The one-paragraph answer
Chemotherapy poisons cells that divide quickly — cancer above all, but also hair, gut and blood cells, which is why it causes the side effects everyone knows. Targeted therapy blocks one specific molecular fault that the tumour depends on, so it only works if your tumour has that fault. Immunotherapy does not attack the cancer directly at all — it releases or re-engineers your own immune system to do it.
A side-by-side view
| Chemotherapy | Targeted therapy | Immunotherapy | |
|---|---|---|---|
| Attacks | All fast-dividing cells | One specific fault (e.g. HER2, FGFR2, EGFR) | Nothing directly — activates immune cells |
| Needs a biomarker? | No | Yes — testing decides eligibility | Sometimes (e.g. PD-L1, MSI-high) |
| Typical form | IV infusion cycles | Often daily pills | Infusions; CAR-T is a one-time cell product |
| Signature side effects | Low blood counts, nausea, hair loss | Fault-specific (skin, blood pressure, eyes…) | Immune overactivation — “-itis” side effects |
Where CAR-T fits
CAR-T therapy is immunotherapy’s most engineered form: your own T-cells are collected, genetically re-armed to recognise the cancer, multiplied, and returned. It has produced durable remissions in several blood cancers. One insight from our published lymphoma research: CAR-T’s power depends on the fitness of your immune cells — many prior rounds of chemotherapy can exhaust them, which is one reason timing CAR-T earlier, per written escalation rules, matters so much.
Why most modern plans are combinations
These families are not rivals. A common modern strategy pairs a chemotherapy backbone with a targeted drug matched to your tumour’s fault, or follows chemotherapy with immunotherapy. The right mix is exactly what molecular testing plus an experienced team — and, we would argue, a systematic computational check of the options — is for.
Unsure which family your current drugs belong to, or why? Attach your prescription list to a ticket — we will map each drug to its mechanism in plain words.