📚 THE BASICS
What Is Actinic Keratosis?
Start here before anything else
Actinic keratosis (AK) is a pre-malignantNot cancer yet. But it's standing in the cancer waiting room. The cells are abnormal but haven't punched through the basement membrane yet. skin lesion caused by cumulative UVB radiation damage to keratinocytes.
Think of it like this: every unprotected sun exposure is a tiny mutation stored in your DNA. After 30 years of landscaping without sunscreen, those mutations pile up. AK is the skin's way of saying "the bill is coming due."
The key word is cumulative. This isn't about one bad sunburn. This is decades of UV exposure quietly damaging the same keratinocytes on the same sun-exposed areas, over and over, until the DNA can't keep up.
⚙️ THE MECHANISM
UVB Destroys the Skin's Editor
p53 is what catches and fixes DNA errors. UV breaks it.
UVB radiation causes a very specific type of DNA damage: it fuses adjacent thymine bases together (called pyrimidine dimersTwo adjacent thymines (T-T) stuck together by UV energy. The DNA proofreader can't read it correctly. If p53 is also broken, the cell divides with this error baked in.). Normally your cells catch these errors using p53Tumor suppressor gene. When DNA is damaged, p53 STOPS the cell from dividing until repairs are made. Or, if damage is too severe, p53 tells the cell to self-destruct (apoptosis). Break p53 and you remove the brake pad entirely..
Here's the problem: UVB also mutates p53 itself. So you get damaged DNA AND no editor to catch it. The cell divides. The daughter cells have the same mutation. This keeps happening for years until you get a clonal population of dysplastic keratinocytes sitting in the epidermis.
That clonal dysplastic population is the actinic keratosis.
🧬 The AK-to-SCC Story in One Chain
→ UV also mutates p53 (the DNA repair cop)
→ Dysplastic cells divide unchecked (= AK)
→ More mutations accumulate over time
→ Cells break through the basement membrane (= invasive SCC)
👨🏭 WHO GETS IT
Risk Factors
The profile is very specific
| Risk Factor | Why It Matters | Board Clue |
|---|---|---|
| Chronic sun exposure | Cumulative UVB damage over years (not single burn) | Outdoor worker, farmer, landscaper, sailor |
| Fair skin (Fitzpatrick I-II) | Less melanin = less UV protection | Blue/green eyes, light hair, burns easily |
| Immunosuppression | Immune surveillance fails, dysplastic cells aren't cleared | Transplant patient on tacrolimus, HIV |
| Age >60 | Decades of accumulated UV damage | Combined with outdoor work = highest risk |
| Prior AK or skin cancer | Same UV-damaged field produces more lesions | Field cancerization (covered below) |
