====== Pro-inflammatory Oncogenic Driver ======

**Definition:**  
A *pro-inflammatory oncogenic driver* is a genetic or molecular alteration that simultaneously promotes **malignant transformation** (oncogenesis) and **chronic inflammation**, fostering tumor development and progression.

===== Key Features =====

  * Activates inflammatory signaling pathways (e.g., NF-κB, STAT3).
  * Promotes cell proliferation, survival, and immune evasion.
  * Shapes the tumor microenvironment to support angiogenesis and metastasis.
  * Creates a positive feedback loop between inflammation and tumor growth.

===== Common Examples =====

^ Driver / Pathway           ^ Role in Inflammation and Cancer                                        ^
| **Mutated KRAS**          | Activates MAPK and NF-κB → increases pro-inflammatory cytokines.        |
| **MYC overexpression**    | Regulates inflammatory and metabolic genes in the tumor environment.    |
| **Constitutive NF-κB**    | Drives chronic inflammation and survival gene expression.               |
| **Activated STAT3**       | Induces IL-6, VEGF, and other oncogenic inflammatory mediators.         |
| **TP53 loss**             | Impairs immune surveillance → unresolved inflammation.                  |
| **COX-2 overexpression**  | Elevates prostaglandins → enhances inflammation and tumor growth.       |

===== Clinical Relevance =====

  * **Therapeutic Targeting:** These drivers are candidates for combined oncologic and anti-inflammatory therapies.
  * **Biomarkers:** Their dual role makes them valuable prognostic or predictive biomarkers.
  * **Immunotherapy Modulation:** Targeting these pathways may enhance immune responses against tumors.

===== References =====
  * Greten, F.R., Grivennikov, S.I. (2019). Inflammation and Cancer: Triggers, Mechanisms, and Consequences. *Immunity*.
  * Mantovani, A., et al. (2008). Cancer-related inflammation. *Nature*.