Core Framework & Diagram What Is the Tumor Immune Atlas?

Currently tumor immune typing is mainly completed through gene expression analysis of tumor tissue (requiring RNA sequencing data from tumor biopsy). In clinical practice, PD-L1 immunohistochemistry, TMB detection, and MSI testing are usually used as surrogate biomarkers to guide treatment decisions. At cancer centers with appropriate capabilities, you can ask whether comprehensive molecular pathology analysis (including transcriptome data) is available — some centers already provide clinical versions similar to TIMER analysis.

Absolutely, and this is routine. The same lung adenocarcinoma may have C2 type in some patients (high IFN-γ, good PD-1 response) and C5 type in others (immune desert, poor response). This immune heterogeneity within the same cancer type is the fundamental reason why the 'one drug for all lung cancers' approach has unstable effects — and the reason personalized immunotherapy exists.

Yes, and this is one of the important mechanisms of treatment resistance. Chemotherapy, radiation, and targeted therapy can all change tumor immune microenvironment — some treatments 'warm up' cold tumors (increasing immune infiltration), some treatments cause tumor evolution with new immune escape mechanisms. This is why continuous tumor immune monitoring (dynamic atlas) has extreme value during treatment.

For non-researchers, TIMER2.0 itself is fairly specialized. But it provides intuitive data visualization for understanding 'why immunotherapy works well for some cancers and poorly for others.' For medically knowledgeable patients or families, it can be an educational tool for understanding tumor immune biology; for healthcare professionals, it's a research aid resource for quickly consulting different cancer types' immune characteristics.