The objective of this research was to develop a robust classification system that accurately predicts the prognosis and therapeutic efficacy of neoadjuvant chemoradiotherapy (NCRT) in patients with rectal cancer.

We generated an immune cell gene signature (ICGS) model employing univariate Cox regression and Lasso regression methods. Subsequently, the predictive capabilities of the ICGS model were assessed and validated for NCRT efficacy, survival outcomes, and immunotherapy benefits. Furthermore, we conducted functional annotation, investigated genomic alterations, and explored potential immune escape mechanisms.

Initially, we developed three ICGS models with prognostic implications: the B cell signature, macrophage signature, and combined signature. The immune cell-related genes were highly associated with immune function, immune response, and immunological pathways. The ROC analysis revealed that the ICGS model demonstrated a relatively strong predictive capability for the response to NCRT. Patients exhibiting high ICGS scores experienced a significantly reduced overall survival. Furthermore, multivariate Cox regression analysis verified the ICGS as an independent factor, and we constructed a predictive nomogram. The AUC value confirmed that the ICGS model was comparable to and superior to the clinical stage in predicting overall patient survival. Additionally, the low-risk group for the macrophage signature showed a better survival advantage from immunotherapy. Finally, we systematically correlated the ICGS model with genomic alterations and uncovered potential immune escape mechanisms.

The ICGS model can be considered a reliable tool for evaluating the efficacy of neoadjuvant therapy in rectal cancer and can further assist in guiding risk stratification and treatment decisions.

The glymphatic system is a cerebrospinal fluid-interstitial fluid exchange pathway that clears metabolic waste and maintains brain fluid homeostasis. Aquaporin-4 (AQP4), a water channel at astrocytic endfeet along the neurovascular interface, supports perivascular water transport and glymphatic flow. Disruption of this glymphatic-AQP4 unit is implicated in conditions with altered fluid dynamics, including traumatic brain injury (TBI) and brain tumors. We reviewed experimental and clinical studies examining glymphatic pathways and AQP4 regulation in TBI and brain tumors, and synthesized evidence on glymphatic physiology, AQP4 polarization, and imaging-based assessment to compare mechanisms of disruption in injury versus tumor remodeling. Evidence shows reduced glymphatic transport in both conditions, commonly accompanied by altered AQP4 localization. In TBI, mechanical injury triggers astrocytic reactivity, blood-brain barrier disruption, and loss of perivascular AQP4 polarization, impairing clearance across phases of injury. In brain tumors, parenchymal remodeling, vascular compression, and vasogenic edema disrupt cerebrospinal fluid dynamics and glymphatic pathways. Across disease states, total AQP4 expression alone poorly predicts glymphatic function; instead, spatial localization and polarization of AQP4 at astrocytic endfeet more consistently correlate with clearance efficiency. Emerging imaging approaches, including diffusion-based MRI metrics and perivascular space quantification, offer potential noninvasive methods for assessing glymphatic alterations in vivo, although their reliability and biological specificity remain debated and under active investigation. Overall, the glymphatic-AQP4 system is a key neurovascular interface regulating brain fluid balance. Disrupted AQP4 polarization and glymphatic transport contribute to edema and impaired solute clearance in both TBI and brain tumors. Future work should prioritize standardized imaging biomarkers and time-dependent strategies to restore glymphatic function and perivascular AQP4 organization.

Candidemia poses a life-threatening complication for immunocompromised patients, including those undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT). Non-albicans Candida species are increasingly recognized as causative pathogens in this population, with azole resistance having emerged as a global concern. Candida orthopsilosis, a member of the Candida parapsilosis species complex, is generally considered susceptible to azole antifungal agents. Although sporadic reports of azole-resistant isolates have surfaced worldwide, no such cases have been documented in Japan. Furthermore, genetic evaluations of azole-resistant C. orthopsilosis have primarily been conducted in Europe. We present the first case of fluconazole-resistant C. orthopsilosis bloodstream infection in a 73-year-old man following allo-HSCT for acute myeloid leukemia in Japan. Whole-genome sequencing identified an ERG11 G458S substitution, a known mechanism of fluconazole resistance in C. orthopsilosis, representing the first identification of this mutation outside Europe. Our findings highlight the importance of continued surveillance of antifungal resistance in C. orthopsilosis.

Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by high invasiveness, limited therapeutic options, and unfavorable clinical outcomes. Ribosomal protein L5 (RPL5), a component of the large ribosomal subunit, has been implicated in ribosome biogenesis, translational regulation, and p53-associated cellular processes. This study investigated the immunohistochemical expression pattern of RPL5 in TNBC tissues and explored its potential biological significance through integrated transcriptomic analyses. Tumor tissues from 37 patients with TNBC and 7 adjacent non-tumorous breast tissues were collected from the Affiliated Tumor Hospital of Xinjiang Medical University between December 2017 and December 2023. RPL5 protein expression was evaluated by immunohistochemistry, and its association with clinicopathological characteristics was analyzed. Public transcriptomic datasets from TCGA-BRCA and GEO were further used to validate RPL5 expression patterns in TNBC. Co-expression analysis and Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to investigate potential biological functions and signaling pathways associated with RPL5. Immunohistochemical analysis demonstrated significantly lower RPL5 protein expression in TNBC tissues compared with adjacent normal breast tissues (p=0.001). In contrast, transcriptomic analyses revealed significantly higher RPL5 expression in TNBC compared with non-TNBC breast cancer subtypes (p<0.001). No significant associations were observed between RPL5 expression and clinicopathological parameters, including age, tumor size, menopausal status, TNM stage, histological grade, or lymph node metastasis (all p>0.05). Survival analysis showed no significant difference in overall survival between patients with high and low RPL5 expression. Functional enrichment analyses indicated that RPL5-related genes were predominantly involved in ribosome biogenesis, translational regulation, and p53-related signaling pathways. These findings suggest that abnormal RPL5 expression may be associated with TNBC biology through ribosome-related programs, although causal roles require functional validation. RPL5 may represent a potential histopathological and molecular indicator associated with TNBC biology, although its precise functional role requires further experimental validation.

Prostate cancer (PCa) is a common malignancy in men with limited therapeutic options at advanced stages. Statins, widely prescribed lipid-lowering agents, have demonstrated antitumor activity in PCa, but underlying mechanisms are not fully understood. Studies suggested that tumor progression is facilitated upon activation of mevalonate (MVA) pathway, while it is reduced via MVA pathway inhibition-induced ferroptosis. Therefore, this study aimed to determine whether lovastatin suppresses prostate cancer progression by inducing ferroptosis through inhibition of the MVA pathway. Five clinically used statins were screened in prostate cancer cell lines to identify the most effective compound. Cell proliferation, migration, and invasion were assessed. Ferroptosis was evaluated by measuring intracellular Fe2+ and reactive oxygen species (ROS) levels, mitochondrial membrane potential, ferroptosis-related protein expression, and ultrastructural mitochondrial alterations. Rescue experiments were performed using the ferroptosis inhibitor deferoxamine and MVA supplementation. Lovastatin exhibited the strongest inhibitory effect, significantly reducing proliferation, migration, and invasion. Lovastatin significantly suppressing PCa cell aggressiveness and inducing ferroptosis, as evidenced by typical biochemical and morphological markers, all of which were reversed by deferoxamine. MVA supplementation restored cell viability, normalized oxidative stress and iron levels, and reversed alterations in MVA pathway enzymes and ferroptosis-associated proteins. Lovastatin suppresses prostate cancer cell growth and invasiveness by inhibiting the MVA pathway and inducing ferroptosis, highlighting the MVA-ferroptosis axis as a potential therapeutic target for PCa.

A 68-year-old woman visited a gynecological clinic complaining of abdominal distension and pain. A large immobile tumor was palpable in the upper left abdominal area. Computed tomography showed an ovarian tumor measuring 20 cm in diameter anterior to the left kidney. A barium enema revealed that the descending colon was narrow, with a wall that was irregularly transformed by the tumor. Cytoreductive debulking surgery was performed. A histological examination demonstrated squamous cell carcinoma arising from a mature cystic teratoma of the ovary. The descending colon was invaded by cancer cells up to the mucosal tissue, and four lymph nodes were metastatic. After surgery, she received eight cycles of adjuvant chemotherapy. After the last treatment, she has been free of the disease for longer than 18 years. We describe the clinical characteristics of this case and speculate on the reason for the long-term survival.

