Survival outcomes for early-stage breast cancer have improved substantially; however, many survivors experience persistent treatment-related toxicities that adversely affect long-term quality of life (QoL) and functional recovery. Prospective survivorship data from China remain limited. The PERSEVERE study aims to characterise longitudinal trajectories of QoL and treatment-related toxicities among Chinese women treated for stage I-III breast cancer and to identify factors associated with suboptimal recovery.

Hepatocellular carcinoma (HCC), a prevalent malignant tumor, is characterized by occult early symptoms, leading to most patients being diagnosed at advanced stages. This diagnostic delay significantly contributes to the high mortality and limited therapeutic efficacy observed in HCC. Therefore, the development and application of accurate early detection methods and efficacious treatment strategies are essential for improving patient survival and overall clinical outcomes. Glycoproteomics focuses on the characterization of glycosylation sites and site-specific glycans. As one of the most prevalent post-translational modifications of proteins, aberrant glycosylation plays a critical role in the initiation, progression, diagnosis and treatment of HCC. In-depth investigation of abnormal glycoproteins in HCC holds substantial scientific and clinical significance for unraveling its pathogenesis, identifying effective diagnostic biomarkers, and pinpointing potential therapeutic targets. Body fluids and the derived exosomes have emerged as a pivotal research frontier, owing to their distinctive advantages: non-invasiveness, a wealth of disease-associated information, and ease of collection. Based on this, this review elaborates on the research strategies of HCC glycoproteomics and provides a detailed description of the analysis of body fluids and derived exosomes, to explore potential biomarkers in the pathogenesis of HCC, thereby providing strong support for the early detection and personalized treatment.

We present the first metastatic castration-resistant prostate cancer (mCRPC) patient, heavily pretreated with multiple systemic and radioligand therapies, who received [212Pb]Pb-PSMA radioligand therapy (PRLT) combined with the metabotropic glutamate receptor (mGluR)-inhibitor Riluzole due to disease progression. This novel combination, aimed at targeting glutamine addiction in prostate cancer and exploiting radio-sensitization, was well tolerated leading to partial remission of the disease, decrease in PSA values, and stability of symptoms. This represents the first-in-human clinical application of [212Pb]Pb-PSMA PRLT combined with mGluR inhibition in mCRPC, representing a promising therapeutic strategy for advanced, treatment-refractory, progressing patients, supported by molecular imaging and clinical benefit.

A 79-year-old patient with a history of renal cell carcinoma (RCC) presented with nonspecific upper abdominal pain 6 months ago. Contrast-enhanced CT and MRI did not reveal definitive evidence of malignancy. However, 68Ga-LNC1007 (68Ga-FAPI-RGD) PET/CT demonstrated a significant radiotracer-avid focus in the tail of the pancreas, initially interpreted as a metastatic RCC lesion. Surgical pathology later confirmed the lesion as a neuroendocrine neoplasm (NEN). This case illustrates that neuroendocrine tumors may occasionally be missed by conventional imaging modalities or suspected as other malignancies in certain scenarios, and highlights the potential diagnostic value of 68Ga-LNC1007 PET/CT in detecting neuroendocrine tumors.

A 51-year-old woman presented with intermittent upper abdominal pain for two years and unintentional weight loss recently. Gastroscopy revealed a large cardia mass protruding into the gastric lumen. CT examination suggested malignant gastric tumor. Subsequently, ¹⁸F-FDG PET/CT demonstrated heterogeneous intense uptake in the gastric mass. Pathologic examination identified a gastric pyloric gland adenoma by immunohistochemistry. The lesion was resected locally, and the patient recovered well.

A 57-year-old woman presented with fever was incidentally found to have a large hepatogastric space mass with coarse calcifications on CT, accompanied by a markedly elevated serum CA-125 level (3082 U/mL). 18F-FDG PET/MR revealed intense metabolic activity (SUVmax= 10.82) and restricted diffusion without ascites, while both ovaries appeared unremarkable. Pathology confirmed primary peritoneal high-grade serous carcinoma (PPHGSC). This case illustrates atypical imaging features of this rare malignancy, including lesion localization, coarse calcification, and absence of ascites.

Fibroblast activation protein (FAP) has emerged as a promising molecular target for theranostic strategies. Here is a case of a 37-year-old woman with poorly differentiated pancreatic adenocarcinoma with lymph node metastasis who received 1 cycle of gemcitabine plus nab-paclitaxel, but relapsed a year ago. She then received 3 cycles of 177Lu-FAP-2286 treatment, in combination with 6 cycles of gemcitabine plus nab-paclitaxel therapy. After that, the patient received an additional 2 cycles of 225Ac-FAP-2286 treatment. A follow-up 68Ga-FAP-2286 PET/CT scan revealed complete metabolic response of the lesions, and no severe adverse reactions were reported.

