🔬 Why HOX Genes?
HOX (Homeobox) genes are essential during embryonic development. Like master architects, they determine where the head, tail, arms, and legs form. These genes are highly conserved across species and play a crucial role in organizing the body’s structure along the anterior-posterior axis.
But in recent years, researchers have discovered that HOX genes can be reactivated or dysregulated in cancer—and not just any cancer. In glioblastoma (GBM), one of the deadliest forms of brain tumor, abnormal HOX gene expression has been linked to:
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Tumor growth
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Therapeutic resistance
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Poor survival outcomes
This unexpected connection between developmental biology and cancer progression caught our attention.
🧠 The Glioblastoma Challenge
Glioblastoma is an aggressive, fast-growing tumor with a notoriously poor prognosis. Despite surgery, radiation, and chemotherapy, the average survival time remains just 12–15 months after diagnosis.
We wondered—could HOX genes be one of the hidden drivers behind glioblastoma’s resistance and rapid progression?
🧾 What We Did?
We conducted an in-depth review of the scientific literature to answer this question. Our article:
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Summarizes the current knowledge about HOX gene expression in GBM
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Highlights specific HOX genes (like HOXA9, HOXA10, and HOXD10) that are linked to treatment resistance
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Explores the connection between HOX gene activity and glioma stem cells, tumor microenvironment, and immune evasion
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Discusses the implications of HOX genes as biomarkers and therapeutic targets
This is the first narrative review focused specifically on HOX gene dysregulation in GBM.
🚀 Why It Matters
Our findings suggest that HOX genes are more than developmental relics—they may be active participants in the progression and treatment resistance of glioblastoma.
Understanding how and why these genes become dysregulated could lead to:
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Improved diagnostic tools
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Personalized treatment strategies
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New targets for drug development
📖 Behind the Scenes
This project brought together my passion for computational genomics and my fascination with developmental biology. It reminded me how genes that build life can also contribute to its breakdown, depending on the context.
Writing this review wasn’t just an academic task—it was an effort to bridge two fields and encourage researchers to see cancer through a broader genetic lens.