Orbital vascular malformation often encircles normal tissue with ill-defined borders. It is easy to bleed during resection operation, making surgical treatment difficult and lesions hard to be removed completely. In this study we aimed to summarize the treatment outcomes by embolizing orbital vascular malformation with intraoperative intracavitary injection of medical glue . A retrospective observational and cross-sectional case series study enrolled 31 patients (male = 9, female = 22) with orbital vascular malformations, who were treated from March 2008 to September 2017 at our institution. The clinical features, operation records, pathological reports and follow-up data were analyzed. The location of vascular malformations involved intraorbital (14 cases), superficial area of eyelid and/or face (7 cases), both intraorbital and superficial area (10 cases). Imaging examination showed a solitary mass with regular shape in 8 cases and a space occupying lesion with irregular shape and ill-defined margins in 23 cases. There were 9 cases had optic nerve involved. Surgical debulkling were performed via skin incision on the mass surface (5 cases), lateral orbitotomy (2 cases), and anterior orbitotomy (24 cases). During the operation, lesions were partly exposed and injected with medical glue. The amount of injected glue was 0.25 ml to 2.5 ml in divided doses. The lesions and remnant glue were removed after the glue had turned hard. The whole procedure caused less bleeding and was easier performing than usual. Topical skin aseptic inflammation took place on the same side of the superficial eyelid lesions in 3 cases. One patient suffered from sudden central retinal artery embolism on the third day post operation. With timely rescue and appropriate procedure, visual acuity recovered to 20/32. There were no recurrences in 29 cases. Embolization of orbital vascular malformation with medical glue intraoperatively made it easy to control hemorrhage. Surgeons should be careful with glue application methods in order to avoid complications.

Mesenchymal chondrosarcoma (MC) is an uncommon type of malignant soft tissue tumor. The skeleton is the most common site of MC. Extraosseous sarcoma is rare, especially that of the orbit. Fusion gene HEY1–NCOA2 has diagnostic significance for MC, but there is a lack of research on its related pathways. To analyze the characteristics of orbital mesenchymal chondrosarcoma (MC), and search for HEY1-NCOA2-related pathways in orbital MCs, four cases of orbital MC were included in the study. From January 2018 to December 2022, four MC patients hospitalized at Tianjin Medical University Eye Hospital were collected for a retrospective series of case studies. HEY1-NCOA2 of the assay specimens was detected by fluorescence in situ hybridization, and immunohistochemical staining was performed for representative proteins of the relevant pathways. For figure modification and statistical analysis, GraphPad Prism 8.0 (La Jolla, CA, USA) was utilized. Four orbital MC were reported. Among the 4 ligible MC specimens, two were HEY1-NCOA2-positive and two were HEY1-NCOA2-negative. Immunohistochemistry showed stronger expression of COL2A1, APC, CD99, and Bcl2 in HEY1-NCOA2-positive samples than in HEY1-NCOA2-negative MCs. We summarized the clinical features, treatments, and prognosis of orbital MC, including our cases and the literature. The expression of COL2A1 and Bcl2 is elevated in HEY1-NCOA2-positive tissues, and they promote tumor cell growth by regulating cell proliferation, apoptosis, epithelial–mesenchymal transition, and drug resistance. For HEY1-NCOA2-positive patients, given the high expression of CD99, drugs targeting the MAPK pathway may be an effective treatment.

Meibomian Gland Carcinoma (MGC) is a highly malignant eyelid tumor with a poor prognosis. This study investigates the molecular mechanisms underlying MGC, focusing on the abnormal expression of E2F transcription factor 2 (E2F2), often observed in tumors and potentially linked to DNA methylation. E2F2 expression was measured in MGC cells and tissues. Tissue samples from 3 normal meibomian glands (MG) and 36 MGC patients were used to construct a tissue microarray. Functional assays were performed by modifying E2F2 expression, including CCK8, wound healing, Transwell, and analysis of epithelial-mesenchymal transition (EMT)-related markers. Flow cytometry was used to assess cell apoptosis and cell cycle. RNA sequencing was conducted to identify differential genes after treating MGC cells with the methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-2-dc), to explore the relationship between E2F2 downregulation in MGC and methylation. E2F2 expression was significantly lower in MGC cells compared to normal MG cells. Immunohistochemical analysis showed low E2F2 expression in MGC. Specifically, immunohistochemical staining results have revealed a negative correlation trend between E2F2 and Ki-67 expression, as well as a positive correlation trend between E2F2 and P21, P27 expression. E2F2 knockdown increased MGC cell proliferation, migration, and invasion. Flow cytometry revealed that E2F2 knockdown reduced apoptosis, decreased the G0/G1 phase, and increased the S phase, while E2F2 overexpression produced opposite effects. RNA sequencing revealed that a total of 87 genes were differentially expressed in the 5-aza-2-dc experimental group compared to the control group, with 72 mRNAs showing upregulated expression and 15 mRNAs showing downregulated expression. Bioinformatics analysis results indicated that the functions of these differentially expressed genes were concentrated, and the biological processes mainly involved DNA replication, among others. The signaling pathways associated with these genes primarily included DNA replication and the cell cycle. RNA sequencing identified differential gene expression after methylation inhibition in MGC cells with 5-aza-2-dc, demonstrating that demethylation significantly upregulated E2F2. MSP assays confirmed reduced methylation levels. Additionally, inhibiting gene methylation in MGC cells suppressed proliferation, migration, and invasion. E2F2 presents a promising therapeutic target for MGC. Overexpression of E2F2 and methylation inhibition in MGC cells may reverse E2F2 gene silencing, inhibiting malignant progression. These findings provide new perspectives for targeted therapies and precise, individualized treatment in MGC.

Lacrimal adenoid cystic carcinoma (LACC) is the most common malignant epithelial tumor of the lacrimal gland, with particularly high recurrence and mortality in cases with high-grade transformation (HGT-LACC). This study aims to investigate the functional role of miR-150-5p in regulating the HGT of LACC. MiRNA microarray and proteomic mass spectrometry were performed on paired LACC and HGT-LACC tissues to identify differentially expressed miR-150-5p and its potential target COL1A1. The miR-150-5p/COL1A1 interaction was validated by luciferase reporter assay, and the effects of miR-150-5p on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) were assessed in vitro and in vivo via colony formation, wound healing, Transwell assays, and xenograft models. MiR-150-5p was significantly downregulated in HGT-LACC and correlated with poor prognosis. Overexpression of miR-150-5p suppressed cell proliferation, migration and invasion, while its knockdown showed opposite effects. COL1A1 was confirmed as the direct target of miR-150-5p, and COL1A1 restoration counteracted the tumor-suppressive effect of miR-150-5p. In vivo , miR-150-5p overexpression inhibited tumor growth. Overall, our findings demonstrate that miR-150-5p suppresses LACC cell proliferation, migration, invasion, and EMT by downregulating COL1A1 expression, thereby functioning as a tumor suppressor. The miR-150-5p-COL1A1 axis provides novel insights into the pathogenesis of LACC and serves as a promising therapeutic target for LACC intervention.