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Molecular landscape of eyelid sebaceous gland carcinoma: A comprehensive review

Perumal Jayaraj1, Debjeet Ray1, Kevika Goel1

  • 1Department of Zoology, Sri Venkateswara College, University of Delhi, Delhi, India.

Indian Journal of Ophthalmology
|September 27, 2024
PubMed

Insights

Eyelid sebaceous gland carcinoma (SGC) is aggressive, with unique mutations. Understanding its molecular drivers, like signaling pathways and genetic alterations, is key for developing targeted therapies and improving patient outcomes.

Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • Eyelid sebaceous gland carcinoma (SGC) is an aggressive skin cancer with high recurrence and metastasis rates.
  • Current treatments rely on surgical excision, highlighting the need for advanced molecular insights.
  • Understanding SGC's molecular basis is crucial for developing targeted therapies and improving patient prognosis.

Purpose of the Study:

  • To provide a comprehensive review of the molecular landscape of eyelid SGC.
  • To emphasize key genetic alterations, signaling pathways, and epigenetic modifications in SGC.
  • To identify potential therapeutic targets for personalized medicine approaches.

Main Methods:

  • Literature review synthesizing findings on genetic alterations, signaling pathways (e.g., β-catenin, EGFR, TP53), and epigenetic modifications.
  • Analysis of next-generation sequencing data identifying actionable mutations (e.g., PTEN, ERBB2).
  • Examination of the roles of molecular chaperones (XIAP, BAG3) and epithelial-mesenchymal transition (EMT) markers (E-cadherin, vimentin, ZEB2).

Main Results:

  • Identified key signaling pathway aberrations (β-catenin, LEF, hedgehog, EGFR, P53, P21WAF1) linked to SGC progression and poor prognosis.
  • Eyelid SGC exhibits a distinct mutational profile, lacking UV-signature TP53 mutations, suggesting alternative mutagenic pathways.
  • Actionable mutations in PTEN and ERBB2 were identified, paving the way for personalized medicine.
  • Molecular chaperones XIAP and BAG3, along with EMT regulators, significantly contribute to SGC survival and aggressiveness.
  • DNA methylation and microRNA dysregulation were implicated as important epigenetic modifications.

Conclusions:

  • A comprehensive understanding of eyelid SGC's molecular drivers, including genetic alterations, signaling pathways, and epigenetic factors, has been consolidated.
  • The review highlights potential therapeutic targets and provides a foundation for future research in diagnostic, prognostic, and personalized treatment strategies.
  • Targeting identified molecular pathways and genetic alterations holds promise for advancing SGC treatment and improving patient outcomes.

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