classified as AML, whereas cutaneous manifestations by morphology and immunophenotype were highly suggestive of a pDC neoplasm.

A high-dose cytarabine with anthracycline backbone and venetoclax was administered based on efficacy in AML and BPDCN, respectively. The patient achieved complete remission as well as resolution of FDG-avid activity by PET-CT imaging.

This report highlights that clinical correlation with immunophenotype and molecular testing is important in distinguishing these unique entities to guide appropriate diagnosis and management.

Photodynamic therapy (PDT) may eradicate residual malignant cells following sarcoma resection, through reactive oxygen species (ROS) mediated cytotoxicity, thus improve clinical outcomes. This study aims to assess the efficacy of 5-aminolevulinic acid (5-ALA) as a photosensitizer in combination with red light (RL) for PDT of bone sarcoma cells in vitro.

Three bone sarcoma cell lines underwent treatment with 5-ALA and RL or sham-RL (SL). 5-ALA uptake was assessed using flow cytometry. Production of ROS was measured using CellROX Green staining and fluorescence microscopy. Cell viability was assessed using Cell Counting Kit-8 assays.

All cell lines showed significant 5-ALA uptake in comparison to the 0 mM control (p < 0.05). Production of ROS was significantly increased in cells treated with 5-ALA and RL, compared to those treated with RL and no 5-ALA or SL (p < 0.05). Viability was significantly reduced in cells treated with 5-ALA and RL, compared to SL (p < 0.05). At 72 h post-treatment, cell viability ranged from 6%-12% in 0.5 mM 5-ALA and RL-treated cells vs. 90%-137% in 0.5 mM 5-ALA and SL-treated cells.

5-ALA-based PDT led to the desired increased production of ROS and reduction in cell viability in all cell lines. These preliminary in vitro results warrant further study with multicellular spheroid or animal models and suggest PDT has potential to be used as an adjuvant therapy to surgical resection in sarcoma management.

Acquired resistance to paclitaxel represents a critical barrier to the effective chemotherapy of non-small cell lung cancer (NSCLC). The present study aimed to elucidate the molecular and pharmacological mechanisms promoting paclitaxel resistance in NSCLC and to explore potential strategies for overcoming this resistance.

Here, we report an integrated pharmacological and analytical approach to quantify paclitaxel disposition and overcome resistance in a A549/TAX cell model (paclitaxel-resistant A549 cells).

Cell counting kit-8 (CCK-8) assay, colony formation, and apoptosis assays confirmed that A549/TAX cells exhibited marked resistance to paclitaxel relative to parental A549 cells. Based on transcriptome profiling by RNA sequencing analysis and validation by western blotting assay, we found that the expression of the ATP-binding cassette subfamily B member 1 (ABCB1) (the encoded protein is termed P-glycoprotein) was significantly upregulated in resistant cells. By using ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), we demonstrated that ABCB1 overexpression promotes enhanced efflux of intracellular paclitaxel, thereby lowering its cytotoxic accumulation. Genetic silencing of ABCB1 or pharmacological inhibition with the specific P-glycoprotein modulator elacridar or tariquidar restored intracellular paclitaxel levels, as determined by UPLC-MS/MS, and synergistically decreased cell viability as observed in CCK-8 assay.

These findings reveal that the ABCB1-mediated drug efflux is a crucial mechanism underlying paclitaxel resistance in NSCLC cells, with UPLC-MS/MS serving as a sensitive analytical method to detect paclitaxel concentration. Inhibition of ABCB1 is a promising therapeutic strategy to resensitize resistant tumor cells to paclitaxel.

Uveal melanoma (UM) is the most common intraocular cancer, with approximately 5.2 individuals per million affected annually in the United States. It represents approximately 3% of the global malignant melanoma cases, accounting for 80% of the overall noncutaneous melanomas. Clinically, it remains silent in about 30% of the cases; when symptomatic, it generally causes metamorphopsia (painless loss or distortion of vision) and/or photopsia (flashing or flickering of light in the visual field). Discoloration of the iris, astigmatism, glaucoma, and even blindness are other, less common clinical manifestations. Several pathophysiological mechanisms underlie the development of UM. Genetic mutations, involving especially the G protein subunit alpha q (GNAQ), guanine nucleotide-binding protein subunit alpha-11 (GNA11), BRCA1 associated deubiquitinase 1 (BAP1), splicing factor 3b subunit 1 (SF3B1), and eukaryotic translation initiation factor 1A, X-linked (EIF1AX) genes as well as the MAPK/ERK signaling pathway genes, have been largely associated with the development of UM. Chromosomal aberrations, inflammatory and immunological alterations are often concurrent factors for the development and progression of UM. Therapies targeting specific genetic alterations and immunotherapy agents have been recently developed and introduced in clinical practice for the management of advanced-stage UMs. This review aims to present the latest advances in the clinical molecular pathology of UM, along with the resulting targeted, immunological, and other therapies that have been introduced or are currently under investigation.

