Calcifying epithelial odontogenic tumor (CEOT), or Pindborg tumor, is a rare benign odontogenic neoplasm with a recognized risk of local recurrence. Management of anterior maxillary lesions is particularly challenging due to aesthetic and functional implications. We report the case of a 26-year-old woman who presented with a missing maxillary right canine. Cone beam computed tomography (CBCT) revealed a 2.2 × 1.5 × 1.2 cm, well-defined mixed lesion associated with an impacted tooth 13 with internal calcifications. Incisional biopsy suggested CEOT. Following a multidisciplinary discussion, a conservative surgical approach was selected. Enucleation with curettage and extraction of tooth #13 were performed. Histopathology confirmed CEOT. Complete bone healing was observed at eight months. Secondary reconstruction using guided bone regeneration with a customized titanium mesh was performed, followed by implant placement and prosthetic rehabilitation. At the 30-month follow-up, no evidence of recurrence or implant-related complications was observed. In effect, in selected anterior maxillary CEOTs, conservative surgery followed by staged reconstruction and implant rehabilitation may achieve satisfactory oncologic, functional, and aesthetic outcomes.

Diffuse hemispheric glioma, H3 G34-mutant (DHG-H3-G34), is a rare, newly defined WHO grade 4 glioma. Its nonspecific symptoms and radiologic heterogeneity can mimic infectious, autoimmune, and paraneoplastic neurologic disorders, complicating timely diagnosis. We present a case of a 20-year-old man with a history of suspected systemic lupus erythematosus who presented with acute encephalopathy, seizures, and aphasia. He underwent an extensive workup to evaluate for possible encephalitis. Biopsy ultimately revealed the diagnosis of DHG-H3-G34. This case highlights the importance of maintaining a broad differential in young patients with acute neurologic decline. Early consideration of neoplasms is crucial to avoid diagnostic delays in high-grade gliomas.

Photodynamic therapy (PDT) has emerged as a promising non-invasive therapeutic modality for cancer treatment. Compared with conventional antineoplastic therapies, PDT offers targeted cytotoxic effects and relatively low systemic toxicity, making it an attractive therapeutic option for patients with cancer. The therapeutic efficacy of PDT is largely determined by the intrinsic properties of photosensitizers (PSs), which are the central components of this therapeutic approach. However, currently available PSs still present several inherent limitations, including inadequate penetration into deep tumor tissues, suboptimal accumulation and delivery at tumor sites, and substantial dependence on oxygen availability within the tumor microenvironment. Consequently, the development of high-performance PSs remains a key research priority in the field of PDT. Recent advances in photosensitizer technology have enabled the rational integration of PDT with other therapeutic modalities, including radiotherapy, chemotherapy, and immunotherapy, to achieve synergistic therapeutic effects, thereby significantly improving overall treatment outcomes. This review systematically summarizes the major classifications, key characteristics, and recent advances in the application of nanomaterials for PDT. It evaluates the current progress in the development of nanomaterial-based PSs and examines their potential applications in combination therapeutic strategies for cancer treatment. Collectively, these findings provide valuable insights into the future development of PDT-based anticancer therapies.

Colorectal cancer (CRC) remains a major global health challenge and a leading cause of cancer-related mortality worldwide. Central to its pathogenesis is the dysregulation of interconnected signal transduction networks that govern cellular proliferation, survival, differentiation, apoptosis, and immune modulation. Progressive disruption of these pathways facilitates malignant transformation of the colonic epithelium and underlies disease initiation and progression. In this review, we examine the foundational signaling mechanisms implicated in CRC, with an emphasis on the Wnt/β-catenin, GUCY2C, MAPK/ERK, p53, PI3K/AKT, and SMAD4/TGF-β pathways. We also highlight the genomic and epigenomic hallmarks of CRC to illustrate how genetic and epigenetic alterations contribute to diverse oncogenic processes. Furthermore, we discuss both conventional and emerging precision-based therapeutic strategies aimed at driving mutations in CRC tumorigenesis. By synthesizing advances in signaling biology, this review aims to provide a framework for understanding CRC complexity and to inform the development of more precise and effective therapies.

