Description: <b>Chitosan</b> is a naturally occurring polysaccharide derived from the exoskeletons of crustaceans, such as crabs and shrimp.<br>
Chitosan is a cationic polysaccharide derived from chitin (commonly from crustacean shells). In oncology contexts, chitosan itself is not primarily a direct cytotoxic compound but is widely studied for its immunomodulatory effects, antitumor adjuvant activity, and drug delivery enhancement. Mechanistically, chitosan and its derivatives can activate macrophages, enhance NK cell activity, and stimulate cytokine production (e.g., IL-12, TNF-α), contributing to anti-tumor immune responses in preclinical models. Low–molecular weight chitosan and modified forms have also been reported to inhibit angiogenesis, modulate tumor microenvironment acidity, interfere with metastasis, and induce apoptosis in some in vitro systems. A major translational role of chitosan is as a nanoparticle carrier for chemotherapeutics, genes, and immunotherapies, improving stability and targeted delivery. Effects vary significantly depending on molecular weight, degree of deacetylation, and formulation.<br>
Chitosan has been shown to inhibit the growth of various types of cancer cells, including breast, lung, and colon cancer cells.<br>
Chitosan has been shown to inhibit angiogenesis, stimulate the immune system, and anti-inflammatory.<br>
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Chitosan is only soluble in acidic settings, hence limiting its use in neutral or alkaline pH circumstances<br>
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<h3>Cancer Pathway Table: Chitosan</h3>
<!-- Cancer Pathway Table: Chitosan -->
<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>Innate immune activation (macrophages, NK cells)</td>
<td>NK activity ↑; macrophage activation ↑ (reported)</td>
<td>Immune surveillance support</td>
<td>R, G</td>
<td>Immunostimulatory</td>
<td>Chitosan can activate antigen-presenting cells and enhance anti-tumor immunity in preclinical models.</td>
</tr>
<tr>
<td>2</td>
<td>Cytokine modulation (IL-12, TNF-α, IFN-γ)</td>
<td>Pro-immune cytokines ↑ (reported)</td>
<td>Immune tone modulation</td>
<td>R, G</td>
<td>Immune activation</td>
<td>Immunomodulatory effects vary with formulation and molecular weight.</td>
</tr>
<tr>
<td>3</td>
<td>Angiogenesis signaling (VEGF)</td>
<td>VEGF ↓ (reported in some models)</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic (context-dependent)</td>
<td>Low-molecular-weight and modified derivatives have shown anti-angiogenic activity in vitro.</td>
</tr>
<tr>
<td>4</td>
<td>Apoptosis induction (derivative-dependent)</td>
<td>Caspase activation ↑ (reported in vitro)</td>
<td>Minimal cytotoxicity at moderate exposure</td>
<td>G</td>
<td>Context-dependent apoptosis</td>
<td>Native chitosan is weakly cytotoxic; effects depend strongly on molecular size and chemical modification.</td>
</tr>
<tr>
<td>5</td>
<td>Metastasis / adhesion modulation</td>
<td>Tumor cell adhesion ↓; invasion ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-metastatic (model-dependent)</td>
<td>May interfere with extracellular matrix interactions and tumor cell migration.</td>
</tr>
<tr>
<td>6</td>
<td>Drug delivery enhancement (nanoparticle carrier)</td>
<td>Improved chemo uptake; targeted delivery ↑</td>
<td>Drug exposure optimization</td>
<td>P, R, G</td>
<td>Delivery platform</td>
<td>Major oncology relevance is as a carrier for chemotherapeutics, siRNA, DNA, and immunotherapies.</td>
</tr>
<tr>
<td>7</td>
<td>Tumor microenvironment modulation (acid buffering; charge interaction)</td>
<td>May alter local tumor acidity and cell interactions</td>
<td>↔</td>
<td>R, G</td>
<td>Microenvironment modulation</td>
<td>Cationic nature allows electrostatic interaction with tumor cell membranes and acidic microenvironment.</td>
</tr>
<tr>
<td>8</td>
<td>Redox / ROS effects</td>
<td>Mild ROS modulation (context-dependent)</td>
<td>Antioxidant properties reported in some systems</td>
<td>P, R</td>
<td>Redox modulation (minor)</td>
<td>Not primarily a redox-active compound; effects secondary to immune or metabolic modulation.</td>
</tr>
<tr>
<td>9</td>
<td>Combination therapy synergy</td>
<td>Chemo sensitivity ↑ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Adjunct platform</td>
<td>Often improves stability, targeting, and bioavailability of conventional anticancer agents.</td>
</tr>
<tr>
<td>10</td>
<td>Safety / translational constraint</td>
<td>Low systemic toxicity (generally)</td>
<td>Biocompatible; GI tolerance generally good</td>
<td>—</td>
<td>Biomaterial constraint</td>
<td>Effects depend heavily on molecular weight and degree of deacetylation; shellfish allergy considerations.</td>
</tr>
</table>
<p><small>
TSF: P = 0–30 min (surface interactions), R = 30 min–3 hr (immune signaling shifts), G = >3 hr (phenotype and immune outcomes).
</small></p>