Diffuse Leptomeningeal Glioneuronal Tumor (DLGNT) is a rare neoplasm in children with variable clinical and radiological features, often leading to diagnostic delays.We present the case of a 3-year-old boy with tonic-clonic seizures and gait disturbance. Brain and spine MRI revealed widespread, non-enhancing, cystic lesions along the cerebral sulci and subarachnoid space. Biopsy confirmed the diagnosis of DLGNT. This case demonstrates a unique radiological presentation of DLGNT as diffuse, non-enhancing cystic lesions. Recognizing this unique imaging pattern is crucial for early diagnosis, especially in pediatric patients.

Pathologies affecting the conus medullaris and cauda equina can present with overlapping clinical symptoms, making an accurate diagnosis essential. Conus medullaris syndrome results from damage at the T12-L2 level, while cauda equina syndrome arises from nerve root compression below the conus. Both conditions may cause motor deficits, sensory disturbances, and autonomic dysfunction, necessitating a detailed differential diagnosis.

This educational review highlights common and rare etiologies of conus medullaris and cauda equina lesions, emphasizing imaging characteristics and diagnostic considerations. A comprehensive review of tumors, infections, inflammatory, vascular, and degenerative conditions affecting these regions was performed. Contrast-enhanced MRI was identified as the gold standard for diagnosis.

Tumors: myxopapillary ependymomas and schwannomas are the most frequent neoplasms, while drop metastases and glioblastomas represent rarer entities.

tuberculous arachnoiditis, bacterial radiculitis, schistosomiasis, and neurocysticercosis may mimic neoplastic processes. Inflammatory disorders: Guillain-Barré syndrome, neurosarcoidosis, and MOGAD may cause nerve root thickening and enhancement. Vascular lesions: spinal dural arteriovenous fistulas, infarcts, and arteriovenous malformations can produce conus and cauda equina symptoms. Miscellaneous causes: developmental anomalies like diastematomyelia and ventriculus terminalis, along with degenerative diseases, can mimic other conditions.

Radiologists play a pivotal role in differentiating conus medullaris and cauda equina pathologies. A thorough understanding of imaging findings is essential for accurate diagnosis and effective management.

Conus medullaris and cauda lesions present with overlapping clinical symptoms but show some distinct imaging patterns. It is essential to recognize characteristic features that differentiate neoplastic from infectious or vascular etiologies.

Conus and cauda lesions have varied causes; MRI with contrast is vital for accurate diagnosis. Myxopapillary ependymomas cause vertebral scalloping; schwannomas may be cystic; intramedullary gliomas expand the cord. Conus medullaris and cauda lesions overlap clinically; imaging helps distinguish neoplastic from infectious or vascular causes.

Epigenetic research, particularly involving m6A RNA methylation-a dynamic and reversible posttranscriptional modification-has increasingly demonstrated its critical involvement in cancer pathogenesis. Although the m6A demethylase FTO is implicated in breast cancer (BC), its specific regulatory mechanisms against triple-negative breast cancer (TNBC) has not been clearly defined. Quantitative PCR (qPCR) was used to compare m6A regulatory enzyme expression in TNBC patient tissues with that in normal breast tissues, identifying FTO as the most differentially expressed enzyme. Two randomly selected TNBC/normal tissue pairs were subjected to methylated RNA immunoprecipitation sequencing (MeRIP-Seq). Integrated analysis utilizing the SRAMP and RMBase databases predicted potential FTO target genes. Transcriptome sequencing of FTO-overexpressing TNBC cell lines identified downstream pathways. Dual-luciferase reporter assays and MeRIP-qPCR validated the functional role of FTO and its target, NFKBIE, and their regulatory interaction in TNBC. Compared with normal samples, clinical samples from TNBC patients presented significantly decreased FTO expression (p < 0.05) and correspondingly elevated global m6A levels. MeRIP-Seq confirmed substantial differences in m6A methylation (R = 0.23, p < 0.05). Bioinformatics and transcriptome analyses identified NFKBIE as the primary FTO target. Dual-luciferase assays demonstrated that FTO overexpression specifically modulated wild-type (WT), but not mutant (MT), NFKBIE promoter activity (p < 0.05). MeRIP-qPCR verified the FTO-mediated reduction in m6A methylation at three specific NFKBIE sites (p < 0.05). Functional assays (CCK-8, Transwell invasion/migration, and scratch wound healing) indicated that FTO overexpression significantly enhanced TNBC cell proliferation and motility; these oncogenic phenotypes were partially rescued by concurrent NFKBIE overexpression. FTO regulates NFKBIE expression via m6A-dependent demethylation, establishing a pivotal FTO-NFKBIE regulatory axis that drives TNBC progression. FTO overexpression promotes TNBC cell proliferation, migration, and invasion, effects that are partially reversible through NFKBIE restoration.