Ring finger protein 145 (RNF145), an E3 ubiquitin ligase, is significantly upregulated in hepatocellular carcinoma (HCC). However, its role in HCC remains unknown. The study aimed to investigate the functions and underlying mechanisms of RNF145 in HCC.

The role of RNF145 in HCC was investigated using data from The Cancer Genome Atlas (TCGA) and in vitro experimental assays. Its oncogenic functions were assessed using the transwell migration assay and the wound-healing assay. The molecular mechanism was explored through protein immunoprecipitation and western blot analyses. Data from public databases were analyzed to correlate RNF145 expression with clinicopathological features. Univariate and multivariate Cox analyses established RNF145 as an independent prognostic factor. Subsequently, a prognostic nomogram was constructed.

RNF145 was upregulated in HCC. The expression level of RNF145 in HCC showed significant correlations with histological grade, pathological stage, and vascular invasion. Functionally, knockdown of RNF145 effectively abolished the migratory and invasive capacities of HCC cells. This pro-metastatic effect is mediated through the RNF145-driven ubiquitination and subsequent degradation of protocadherin 9 (PCDH9).

Our findings confirm the significant upregulation of RNF145 in HCC and promote metastasis by facilitating PCDH9 ubiquitination and degradation, highlighting its role as a prognostic biomarker and a potential therapeutic target.

Gastric cancer (GC) remains a major global health concern, and Phosphoinositide-3-Kinase Regulatory Subunit 1 (PIK3R1), a regulatory subunit of the PI3K signaling pathway, may play a critical yet underexplored role in GC progression. This study aimed to investigate the prognostic significance of PIK3R1 in GC and its association with the tumor immune microenvironment.

PIK3R1 expression and its clinical relevance were analyzed using datasets from GC patients who underwent gastrectomy, including cohorts from The Cancer Genome Atlas (TCGA) and the Sun Yat-sen University Cancer Center (SYSUCC). Prognostic models integrating PIK3R1 expression with clinical parameters were constructed for both cohorts. The immune microenvironment associated with PIK3R1 expression was assessed through immunohistochemistry and single-cell RNA sequencing. In vitro assays were conducted to evaluate the effects of PIK3R1 on GC cell proliferation and migration.

PIK3R1 was significantly overexpressed in GC tissues and was closely associated with aggressive tumor characteristics and poor clinical outcomes. A nomogram combining PIK3R1 expression with clinicopathological features effectively predicted patient prognosis. Knockdown of PIK3R1 in GC cells reduced proliferation and migration in vitro. Immunological profiling revealed that high PIK3R1 expression correlated with increased infiltration of forkhead box protein P3 (Foxp3⁺) and cluster of differentiation 73 (CD73⁺) T cells. Patients with low PIK3R1 expression and low CD73⁺ T cell infiltration had significantly better survival.

PIK3R1 overexpression is linked to poor prognosis in GC and influences the extent of immune cell infiltration within the tumor microenvironment. A novel prognostic model integrating PIK3R1 and CD73 expression with clinical parameters was established to stratify GC patients into distinct risk groups, offering potential value for personalized therapeutic strategies.

Lung cancer is the most common but fatal malignant tumor worldwide. Patients with lung cancer experienced a relatively low 5-year overall survival rate, and issues such as metastasis and drug resistance remain prominent challenges in its clinical management. Neddylation, a novel type of post-translational modification, was overactivated in lung cancer and was closely associated with its occurrence, development, metastasis, and drug resistance. This review systematically summarizes the biological process of neddylation and deeply explores the latest research progress on how neddylation affects lung cancer cell proliferation, metastasis, and drug resistance mechanisms, with a focus on its regulation of key molecules such as Cullin-RING E3 ligases and the SCCRO family. Meanwhile, it concludes the current advances in potential therapeutic agents targeting neddylation-related targets, including small-molecule compounds (such as Pevonedistat) and natural extracts (such as arctigenin). Finally, the review prospectively evaluates the application potential and questions requiring further exploration of neddylation in lung cancer treatment. In conclusion, we aim to systematically summarize the biological process of neddylation, critically explore its roles in lung cancer proliferation, metastasis, and drug resistance, and evaluate the therapeutic potential of neddylation-targeting agents.