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2026
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| Accés en línia: | https://doi.org/10.5281/zenodo.20002352 |
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| _version_ | 1866901963933745152 |
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| author | Abuamra, Mohammed Fuad Yousef |
| author_facet | Abuamra, Mohammed Fuad Yousef |
| contents | <p>The original Sugar-Iron Bomb Model proposed that chronic hyperglycemia, glycated hemoglobin (HbA1c), iron dysregulation, and oxidative stress may interact to create a pro-carcinogenic systemic environment. In this extension, we propose a complementary tumor-local amplification mechanism operating within the tumor microenvironment. Specifically, abnormal tumor angiogenesis, microvascular fragility, and intermittent microhemorrhage may permit erythrocyte extravasation into tumor tissue. Subsequent macrophage-mediated erythrophagocytosis could release heme and redox-active iron, enhancing reactive oxygen species (ROS) generation through Fenton chemistry. This process may intensify DNA damage, inflammatory signaling, extracellular matrix remodeling, and tumor adaptation. We hypothesize that this local iron-recycling circuit may synergize with systemic hyperglycemia to amplify malignant progression.</p> |
| format | Recurso digital |
| id | zenodo_https___doi_org_10_5281_zenodo_20002352 |
| institution | Zenodo |
| language | |
| publishDate | 2026 |
| publisher | Zenodo |
| record_format | zenodo |
| spellingShingle | The Sugar-Iron Bomb Model of Carcinogenesis - Part II: Tumor Microenvironment Iron Recycling and Oxidative Amplification Extension Abuamra, Mohammed Fuad Yousef Cancer metabolism Iron HbA1c Macrophages Microhemorrhage Tumor microenvironment Fenton reaction Oxidative stress Hyperglycemia Carcinogenesis <p>The original Sugar-Iron Bomb Model proposed that chronic hyperglycemia, glycated hemoglobin (HbA1c), iron dysregulation, and oxidative stress may interact to create a pro-carcinogenic systemic environment. In this extension, we propose a complementary tumor-local amplification mechanism operating within the tumor microenvironment. Specifically, abnormal tumor angiogenesis, microvascular fragility, and intermittent microhemorrhage may permit erythrocyte extravasation into tumor tissue. Subsequent macrophage-mediated erythrophagocytosis could release heme and redox-active iron, enhancing reactive oxygen species (ROS) generation through Fenton chemistry. This process may intensify DNA damage, inflammatory signaling, extracellular matrix remodeling, and tumor adaptation. We hypothesize that this local iron-recycling circuit may synergize with systemic hyperglycemia to amplify malignant progression.</p> |
| title | The Sugar-Iron Bomb Model of Carcinogenesis - Part II: Tumor Microenvironment Iron Recycling and Oxidative Amplification Extension |
| topic | Cancer metabolism Iron HbA1c Macrophages Microhemorrhage Tumor microenvironment Fenton reaction Oxidative stress Hyperglycemia Carcinogenesis |
| url | https://doi.org/10.5281/zenodo.20002352 |