The efficacy of CD19 CAR-T cells in B-cell lymphoma patients is not as good as that in B-cell acute lymphoblastic leukemia (B-ALL) patients. This might be attributed to the intricate tumor microenvironment of B-cell lymphoma, which leads to CAR-T cell exhaustion, inability to sustain function, and difficulty infiltrating into the tumor interior. We developed CD19 CAR structures that simultaneously produce membrane-bound IL-15 (mbIL-15) and CXCR5. This design aims to enhance the migration of CAR-T cells into CXCL13+ B-cell lymphomas and their long-term antitumor ability. Compared with CD19 CAR-T cells, CD19 mbIL15-CXCR5 CAR-T cells exhibited greater cytotoxicity against CD19+ tumor cell lines in vitro. In particular, when exposed to recurrent tumor antigen stimulation, CD19 mbIL15-CXCR5 CAR-T cells still exerted long-lasting antitumor effects. CD19 mbIL15-CXCR5 CAR-T cells had a greater proportion of central memory T (TCM) and effector memory T (TEM) cells, which allowed them to exhibit more long-lasting antitumor effects. Moreover, in Transwell assays and mouse models, compared with CD19 CAR-T cells, CD19 mbIL15-CXCR5-CAR-T cells exhibited significant chemotaxis toward CXCL13+ tumor cells and superior tumor infiltration ability. The Xenogram animal model demonstrated better and more persistent tumor suppression ability than did the CD19 CAR-T cells. We preliminarily demonstrated the safety of CD19 mbIL15-CXCR5-CAR-T cells in vivo by evaluating liver and kidney function and major organ morphology in mice. In summary, the use of CD19 mbIL15-CXCR5-CAR-T cells is a relatively safe and effective option for the treatment of B-cell malignancies.

To validate a standardized MRI scoring system, tracheal invasion score (T-score) and vascular invasion score (V-score) against CT for detecting tracheal and major-vessel invasion in esophageal cancer, based on imaging obtained after neoadjuvant therapy.

Twenty-six patients (mean age 65 years) who underwent both MRI and CT after preoperative therapy and prior to esophagectomy were retrospectively reviewed. Two radiologists independently assigned T- and V-scores on MRI and CT-based T-stage (12th Japanese Classification). Diagnostic performance was measured by the area under the ROC curve (AUC) and κ for inter-reader agreement. Patient-level bootstrap resampling (2000 iterations) compared the combined MRI score-defined as max (T, V)-with CT.

MRI yielded higher AUCs than CT for tracheal invasion (0.943-0.990 vs. 0.529-0.706) and vascular invasion (0.878 for both readers). MRI achieved substantial-to-almost-perfect agreement (κ = 0.771-1.000), whereas CT was only moderate (κ = 0.369-0.487). Bootstrap analysis confirmed superior discrimination of the combined MRI score: ΔAUC + 0.19 (-0.05-0.43, p = 0.11) for Reader A and +0.38 (0.07-0.66, p = 0.02) for Reader B.

