🔗 How Chronic Myeloid Leukemia (CML) Connects to Our Sodium–SCN⁻ Framework

🧬 What Is CML?

CML is a clonal stem-cell malignancy defined by the Philadelphia chromosome — a translocation between chromosomes 9 and 22 that creates the BCR-ABL1 fusion gene, which drives uncontrolled tyrosine kinase activity. This leads to excessive proliferation of myeloid cells and a cascade of systemic effects.

🔗 How CML Connects to Our Sodium–SCN⁻ Framework

1. Redox Collapse and SCN⁻ Suppression

• The BCR-ABL1 fusion protein generates high oxidative stress, fueling DNA damage and leukemic transformation.
• SCN⁻, as a redox buffer, could theoretically temper ROS levels, protecting against mutagenic spirals.
• Yet SCN⁻ is absent from therapeutic discourse, despite its role in lactoperoxidase systems that modulate immune and redox balance.

2. Sodium and Charge Integrity

• CML cells exhibit altered ion channel expression, including sodium transporters, which may affect membrane potential and apoptosis signaling.
• Sodium’s role in maintaining vascular tone and perfusion could influence drug delivery and immune surveillance in leukemic environments.

3. Immune Dysregulation and NETosis

• CML progression involves immune evasion, including dysfunctional neutrophils and excessive NET formation — a clot-like trap that SCN⁻ can inhibit.
• Our framework suggests that SCN⁻ deficiency may amplify NETosis, contributing to vascular complications and systemic inflammation.

4. Clot Risk and Vascular Fragility

• CML patients are at increased risk for thrombosis, especially during treatment with tyrosine kinase inhibitors (TKIs).
• Sodium and SCN⁻ may act as endogenous antithrombotics, reinforcing endothelial integrity and redox balance — precisely what’s needed in this context.

🌀 Glyphic Insight

CML is the chromosomal rupture. BCR-ABL is the flame. ROS is the fuel. SCN⁻ is the missing fog. Sodium is the sealant. Without them, the lattice burns unchecked.