Description: <b>Hyperbaric oxygen (HBO) therapy</b> is a treatment where patients breathe 100% oxygen inside a pressurized chamber.(typically 1.5–3.0 ATA) This approach increases the oxygen concentration in the blood and tissues.<br>
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Its strongest evidence base is:
-Radiation enhancement (oxygen fixation)
-Treatment of radiation necrosis
-Wound healing in oncology patients
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Enhanced Oxygenation of Tumors:<br>
-Many tumors are hypoxic (low in oxygen), which can make them more resistant to radiation and some forms of chemotherapy. Enhanced oxygenation through HBO may help overcome this hypoxia.<br>
Increased oxygen levels can lead to the formation of reactive oxygen species (ROS), which may damage cancer cells and sensitize them to treatment.<br>
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Synergistic Effects with Radiation Therapy:<br>
-Oxygen acts as a radiosensitizer. Radiation-induced DNA damage can be more effective in the presence of oxygen, potentially improving the efficacy of radiotherapy.<br>
Some studies have explored combining HBO with radiotherapy to overcome radioresistance in hypoxic tumor regions.<br>
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Improved Delivery of Chemotherapeutic Agents:<br>
-Elevated tissue oxygenation might enhance the delivery and efficacy of certain chemotherapeutic drugs, although this area is still under investigation.<br>
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Potential Immune Modulation:<br>
-There is ongoing research into whether HBO can modulate the tumor microenvironment in a way that is more favorable for anti-tumor immune responses.<br>
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Possible problems:<br>
-Implanted device (such as an insulin pump or pacemaker)<br>
-Avoid with recent perforated ear drum<br>
-Pneumothorax<br>
-Wait for 4 wks after chemo?<br>
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<!-- Hyperbaric Oxygen (HBOT) — Cancer-Oriented Time-Scale Flagged Pathway Table -->
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer / Tumor Context</th>
<th>Normal Tissue Context</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>Tumor hypoxia reduction</td>
<td>Hypoxia ↓; HIF-1α signaling ↓ (context-dependent)</td>
<td>Tissue oxygenation ↑</td>
<td>P, R</td>
<td>Microenvironment normalization</td>
<td>Elevated dissolved oxygen increases tumor pO₂, potentially reducing hypoxia-driven survival programs.</td>
</tr>
<tr>
<td>2</td>
<td>Radiation sensitization (oxygen fixation effect)</td>
<td>Radiotherapy efficacy ↑</td>
<td>—</td>
<td>R</td>
<td>DNA damage amplification</td>
<td>Oxygen stabilizes radiation-induced DNA radicals, increasing double-strand break lethality.</td>
</tr>
<tr>
<td>3</td>
<td>ROS generation (hyperoxia-driven)</td>
<td>ROS ↑ (transient); oxidative stress ↑</td>
<td>ROS ↑; antioxidant response ↑</td>
<td>P, R</td>
<td>Redox amplification</td>
<td>Elevated O₂ increases mitochondrial and enzymatic ROS production; magnitude depends on exposure pressure and duration.</td>
</tr>
<tr>
<td>4</td>
<td>NRF2 antioxidant response</td>
<td>Adaptive NRF2 activation ↑ (reported)</td>
<td>NRF2 ↑; antioxidant enzymes ↑</td>
<td>R, G</td>
<td>Redox adaptation</td>
<td>Repeated hyperoxic exposure can induce antioxidant defense systems; may influence redox-sensitive therapies.</td>
</tr>
<tr>
<td>5</td>
<td>HIF-1α / hypoxia signaling modulation</td>
<td>HIF-1α ↓ (acute hyperoxia); VEGF modulation</td>
<td>Hypoxia signaling ↓</td>
<td>R</td>
<td>Hypoxia pathway suppression</td>
<td>Reduced hypoxia may decrease glycolytic shift and angiogenic drive in some tumors.</td>
</tr>
<tr>
<td>6</td>
<td>Angiogenesis modulation</td>
<td>VEGF modulation (context-dependent)</td>
<td>Wound-healing angiogenesis ↑</td>
<td>G</td>
<td>Vascular remodeling</td>
<td>HBOT stimulates angiogenesis in ischemic tissue; tumor angiogenic response varies by context.</td>
</tr>
<tr>
<td>7</td>
<td>Immune modulation</td>
<td>Innate immune activity modulation</td>
<td>Neutrophil function ↑; inflammation modulation</td>
<td>R</td>
<td>Inflammatory modulation</td>
<td>Hyperoxia can alter cytokine signaling and leukocyte behavior.</td>
</tr>
<tr>
<td>8</td>
<td>Combination therapy interaction</td>
<td>May enhance radiotherapy; effects with chemo variable</td>
<td>—</td>
<td>R, G</td>
<td>Adjunctive leverage</td>
<td>Most consistent evidence supports radiosensitization; chemotherapy interactions are drug-specific.</td>
</tr>
<tr>
<td>9</td>
<td>Safety constraints</td>
<td>—</td>
<td>Oxygen toxicity (CNS/pulmonary); barotrauma risk</td>
<td>—</td>
<td>Exposure limitation</td>
<td>High-pressure or prolonged exposure can cause oxygen toxicity seizures or lung injury.</td>
</tr>
</table>
<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (hyperoxia; ROS surge)</li>
<li><b>R</b>: 30 min–3 hr (HIF modulation; radiation sensitization window)</li>
<li><b>G</b>: >3 hr (angiogenesis remodeling; adaptive antioxidant response)</li>
</ul>