Breast schwannomas are rare benign tumors originating from Schwann cells of peripheral nerves. They are exceedingly uncommon in the male breast and are often misdiagnosed as gynecomastia, particularly in patients on prolactin-elevating medications. We report a case of a 40-year-old male with a longstanding palpable mass in the upper outer quadrant of the left chest wall. The patient had a history of schizoaffective disorder and was on antipsychotic therapy, initially leading to the clinical presumption of gynecomastia. Diagnostic mammography revealed a well-circumscribed, noncalcified mass adjacent to the pectoralis muscle. Ultrasound demonstrated a heterogeneously hypoechoic lesion with cystic changes, classified as BI-RADS 4. Ultrasound-guided core biopsy revealed a schwannoma with S100 positivity which was confirmed on final surgical pathology after excision. This case underscores the importance of maintaining a broad differential for male breast masses and highlights the limitations of imaging alone in distinguishing rare benign neoplasms from malignancy. Biopsy remains essential for diagnosis, particularly in patients with confounding clinical risk factors.

Tumor immunotherapy can activate host antitumor immune responses and specifically eliminate tumor cells, making it a research frontier in tumor therapy. However, its clinical efficacy remains limitations by the immunosuppressive tumor microenvironment (TME) and insufficient tumor immunogenicity. Cascade nanozymes possess the capability to mimic diverse enzymatic activities, catalyze multi-step reactions, regulate the redox equilibrium of the TME, generate reactive oxygen species (ROS) for the eradication of tumor cells, induce immunogenic cell death (ICD), and modulate innate immune signaling pathways. These effects further trigger both innate and adaptive immune responses, thereby suppressing tumor metastasis and recurrence. Nevertheless, achieving selective killing of tumor cells without damaging normal cells via enzymatic reactions and clarifying the underlying mechanisms of cascade nanozyme-based immunotherapy remains a major challenge in cancer treatment. This review summarizes the latest advances of cascade nanozymes in cancer immunotherapy. It critically evaluates the design strategies and mechanisms of cascade nanozymes for immunotherapeutic applications, and highlights the key challenges and future perspectives in this field. It is expected to provide new insights for developing more efficient and targeted tumor immunotherapy strategies.

Folate deficiency is common and often asymptomatic, but severe cases can cause megaloblastic anemia. Rarely, it presents with pancytopenia and bone marrow changes resembling myelodysplastic syndrome/neoplasm (MDS) and/or acute myeloid leukemia (AML), complicating diagnosis and management. We present a case of a patient with severe folate deficiency, in the setting of normal vitamin B12 levels, who presented with hematologic and bone marrow findings initially suggestive of MDS/AML that resolved with folate supplementation. This case highlights that the clinical and morphologic findings associated with severe folate deficiency can closely resemble those of high-risk MDS or MDS/AML. Careful diagnostic evaluation, including nutritional assessment, is essential to avoid the misclassification of reversible nutritional deficiencies as myeloid neoplasms requiring cytotoxic therapy.

Single-cell transcriptomics and machine learning methods are increasingly used to identify immune-related biomarkers in solid tumors, yet their combined application to microenvironment-related drivers of therapeutic resistance in clear cell renal cell carcinoma (ccRCC) is still limited. Here, we investigated the biological and clinical significance of myeloid-derived growth factor (MYDGF) through an integrative strategy spanning single-cell profiling, bulk multiomics, and functional validation. Analysis of scRNA-seq data (GSE156632) revealed that MYDGF is preferentially detected in malignant epithelial subpopulations and associated with the composition of myeloid and lymphoid compartments. Integration with TCGA-KIRC transcriptomic and clinical datasets demonstrated strong associations between MYDGF expression and immune-checkpoint activation, immune dysfunction signatures, and PI3K/AKT-MAPK pathway activity. Tumors with high MYDGF expression exhibited an immune-infiltrated yet functionally impaired microenvironment and were predicted to show reduced responsiveness to immune checkpoint blockade. Differential expression and enrichment analyses further highlighted MYDGF-associated genes involved in inflammatory, extracellular, and receptor-binding functions. A machine learning pipeline using LASSO Cox regression identified a preliminary 19-gene MYDGF-related prognostic gene set that requires further validation. Functional experiments confirmed that MYDGF knockdown suppressed proliferation, migration, and invasion in ccRCC cells. Overall, our analyses characterize MYDGF as a microenvironment-related biomarker linked to immune-associated features, signaling-associated alterations, and adverse prognosis in ccRCC. These results nominate MYDGF as a candidate prognostic biomarker and show the value of pairing single-cell resolution with computational modeling for biomarker discovery in renal cancer.

