Surgery Curiosities
How do cancer cells evade the immune system?
Assoc. Prof. Cengiz Dibekoğlu, MD
The immune system can recognize and clear damaged or foreign cells. So “why doesn’t it always clear cancer?” is a fair question. Short answer: defense exists — but some tumors escape it or tip the balance in their favor. Tumors do not “decide” this; cells that can escape survive and grow. That balance helps explain why immunotherapy is discussed for selected patients.
Educational schematic. Some structures may be simplified or emphasized for clarity; not an exact anatomical depiction.
© Cengiz Dibekoğlu — illustrative; not for unauthorized use
Learn in 30 seconds
The main points of this article:
- Immunity can be a strong defense against a tumor; escape is also possible.
- The immune–tumor relationship is often framed in three states: elimination, equilibrium, and escape (3E).
- Immune cells have a gas pedal and a brake. Some tumors press the brake.
- In selected patients, drugs that loosen that brake (checkpoint inhibitors) may be used.
- A PD-L1 test does not mean the same thing in every cancer type.
- When appropriate, surgery reduces disease burden; the immune side is planned separately.
What can immunity do against cancer?
Immune cells can recognize cells that look “different from normal.” Sometimes that recognition helps destroy tumor cells — immune surveillance. Tumor and immunity can interact for a long time. Science calls this immunoediting. Three states are often taught; their English initials give the 3E label:
- Elimination — immunity may clear some tumor cells.
- Equilibrium — tumor and immunity may coexist for a long time.
- Escape — the tumor develops ways past that control.
Source: Dunn et al., 2002 / 2004.
How can tumors escape that control?
There is no single hide button. Roughly three paths. Also: some tumors are richer in immune cells; others have fewer (older language sometimes said “hot / cold”).
- Less recognition — surface “see me” signals may weaken so immune cells lose a clear target.
- A suppressing neighborhood — cells and signals that tire the immune response can accumulate (linked to the tumor microenvironment — separate article).
- Checkpoint pathways — the “brake” — natural brakes keep immunity from over-firing; these are immune checkpoints.
- Immune escape is related to resistance to programmed cell death (apoptosis) but is not the same thing (apoptosis is covered separately).
Sources: Dunn 2002/2004; Hanahan & Weinberg 2011; Hanahan 2022.
What is PD-L1? How does the immune brake work?
Immune cells have a gas pedal and a brake. A tumor may press the brake. Checkpoint drugs aim to lift that foot. A common pair: PD-1 (brake receptor on the immune cell) and PD-L1. PD-L1 binds PD-1 and engages the brake. Some tumor cells carry a lot of it on their surface; PD-L1 can also appear on some immune cells. PD-L1 does not mean the same thing in every cancer; immunotherapy fitness depends on cancer type, stage, and biomarkers.
Immunotherapy can sometimes harm healthy tissues too — for example inflammation of bowel, thyroid, lung, or liver.
Understand with an example
In a short infection, immunity often answers a clear target quickly. A tumor can be a quieter, years-long interaction: cells change slowly, immunity partly suppresses and partly adapts, escape routes may accumulate. When appropriate, surgery reduces disease amount by removing the main mass. Surgery alone does not “fix” the immune problem; whole-body risk is discussed separately.
Who may receive immunotherapy?
In selected patients, checkpoint inhibitors that loosen the immune brake may be used. Fitness depends on tumor type, clinical criteria, and side-effect risk. In some colorectal cancers with MSI-H / dMMR, immunotherapy is discussed more often — found via molecular tests. Tests such as PD-L1 may help in some tumors; meaning varies by cancer type.
- Surgery is often the main path to reduce visible disease and local control.
- Immunotherapy is considered for selected patients and clinical criteria.
- Checkpoint drugs aim to loosen the immune brake.
Sources: Dunn 2002/2004; Hanahan 2011/2022.
What science accepts
Solid points in this field include:
- Immunity has real power against tumors.
- Escape is possible; the simple 3E model is widely used.
- Immune evasion is one of cancer’s core features.
- Checkpoint inhibitors are clinical options in selected settings.
- PD-L1’s clinical meaning varies by tumor type.
Not yet settled
These claims are not generalizable to every patient:
- That every tumor uses the same escape switch.
- That having infections or “immune boosters” prevents cancer.
- That PD-L1 is the same decision key in every cancer.
- That immunotherapy suits everyone.
- That early lab findings mean “guaranteed treatment tomorrow.”
Questions patients ask most
Common myths
“If immunity is strong, cancer cannot occur.”
Immunity matters, but cancer is multi-step; one factor does not explain it.
“Immunotherapy is for everyone.”
No. Selected patients and clinical criteria apply. It can also harm healthy tissues.
“Surgery is unnecessary because of immune escape.”
No. Surgery often reduces disease burden and may aim for clearance. The immune dimension is planned separately.
“Infection or an “immune booster” prevents cancer.”
Not a general rule. Some infections (HPV, hepatitis B/C, H. pylori) can raise cancer risk.
“Hearing “PD-L1” means a specific drug at once.”
Meaning depends on the tumor; results are read in clinical context.
Summary
Cancer “hiding” is a balance between immune surveillance and escape routes. There is no single switch. The immune–tumor struggle (3E: elimination–equilibrium–escape) is a teaching model. Natural immune brakes (e.g. PD-1 / PD-L1) can strengthen in some tumors; PD-L1 does not mean the same in every cancer. In selected patients, checkpoint inhibitors may target those brakes — with side-effect risk. When appropriate, surgery reduces disease burden.
Scientific references
- Dunn GP, Bruce AT, Ikeda H, Old LJ, Schreiber RD. Cancer immunoediting: from immunosurveillance to tumor escape. Nat Immunol. 2002. — PMID: 12407406 · DOI: 10.1038/ni1102-991 — Immune surveillance and tumor escape
- Dunn GP, Old LJ, Schreiber RD. The three Es of cancer immunoediting. Annu Rev Immunol. 2004. — PMID: 15032581 · DOI: 10.1146/annurev.immunol.22.012703.104803 — Elimination, equilibrium, escape
- Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011. — PMID: 21376230 · DOI: 10.1016/j.cell.2011.02.013 — Immune evasion as a hallmark
- Hanahan D. Hallmarks of Cancer: New Dimensions. Cancer Discov. 2022. — PMID: 35022204 · DOI: 10.1158/2159-8290.cd-21-1059 — Updated dimensions; immune escape context