Colorectal cancer (CRC) remains a leading cause of cancer-related death worldwide, prompting ongoing research into infectious agents that may contribute to colorectal carcinogenesis. Among candidate oncogenic viruses, JC polyomavirus (JCPyV), a ubiquitous human polyomavirus, has attracted considerable attention due to its potential involvement in tumour initiation and progression. Although several studies have reported the presence of JCPyV viral DNA, transcripts, and proteins in colorectal adenomas and carcinomas, the prevalence and clinical significance of these findings vary considerably across populations and diagnostic methods. Mechanistically, the viral Large T Antigen (TAg) is implicated in several oncogenic processes through its interactions with key cellular regulators, including p53, retinoblastoma protein (pRb), and components of the Wnt/β-catenin signalling pathway. These interactions may cause genomic instability, aberrant cell cycle progression, impaired DNA repair, and aberrant cell proliferation, thereby creating an environment conducive to malignant transformation. In addition, emerging evidence suggests that JCPyV may contribute to chromosomal instability and epigenetic changes that facilitate tumour progression. Despite these observations, the causal role of JCPyV in colorectal cancer remains controversial. Inconsistent epidemiological data, discrepancies in virus detection, geographic variation, and the inability to confirm direct causation of carcinogenesis have generated ongoing debates about the involvement of JCPyV as a stimulator factor or cofactor in colorectal tumourigenesis. This review critically evaluates the current evidence linking JCPyV to colorectal cancer, summarises the proposed molecular mechanisms of viral carcinogenesis, and highlights key unresolved questions that need to be addressed to clarify the biological and clinical significance of JCPyV in colorectal carcinogenesis.

Arginine methylation is a common post-translational modification that exists in three distinct forms-monomethylation, asymmetric dimethylation, and symmetric dimethylation-through which it regulates precursor RNA splicing and maintains cellular homeostasis. Dysregulation of the writing, reading, or erasure of arginine methylation promotes cancer development. Recent studies have identified PRMTs as key regulators of alternative splicing, and aberrant PRMT-driven splicing directly impacts multiple biological processes, including tumor proliferation, apoptosis resistance, metastasis, and immune evasion. This review focuses on the molecular mechanisms by which PRMTs regulate alternative splicing, their connections to oncogenic processes, and the therapeutic implications and challenges of targeting the PRMT-splicing axis in cancer.

Fibroadenomas are common benign lesions that are typically managed conservatively. However, transformation into malignant phyllodes tumor is a rare but critical progression that demands a shift from surveillance to surgical intervention. We present the case of a patient who underwent multiple core-needle biopsies over several years, all confirming a fibroadenoma, yet the mass demonstrated progressive growth, ultimately exceeding 7 cm. Ultimately, surgical excision revealed a malignant phyllodes tumor characterized by stromal overgrowth, cellular atypia, increased mitotic activity, and infiltrative margins. This case highlights the diagnostic limitations of core-needle biopsy in fibroepithelial lesions. Although the vast majority of fibroadenomas remain benign, a minority may undergo malignant transformation. Physicians must maintain a high degree of clinical suspicion and closely monitor longstanding lesions for any signs of growth or change. Early distinction between fibroadenomas and phyllodes tumors is essential, as management strategies differ substantially.

Intra-orbital ancient schwannomas are exceedingly rare nerve sheath tumors characterized by degenerative changes such as cystic necrosis, hyalinization, and calcification. These benign neoplasms often present diagnostic challenges due to their nonspecific clinical manifestations and potential for extensive local growth. A 57-year-old male farmer presented with a 20-year history of progressive swelling in the right upper eyelid, which had enlarged to the size of a golf ball.The lesion was associated with proptosis, inferior globe dystopia, exposure keratopathy, and complete vision loss in the affected eye. Systemic symptoms included intermittent headaches, low-grade fever, and weight loss. Magnetic resonance imaging revealed a large, heterogeneously enhancing mass arising from the superior aspect of the right orbit, with intracranial extension into the anterior cranial fossa and involvement of adjacent paranasal sinuses. Histopathological examination of the excised tumor demonstrated features consistent with an ancient schwannoma, and immunohistochemistry confirmed the diagnosis.This case highlights the indolent yet locally aggressive nature of intra-orbital ancient schwannomas, emphasizing the importance of early diagnosis and multidisciplinary management. Surgical excision remains the mainstay of treatment, with a favorable prognosis following complete resection. However, intracranial extension and prolonged symptom duration, as seen in this case, underscore the need for heightened clinical suspicion and timely intervention.

Intra-orbital ancient schwannomas are rare but should be considered in the differential diagnosis of orbital masses. Early imaging and histopathological confirmation are critical for optimal management and preservation of visual function.