Ovarian cancer keeps claiming lives silently due to its late detection and high recurrence rates. One key reason is the role of chronic inflammation, which drives cancer progression. Specific cytokines like IL-6, TNF-α, and IL-8, along with pathways like NF-kB and STAT3, get overactive in ovarian cancer, helping tumors grow and spread.

The area around the tumor, known as the tumor microenvironment (TME), sees a lot of immune cells that actually support the cancer. Cells like tumor-associated macrophages (TAMs) and regulatory T cells (Tregs) dampen the body's natural fight against the tumor.

Ovarian cancer cells have another trick up their sleeve: they use immune checkpoint paths, particularly PD-1/PD-L1, to weaken the activity of cells meant to kill them.

Scientists are exploring ways to fight back by targeting these inflammatory and immune evasion mechanisms. Drugs that block NF-kB, COX-2, and JAK/STAT pathways are showing promise in lab tests. Immune checkpoint inhibitors, which target PD-1/PD-L1 and CTLA-4, are being tested, but the results are mixed so far.

Recent research is digging into the microbiome and substances linked to inflammation, like microRNAs (miRNAs) and exosomes, for early detection and personalized treatments.

To truly beat ovarian cancer, future treatments need to focus on personalized strategies that fight inflammation in the TME and combine anti-inflammatory treatments with immunotherapy.

Ovarian Cancer: The Secret Battle Against Inflammation and the Immune System

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