A combined MRI T/V-score provides better accuracy and inter-reader reliability than CT for evaluating critical local invasion, even after preoperative therapy, supporting routine integration of MRI when CT findings are equivocal.

Question Determine whether a standardized MRI scoring system for tracheal and vascular invasion improves diagnostic accuracy compared with contrast‑enhanced CT in esophageal cancer. Findings MRI outperforms CT in detecting tracheal and vascular invasion, with higher specificity and superior inter-reader agreement using standardized scoring criteria. Clinical relevance Standardized MRI scoring improves staging accuracy in suspected T4 esophageal cancer, aiding surgical decision-making and helping to avoid unnecessary surgery in inoperable patients as well as incomplete (R1/R2) resections.

Glioblastoma multiforme (GBM) remains one of the most lethal malignancies due to its marked resistance to standard therapies and a profoundly immunosuppressive tumor microenvironment. Cyclooxygenase-2 (COX-2), via its enzymatic product prostaglandin E2 (PGE2), has emerged as a central driver of multiple oncogenic processes in GBM, including immune evasion, therapy resistance, glioma stemness, and vascular mimicry. This review consolidates recent molecular findings on the COX-2/PGE2 axis, with particular focus on EP2/EP4-mediated signaling pathways such as PI3K/AKT, MAPK, β-catenin/TCF4, and JAK/STAT3, which collectively contribute to tumor proliferation, radioresistance, and PD-L1 expression. Notably, COX-2 promotes extracellular matrix degradation and glioma invasiveness by upregulating matrix metalloproteinase-9 (MMP-9) through TGF-β1 derived from tumor-associated macrophages (TAMs). In parallel, COX-2 facilitates TAM polarization toward an M2-like phenotype and supports the self-renewal of glioblastoma stem cells (GSCs), reinforcing both immune suppression and therapeutic escape. Furthermore, recent data reveal that COX-2 inhibition by celecoxib contributes to mitochondrial dysfunction by downregulating respiratory complexes and mitochondrial biogenesis regulators such as TFAM and NRF2, ultimately leading to bioenergetic collapse and sensitization to chemotherapy-induced apoptosis. By integrating diverse yet interconnected mechanisms under the umbrella of COX-2 signaling, this review outlines potential therapeutic opportunities aimed at disrupting its multifaceted role in GBM pathogenesis and treatment resistance.

Actin-like protein 6A (ACTL6A) is thought to be associated with the survival and prognosis of patients with a variety of human cancers. This study investigates the effect of ACTL6A knockdown on ESCC radiosensitivity and explores molecular mechanisms that may enhance radiotherapy efficacy. The ACTL6A expression level was increased in esophageal squamous carcinoma cells after radiation irradiation. The protein expression level of ACTL6A in tumor tissue samples of clinical esophageal squamous cell carcinoma patients was analyzed by immunohistochemistry, and it was found that the prognosis of the high expression group was worse than that of the low expression group. Further knocking down the ACTL6A gene in esophageal squamous cell carcinoma cells, it was found that ACTL6A could regulate the proliferation, migration, invasion, DNA damage repair, cell cycle, and apoptosis of esophageal squamous cell carcinoma cells, which further affected the radiosensitivity of esophageal squamous cell carcinoma cells. Through functional enrichment analysis of gene set enrichment and validation of the mechanism using the Wnt pathway inhibitor XAV939, it was shown that ACTL6A is involved in the regulation of the Wnt/β-catenin signaling pathway. Knockdown of ACTL6A can inhibit the activity of this pathway, thereby increasing the radiosensitivity of esophageal squamous cell carcinoma. ACTL6A may become an important therapeutic target for esophageal squamous cell carcinoma, providing a necessary theoretical basis for future treatment strategies.

