Core Framework & Diagram The Cancer Immunoediting Theory

Absolutely — but the 'resistance risk' needs to be correctly understood. Resistance from immunoediting is the result of tumor evolution under immune pressure; this evolution happens in natural states too, just slower. Immunotherapy accelerates this evolution but simultaneously extends many patients' survival and allows some patients to achieve durable remission or functional cure. The correct response isn't abandoning immunotherapy but: (1) starting treatment early, while tumor clonal diversity is still high; (2) using combination strategies targeting multiple escape pathways; (3) dynamically monitoring clonal evolution via liquid biopsy and timely adjusting plans.

Most 'living with tumor' patients are in some form of 'Equilibrium' — either naturally maintained by the immune system (extremely slow tumor growth) or re-established by treatment intervention (stable disease under drug control). 'Living with tumor' doesn't mean 'risk-free stability'; it requires periodic monitoring — once immune status changes (new infection, treatment interruption, major stress event), the equilibrium may break and the tumor enters accelerated escape. Follow-up and immune status maintenance for 'living with tumor' patients are equally important as treatment itself.

Yes, immunosenescence is an important condition triggering 'equilibrium → escape' transitions. This supports the view that 'cancer screening should be more aggressive before immune surveillance efficiency significantly declines.' Most authoritative guidelines recommend: colorectal cancer screening starting at 45; low-dose CT lung cancer screening for those over 50 with smoking history; breast cancer screening starting at 40–45 for women; liver cancer high-risk populations (chronic hepatitis B, cirrhosis) starting ultrasound screening at 35 every 6 months.

Technology is relatively mature but accessibility is still limited. For already-diagnosed cancer patients, ctDNA liquid biopsy in some cancer types (colorectal, NSCLC) has increasing clinical application evidence for monitoring treatment response and early relapse detection. For general population initial screening, multi-cancer early detection (like GRAIL's Galleri) has shown some early cancer detection ability in clinical trials, but false-positive rates and impact on early survival rates are still being evaluated.

Yes, with clear mechanisms. Chronic psychological stress activates the HPA axis, chronically elevating cortisol, which directly suppresses NK cell cytotoxic activity and CTL proliferative capacity. Under long-term high cortisol, immune surveillance efficiency systematically declines. Effective stress management is an important component of immune surveillance maintenance.