Lumican (LUM), a small leucine-rich proteoglycan, is a component of the extracellular matrix. Abnormal LUM expression is potentially associated with cancer progression. In the present study, we confirmed high LUM mRNA expression in colorectal adenocarcinoma (COAD) through the UALCAN database. The Kaplan-Meier method, univariate, and multivariate COX analysis showed that high LUM expression is an independent determinant of poor prognosis in COAD. A COX regression model was constructed based on clinical information and LUM expression. The receiver operating characteristic (ROC) curve indicated that this model was highly accurate in monitoring COAD prognosis. The co-expression network of LUM was determined by LinkedOmics, which showed that LUM expression was closely related to immune escape and the miR200 family. Furthermore, we studied the co-expression network of LUM and found that LUM could promote tumor metastasis and invasion. The Tumor Immune Estimation Resource website showed that LUM was closely related to immune infiltration and correlated with regulatory T cells, tumour-associated macrophages, and dendritic cells. We found that LUM cultivated cancer progression by targeting the miR200 family to promote epithelial-to-mesenchymal transition. These findings suggest that LUM is a potential target for inhibiting immune escape and carcinogenic pathways.

Purpose: The involvement of dedicator for cytokinesis 4 (DOCK4), a guanine nucleotide exchange factor for Rac1, in immune infiltration in stomach adenocarcinoma (STAD) remains unclear. Methods: The UALCAN database was used to analyze the expression of the DOCK family. The Kaplan–Meier method and Gene Expression Profiling Interactive Analysis (GEPIA) databases were used to assess the prognostic value of the DOCK family in STAD. Furthermore, the correlation between expression of DOCK4 as well as other immune-related marker genes and tumor immune infiltration in STAD was explored using the TIMER and GEPIA websites. Subsequently, the relationship between DOCK4 expression and clinical characteristics was verified using the UALCAN database. Finally, DOCK4 mutation was analyzed via the TIMER2.0 and cBioPortal databases and the DOCK4 protein-protein interaction networks were constructed using the GeneMANIA and STRING websites. Results: DOCK4 was found to be a new prognostic biomarker in STAD. DOCK4 expression in tumors was thoroughly evaluated relative to paracancerous tissues; overexpression of DOCK4 had a negative impact on the prognosis of patients with STAD. DOCK4 was found to be significantly associated with tumor immune infiltration in STAD. Conclusion: In summary, DOCK4 is a potential regulator of the recruitment and regulation of immune-infiltrating cells, thus serving as a valuable prognostic biomarker in STAD.

The activities of the ephrin family in breast cancer (BrCa) are complex. Family A receptors (EPHA) and ligands (EFNA) can act as oncogenes or tumor suppressors and are implicated in chemoresistance. Here, we examined the expression pattern and prognostic value of the EPHA/EFNA family in patients with breast cancer, including patients with different subtypes or different chemotherapy cohorts. In the UALCAN database, the mRNA expression of EPHA1, EPHA10, EFNA1, EFNA3, and EFNA4 was significantly higher, whereas that of EPHA2, EPHA4, EPHA5, and EFNA5 was significantly lower in breast cancer tissues than in paracancerous tissues. The transcriptional levels of EPHA/EFNA family members were correlated with intrinsic subclasses of breast cancer. The relationship between EPHA/EFNA and the clinicopathological parameters of BrCa was analyzed using bc‐GenExMiner V4.5. EPHA1, EPHA2, EPHA4, EPHA7, EFNA3, EFNA4, and EFNA5 were upregulated in estrogen receptor‐ (ER‐) and progesterone receptor‐ (PR‐) negative tumors, whereas EPHA3, EPHA6, and EFNA1 were upregulated in ER‐ and PR‐positive tumors. EPHA1, EPHA2, EFNA3, and EFNA4 mRNA expression was significantly higher in human epidermal growth factor receptor 2‐ (HER2‐) positive tumors than in HER2‐negative tumors. Triple‐negative status was positively correlated with EPHA1, EPHA2, EPHA4, EPHA7, EFNA3, EFNA4, and EFNA5 and negatively correlated with EPHA3 and EPHA10 mRNA expression. Genetic alterations of EPHA/EFNA in breast cancer varied from 1.1% to 10% for individual genes, as determined by the cBioPortal database. The Kaplan–Meier plotter indicated that high EphA7 mRNA expression was associated with poor overall survival (OS) and recurrence‐free survival (RFS), especially in the HER2 and luminal A subtypes. EFNA4 was predicted to have poor OS and RFS in breast cancers, especially in luminal B, basal‐like subtype, and patients treated with adjuvant chemotherapy. High EPHA3 expression was significantly associated with better OS and RFS, especially in the luminal A subtype, but with poor RFS in BrCa patients receiving chemotherapy. Our findings systematically elucidate the expression pattern and prognostic value of the EPHA/EFNA family in BrCa, which might provide potential prognostic factors and novel targets in BrCa patients, including those with different subtypes or treated with chemotherapy.

