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ABSTRACT
Introduction
Ocular surface squamous neoplasia (OSSN) is the most common ocular malignancy; the pathophysiology is influenced by molecular, genetic, and epigenetic mechanisms. The incidence of OSSN is associated with the anatomy and physiology of the ocular surface, limbal stem cell configuration, limbal vulnerability, cancer stem cells, dysplasia, neoplasia, angiogenesis, invasion, and metastasis. The key etiological factors involved are human papillomavirus (HPV), human immunodeficiency virus (HIV), immunosuppression, p53 tumor suppressor gene, hypovitaminosis A, and failure of Deoxyribonucleic acid (DNA) repair mechanisms.
Areas covered
This special report is a focussed attempt to understand the molecular mechanism, genetic and epigenetic mechanism, and diagnostic modalities for OSSN.
Expert opinion
While these mechanisms contribute to genome instability, promoter-specific hypermethylation might facilitate and promote tumor formation by silencing tumor suppressor genes. OSSN understanding has improved with increased literature available on various genetic, molecular, and epigenetic mechanisms, although the exact genetic and epigenetic mechanisms still need to be elucidated. It is important to note that the molecular mechanisms of OSSN can vary among individuals, and further research is required to elucidate the underlying processes fully. Understanding these mechanisms is crucial for the development of targeted therapies and improved management of OSSN.
Article highlights
Ocular surface squamous neoplasia (OSSN) is the most prevalent ocular cancer, with its pathophysiology being shaped by molecular, genetic, and epigenetic factors. Key contributors to OSSN include human papillomavirus (HPV), HIV, immunosuppression, the p53 tumor suppressor gene, hypovitaminosis A, and failures in DNA repair.
The incidence of OSSN is closely tied to the ocular surface’s anatomy and physiology. Aspects like limbal stem cell configuration, limbal vulnerability, and processes such as angiogenesis, invasion, and metastasis play pivotal roles in its progression.
Molecular, genetic, and epigenetic mechanisms drive OSSN, offering insights into potential diagnostic modalities tailored for the disease.
Epigenetic factors, specifically promoter-specific hypermethylation, may accelerate tumor growth by silencing tumor suppressor genes. However, the precise genetic and epigenetic mechanisms behind OSSN remain somewhat enigmatic.
The molecular mechanisms of OSSN can differ among individuals, underlining the necessity for continued research. Fully understanding these processes is vital to pave the way for targeted treatments and optimized OSSN management.
Abbreviations list
| OSSN | = | Ocular Surface Squamous Neoplasia |
| HPV | = | Human Papilloma Virus |
| HIV | = | Human Immunodeficiency Virus |
| HSV | = | Herpes Simplex Virus |
| DNA | = | Deoxyribonucleic acid |
| PP5 | = | Protein Phosphate 5 |
| CIN | = | Cervical Intraepithelial Neoplasia |
| 5-FU | = | 5-Fluorouracil |
| UV Rays | = | Ultraviolet Rays |
| VEGF | = | Vascular Endothelial Growth Factor |
| LSCD | = | Limbal Stem Cell Deficiency |
| ncRNA | = | non-coding Ribonucleic acid |
| miRNA | = | micro Ribonucleic acid |
| CPDs | = | Cyclobutene Pyrimidine Dimers |
| ROS | = | Reactive Oxygen Species |
| EBV | = | Epstein Bar Virus |
| HEM | = | Human Epithelial Marker |
| CMV | = | Cytomegalovirus |
| KSHV | = | Kaposi Sarcoma Associated Herpesvirus |
| IVCM | = | In Vivo Confocal Microscopy |
| HR-ASOCT | = | High-Resolution Anterior Segment Optical Coherence Tomography |
| UBM | = | Ultrasound Biomicroscopy |
| PCR | = | Polymerase Chain Reaction |
| MMP-9 | = | Matrix Metalloproteinase 9 |
| MMP-11 | = | Matrix Metalloproteinase 11 |
| CGH | = | Comparative Genomic Hybridization |
Declaration of interests
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.