Cell division cycle-associated protein 4 (CDCA4) has the potential to indicate lung adenocarcinoma (LUAD) development, but its regulatory role in mitophagy remains unclear. This study aimed to elucidate the mitophagy regulation and therapeutic implications of CDCA4 in LUAD. CDCA4 expression was significantly elevated in LUAD clinical specimens versus paracancerous tissues and inversely correlated with mitophagy activity. Lentiviral vectors were employed to manipulate established LUAD cells, followed by treatment with chloroquine (CQ; lysosomal inhibitor) and rapamycin (autophagy inducer) in CDCA4-silenced cells. CDCA4 knockdown elevated total and mitochondrial superoxide levels, disrupted mitochondrial membrane potential, activated the PINK1/Parkin pathway, enhanced LC3-II conversion, and degraded mitochondrial membrane proteins, collectively promoting mitophagy. Silencing CDCA4 suppressed malignant phenotypes (proliferation/migration), effects reversed by CQ but exacerbated by rapamycin. Mechanistically, CDCA4 interacted with SERTAD1 and E2F1 and stabilized these proteins. The promotion of mitophagy by CDCA4 silencing was impaired by the overexpression of SERTAD1 and E2F1. LUAD cells silencing CDCA4 were injected into immunodeficient mice for in vivo verification. CDCA4-silenced xenografts exhibited suppressed tumor growth, increased apoptosis, and elevated mitophagy-related markers. This study identifies the CDCA4/SERTAD1/E2F1 complex as a pivotal mitophagy-inhibitory hub in LUAD, proposing this axis as a novel predictive and therapeutic target.

Colorectal cancer (CRC) is one of the most common malignant tumors in the digestive system. Immune checkpoint blockade (ICB) is a promising strategy for CRC treatment, but its limited efficacy poses a challenge. Bioinformatics methods were used to screen ferroptosis-related genes in CRC. Cellular biology methods investigated endothelial PAS domain protein 1 (EPAS1) impact on cellular characteristics, stemness, and ferroptosis. Finally, in vivo experiments validated EPAS1's influence on anti-PD-1 therapy efficacy. We have found that EPAS1 is a risk gene in CRC, which can inhibit the growth, invasion, and stemness of colon cancer cells both in vitro and in vivo, and promote ferroptosis. Mechanistically, caveolin 1 (CAV1) regulates the expression of von Hippel-Lindau tumor suppressor (VHL) to inhibit the ubiquitination of EPAS1, increase its stability, further enhance the expression of nuclear receptor coactivator 4 (NCOA4) and autophagy-lysosome formation, leading to cell iron overload and inducing ferroptosis. Our study confirms EPAS1 regulates ferroptosis, impacting epithelial-mesenchymal transition (EMT) and stemness in CRC cells, and highlights its role in ICB. These findings inform CRC treatment.

B-cell lymphoma, the most common subtype of non-Hodgkin lymphoma, presents major therapeutic challenges due to molecular heterogeneity and high relapse rates. While autologous hematopoietic stem cell transplantation (ASCT) has been a cornerstone for relapsed/refractory (R/R) B-cell lymphoma, its efficacy is often compromised by minimal residual disease (MRD) persistence and an immunosuppressive tumor microenvironment. Chimeric antigen receptor (CAR)-T cell therapy has transformed treatment paradigms but faces limited long-term durability due to antigen escape and T-cell exhaustion. The integration of ASCT with CAR-T therapy may offer a complementary approach to address these limitations, leveraging ASCT-induced immune reconstitution to enhance CAR-T-cell persistence and reprogram the tumor milieu. Emerging clinical evidence supports this approach, indicating improved disease control and progression-free survival. Although preliminary clinical outcomes are encouraging, unresolved challenges persist, particularly in terms of cumulative toxicity, optimal therapeutic sequencing, CAR-T-cell longevity, and financial feasibility associated with these advanced therapies. This review provides a comprehensive overview of mechanistic synergies between ASCT and CAR-T therapy, critically evaluates emerging clinical evidence on treatment sequencing, and explores innovative strategies to increase safety, efficacy, and accessibility.