Primary splenic angiosarcoma is a rare, aggressive malignancy carrying a poor prognosis. A 65-year-old woman with a pathologically confirmed well-differentiated splenic angiosarcoma developed liver metastases 5 months into follow-up. Subsequent 18F-FDG and 68Ga-FAPI PET/CT imaging revealed a "dual-negative" pattern, demonstrating no significant radiotracer uptake in the metastatic liver lesions. Despite well-differentiated histology, the tumor showed rapid progression, confirming aggressive behavior in well-differentiated angiosarcoma. The high-grade splenic angiosarcoma demonstrated negative findings on dual-tracer PET/CT, underscoring that vigilance and comprehensive multimodal evaluation are crucial for such occult malignancies.

Cancer-associated fibroblasts (CAFs) represent a predominant cell population in the tumor microenvironment (TME) of hepatocellular carcinoma (HCC). How the spatial distribution of CAF subtypes relates to immune modulation within the TME remains incompletely understood. This study aimed to characterize the spatial organization of CAF subtypes in HCC and to explore their potential associations with immune contexture.

Mucosal melanoma (MM), an aggressive melanoma subtype arising in mucosal tissues, displays resistance to therapies effective in cutaneous melanoma. To understand how mucosal microenvironment contributes to treatment nonresponsiveness, we performed integrative analysis of single-cell and bulk messenger RNA sequencing data derived from oral mucosa-originated melanoma and revealed that mucosa-specific inflammation induces enrichment of low-pigmented neural crest-like cancer cell, mediated by COX2+ macrophages and their secretome. Maintenance of this inflammation-induced neural crest-like state in cancer cells depends on HER2 and HER3 activation. Inhibition of HER2/3 by pan-HER inhibitors blocks cell state plasticity and overcomes chemoresistance in primary MM cell lines and patient-derived xenograft (PDX) models. These findings provide insights into how the tissue of origin determines cancer aggressiveness, highlight the role of mucosal inflammation in driving melanoma stemness and chemoresistance, and advance the identification of effective treatment options currently lacking for patients with MM.

Early and accurate differentiation of prostate cancer (PC) from benign prostatic hyperplasia (BPH) remains challenging; metabolomics enables biomarker discovery by capturing disease-specific metabolic changes. The study includes 64 expressed prostatic secretion from 31 PC cases and 33 BPH cases. Nuclear magnetic resonance spectroscopy was used for metabolomics. Multivariate analyses, including principal component analysis, orthogonal partial least squares discriminant analysis, and artificial neural network modelling, were performed to identify discriminative metabolites. Diagnostic performance was assessed using receiver operating characteristic curve analysis. Clinical correlations with prostate-specific antigen (PSA) levels, multiparametric MRI (mpMRI), and Gleason score (GS) were executed. Citrate, glutamate, myo-inositol, and cis-aconitate were identified as key metabolites distinguishing PC from BPH, showing significant correlations with PSA, mpMRI-derived Prostate Imaging Reporting and Data System scores and apparent diffusion coefficient values as well as histopathology-based GS. The identified metabolic signature demonstrates strong potential as a noninvasive tool to support early PC detection and clinical decision-making, showing correlation with PSA, mpMRI indices and GS to enhance diagnostic accuracy before structural changes become evident.

Altered cell-surface glycans are established cancer biomarkers, yet no oncogenes have been identified within glycan biosynthesis machinery. This represents a critical gap, as defining a gene as a true oncogene, rather than merely a component of an oncogenic pathway, reveals targetable dependencies that can improve clinical decisions. To date, no gain-of-function mutations have been detected in glycogenes, and the search for such mutations is largely saturated. To address this gap, we developed a bioinformatic-experimental pipeline to identify copy number alteration (CNA)-based driver genes, overcoming noise from passenger genes. The approach recovered known oncogenes and tumor suppressors, while revealing novel candidates, including glyco-oncogenes. Focusing on the glycosphingolipid (GSL) biosynthetic pathway, we validated B4GALT5 as a bona fide glyco-oncogene whose genomic amplification drives proliferation, oncogene addiction, and poor prognosis, effects that can be reversed by targeted pathway inhibition. Mechanistic studies show that B4GALT5 promotes cancer cell survival via integrin-Src signaling under anchorage-independent conditions. Collectively, these findings establish glycosylation enzymes as a druggable oncogene class and provide a resource of high-confidence CNA-based cancer regulatory genes.

BACKGROUND Lymphangioma circumscriptum (LC) is a rare condition characterized by a lymphatic malformation primarily affecting the cutaneous region. Although surgical excision has historically been the first-line treatment, it may be associated with substantial complications and recurrence. This case report presents the first documented use of a simultaneous combination of erbium glass (1540 nm) and CO₂ (10 600 nm) lasers as a targeted therapeutic strategy for LC in a patient with a dark phototype. CASE REPORT A previously untreated 13-year-old Asian girl presented with a 5-month history of multiple reddish and pigmented papules located in the right medial scapular region. After histopathological confirmation, the lesions were simultaneously treated with an erbium glass (4.0 W, 1 millisecond, 4 mJ) and CO₂ (15 W, 0.25 milliseconds, 3.8 mJ) laser system, followed by topical tacrolimus (0.03%). The protocol was well tolerated, with moderate procedural pain and transient effects that resolved within 2 months. Clinical observation suggested a notable reduction in vesicles, reaching near-total clearance at the 2-month follow-up. CONCLUSIONS These results suggest that the simultaneous combination of erbium glass and CO₂ lasers represents a feasible therapeutic option for LC in patients with pigmented skin. Further investigation in larger studies with extended follow-up is required to establish long-term efficacy and safety compared with conventional surgical or laser-based standards.