Rationale: Spindle cell lipoma is a rare, uncommon type of benign lipomatous tumor, a distinct group of lipomas composed of mature adipocytes, uniform spindle cells, and multinucleated giant cells associated with ropey collagen. Immunohistochemically, spindle cell lipoma is characterized by the diffuse expression of CD34. Patient concerns: We present a rare case of a 56-year-old man who complained of vomiting out of a smooth and giant mass in the oral cavity provoked by an intra-abdominal pressure increase. Oral examination revealed an elongated mass protruding from the mouth. Computed tomography of the patient showed a mass from left pyriform to oral cavity, with 2.38 × 2.78 × 16.86 cm in size. The flexible fiberscope showed that the pedicle of the elongated mass originated from the posterior wall of the hypopharynx, corresponding to the left pyriform fossa. Diagnosis: Histopathologically, the tumor was mainly composed of hyperplastic adipocytes, admixed with small blood vessels, and scattered inside adipose tissue spindle cells. The immunohistochemical profile revealed positivity of spindle cells for CD34, negativity for S100, and low proliferation with Ki67, which confirmed the diagnosis of spindle cell lipoma and revealed its benign behavior. Interventions: The patient underwent hypopharyngeal mass resection using transoral suspension laryngoscopy. Outcomes: No recurrence was found after 5 months of follow-up. Lessons: Spindle cell lipoma is difficult to diagnose early because of slow growth and subtle symptomatology. This entity should be differentiated from several benign or malignant subtypes of lipomas, including liposarcomas. In this case, the spindle cell lipoma is large and originates from the hypopharynx, which is a rare entity and presents with atypical symptoms. This case gave rise to further studies on the clinical and pathologic characteristics of this tumor in the future.

Background: Recent studies have unveiled disulfidptosis as a phenomenon intimately associated with cellular damage, heralding new avenues for exploring tumor cell dynamics. We aimed to explore the impact of disulfide cell death on the tumor immune microenvironment and immunotherapy in lung adenocarcinoma (LUAD). Methods: We initially utilized pan-cancer transcriptomics to explore the expression, prognosis, and mutation status of genes related to disulfidptosis. Using the LUAD multi- -omics cohorts in the TCGA database, we explore the molecular characteristics of subtypes related to disulfidptosis. Employing various machine learning algorithms, we construct a robust prognostic model to predict immune therapy responses and explore the model's impact on the tumor microenvironment through single-cell transcriptome data. Finally, the biological functions of genes related to the prognostic model are verified through laboratory experiments. Results: Genes related to disulfidptosis exhibit high expression and significant prognostic value in various cancers, including LUAD. Two disulfidptosis subtypes with distinct prognoses and molecular characteristics have been identified, leading to the development of a robust DSRS prognostic model, where a lower risk score correlates with a higher response rate to immunotherapy and a better patient prognosis. NAPSA, a critical gene in the risk model, was found to inhibit the proliferation and migration of LUAD cells. Conclusion: Our research introduces an innovative prognostic risk model predicated upon disulfidptosis genes for patients afflicted with Lung Adenocarcinoma (LUAD). This model proficiently forecasts the survival rates and therapeutic outcomes for LUAD patients, thereby delineating the high-risk population with distinctive immune cell infiltration and a state of immunosuppression. Furthermore, NAPSA can inhibit the proliferation and invasion capabilities of LUAD cells, thereby identifying new molecules for clinical targeted therapy.

Tumor cell senescence reduces sensitivity to anticancer drugs, making senescent cell elimination an ideal strategy to enhance chemotherapy sensitivity. The interaction between the PI3K/Akt and Hippo/YAP1 pathways is increasingly studied, but the role of PIK3CB, YAP1, and their impact on senescence and chemotherapy sensitivity in head and neck tumors is unclear. Public datasets (GEO, TCGA, HPA) were analyzed for PIK3CB expression and clinical associations. Immunohistochemistry, cell proliferation assays, DNA replication, colony formation, aging markers, and DNA damage assessments were conducted. Bulk and single-cell transcriptomics and proteomics data were analyzed. Cell passage effects on aging and the impact of PIK3CB modulation on YAP1 were evaluated. Potential drugs targeting PIK3CB were identified, and the effects of senescent cell clearance drugs on clonogenic abilities and chemotherapy sensitivity were assessed. Elevated PIK3CB expression in HNSCC tumors correlated with advanced stages, older age, and decreased survival. PIK3CB and YAP1 expressions were strongly correlated, impacting aging pathways and cellular proliferation. Modulation of PIK3CB affected tumor cell proliferation, aging, and DNA damage. The combined application of navitoclax and paclitaxel can reduce tumor cell proliferation and autonomous migration ability, influenced by the levels of PIK3CB. High PIK3CB expression in head and neck cancers is linked to poor prognosis and advanced tumor grades. PIK3CB promotes cell proliferation and reduces aging via the YAP1 pathway. The combination of navitoclax and paclitaxel reduces tumor cell proliferation and autonomous migration ability, providing a basis for further exploration of increasing chemotherapy sensitivity.