Nasopharyngeal cancer (NPC) is a malignant tumor that originates from mucosal epithelial cells of the nasopharynx. As an emerging cancer-associated microRNA, miR-138-5p has been shown to modulate various malignant cell malignancies. However, its precise biological function and regulatory mechanism in NPC remain to be further elucidated. Human NPC cell lines (HK-1 and C666-1) were used for in vitro study, and nude mouse xenograft models were used for in vivo investigations. A bioinformatic method was utilized for the prediction of RNA expression patterns and molecular interactions. RT-qPCR was performed for the detection of miR-138-5p and CENPN expression. Luciferase activity detection and RNA pulldown experiments were used for verification of gene interaction. Flow cytometry and colony formation assays were conducted to evaluate cell cycle distribution, proliferative capacity, and apoptosis rate. Furthermore, extracellular acidification rate, lactate generation, and glucose uptake were assessed to explore the regulatory effects of miR-138-5p and CENPN on glycolysis in NPC cells. Protein levels of CENPN and key molecules associated with cell cycle, apoptosis, glycolysis, and the PI3K signaling pathway were quantified by western blot analysis. CENPN expression is analyzed to be upregulated in head and neck cancer samples, and its high expression is associated with unfavorable clinical prognosis. In NPC cells, miR-138-5p was markedly downregulated and was verified to directly target the 3' untranslated region of CENPN, thereby negatively regulating its expression. Functionally, overexpressing miR-138-5p obstructed malignant phenotype, glycolysis, and tumor growth of NPC cells, where these inhibitory effects were significantly counteracted by enforced CENPN expression. Moreover, miR-138-5p overexpression inactivated the PI3K/Akt/mTOR signaling by reducing CENPN expression in NPC cells. In conlusion, miR-138-5p inhibits cell growth, glycolysis, and tumorigenesis in NPC by directly targeting CENPN, thereby inhibiting the PI3K/Akt/mTOR signaling pathway. These findings highlight the potential utility of miR-138-5p as both a diagnostic indicator and a therapeutic intervention target for NPC management.

Glioblastoma (GBM) exhibits profound metabolic plasticity and resistance to conventional therapies, partly driven by mitochondrial adaptability and stress response mechanisms. ONC212, a second-generation imipridone, targets mitochondrial proteostasis, yet determinants of tumour sensitivity remain unclear. This study aimed to investigate whether ATP-sensitive potassium (KATP) channel expression modulates ONC212-induced mitochondrial dysfunction and integrated stress response (ISR) activation in GBM. Human GBM lines (U87, U251, T98G) and non-malignant SVG p12 astrocytes received ONC212 (0.5-80 μM) for 12-48 h. Viability was assessed by CCK-8. KATP subunit expression (Kir6.2, SUR1, CCDC51) was quantified by qRT-PCR and western blot. Mitochondrial ROS quantification, oxygen consumption rate (Seahorse XF), PERK/ATF4/CHOP activation (western blot, immunofluorescence) and apoptosis (caspase-3/7) were evaluated. KATP was modulated pharmacologically (glibenclamide, diazoxide) and via KCNJ11 (Kir6.2) siRNA. ONC212 induced time-dependent and tumour-selective cytotoxicity, with highest sensitivity observed in KATP-high U87 cells. Treatment significantly increased mitochondrial ROS, impaired oxidative phosphorylation and reduced ATP/ADP ratios, indicating bioenergetic collapse. Concurrently, ONC212 robustly activated the PERK/eIF2α/ATF4/CHOP axis and promoted ATF4 nuclear translocation. PERK inhibition attenuated both stress signalling and cytotoxicity, confirming ISR dependency. KATP inhibition enhanced ONC212-induced mitochondrial dysfunction, ISR activation and apoptosis, whereas KATP activation exerted protective effects. Importantly, KCNJ11 silencing markedly potentiated ONC212 sensitivity, amplifying ROS production, mitochondrial impairment and caspase-dependent apoptosis. KATP channel expression may regulate ONC212 responsiveness in GBM by modulating mitochondrial stress and ISR signalling. Targeting KATP channels may enhance imipridone efficacy and represents a promising strategy for metabolically guided GBM therapy.