Current aromatase inhibitors (AIs) are limited by poor bioavailability and high toxicity, underscoring the need for the development of new therapeutics. In the present study, a series of 12 benzimidazole-pyrazole hybrids was designed, synthesized, and structurally characterized using infrared spectroscopy, mass spectrometry, nuclear magnetic resonance spectroscopy, and elemental analysis. Their anti-breast cancer potential was evaluated against the MCF-7 cell line using the MTT assay. Notably, compounds 5g and 5i exhibited the highest cytotoxicity, reflected by the lowest IC50 values, while showing minimal toxicity toward the normal cell line, NIH3T3. Aromatase inhibitory activity, assessed using the fluorometric assay, further identified compound 5g as the most potent inhibitor. Complementary molecular docking studies demonstrated that compounds 5g and 5i form favorable interactions with the aromatase enzyme, showing higher binding affinity compared to letrozole, providing mechanistic insight into their inhibitory activity. ADMET analysis further confirmed the drug-likeness and pharmacokinetic suitability of the synthesized derivatives. Collectively, these results establish compound 5g as a promising lead for aromatase inhibition, necessitating further in vivo evaluation.

This review is designed to highlight recent research efforts to optimize treatment strategies in men with advanced prostate cancer.

Oligometastatic prostate cancer (oligoPCa) represents a clinical state of limited metastatic spread in which metastasis-directed therapy (MDT) may offer meaningful disease control either alone or with systemic therapy. As imaging, systemic therapy, and biologic characterization evolve, management strategies for both synchronous and metachronous presentations continue to undergo significant refinement.

Body-composition indices beyond body mass index (BMI) are increasingly being investigated as prognostic cancer markers. In pancreatic cancer, the prognostic relevance of skeletal muscle and adipose tissue compartments remains uncertain, with studies yielding inconsistent findings. We examined whether early on-treatment changes in subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), and skeletal muscle index (SMI) are associated with unresectable pancreatic cancer prognosis.

Globally, breast cancer (BC) continues to be the primary cause of cancer-related death for women, underscoring the need for reliable biomarkers for early detection and improved patient outcomes. Because of their stability in biological fluids and their functions in controlling gene expression, microRNAs (miRNAs) have become attractive diagnostic tools.

Head and neck cancers (HNC) significantly impact patients' quality of life (QOL), with oral health often being significantly compromised, especially in advanced stages. Green tea, with its known anti-inflammatory and antioxidant properties, may help to improve oral health in these patients. Therefore, this study aims to investigate the effect of green tea-based mouth rinse on oral health status, pain, and QOL of advanced HNC patients.

Breast cancer remains the most prevalent malignancy among women worldwide, driven by complex interactions between tumor-intrinsic factors and the immune microenvironment. Understanding immune-related molecular regulators is essential to improve diagnostic and therapeutic strategies. Transcriptomic data from the TCGA-BRCA dataset (1109 tumor and 113 normal samples) were analyzed to identify differentially expressed immune-related genes by cross-referencing ImmPort and InnateDB gene sets. Protein-protein interaction networks were constructed using STRING and Cytoscape to identify hub genes. Validation analyses were conducted using GSCA, cBioPortal, and GEO datasets. miRNA-mRNA regulatory interactions were explored using TargetScan, miRDB, miRWalk, and miRTarBase databases, followed by dual-luciferase reporter assays. Functional characterization of CCL5 and CD74 was performed through siRNA-mediated knockdown in breast cancer cell lines, proliferation, colony formation, and wound healing assays, as well as xenograft mouse models. Four key immune-related hub genes, including CXCL9, CXCL13, CCL5, and CD74 were identified as significantly upregulated in breast cancer. Epigenetic and prognostic analyses revealed that these genes were influenced by promoter methylation and correlated with poor survival outcomes. miRNA-mRNA network analysis identified hsa-miR-146a-5p and hsa-miR-200c-3p as central regulators, validated by luciferase assays. Functional studies showed that silencing CCL5 and CD74 significantly reduced cell proliferation, migration, and tumor growth in vivo, confirming their oncogenic roles. This integrative multi-omics and experimental study identified CCL5 and CD74 as key immune-oncogenic drivers of breast cancer progression. Their modulation of the MIF-CD74 signaling axis highlights potential therapeutic targets for immunomodulatory interventions and combination therapy in breast cancer.