Pairings

An ADC kills tumour cells in a way that alerts the immune system; a checkpoint inhibitor lets the immune system finish the job.

Blocking EGFR from inside (a pill) and outside (an antibody that also blocks MET) beat osimertinib and added more than a year of survival.

In bowel cancers that start on the left and have normal RAS and BRAF genes, adding an EGFR antibody to chemotherapy gives the longest survival seen in first-line trials.

Adding the anti-GD2 antibody to relapse chemotherapy doubled response rates in relapsed neuroblastoma, and the idea is now moving into first-line induction.

A pill that switches off the leukaemia's engine plus an immunotherapy that mops up survivors, with no chemotherapy.

Interleaving an immunotherapy with standard chemotherapy cycles improves survival in adults and children with newly diagnosed ALL.

Blocking two consecutive steps in the same relay prevents the pathway from rerouting and reduces side effects.

Block the survival signal and remove the death shield at the same time, for about a year, then stop and stay in remission for years.

Pairing a CD20 bispecific with a CD79b ADC lets two targeted drugs with different mechanisms replace chemotherapy in relapsed lymphoma.

Adding a CD38 antibody to the standard three-drug induction roughly halves progression risk in newly diagnosed myeloma.

Cut the fuel (oestrogen) and jam the engine (CDK4/6) at the same time.

Three trials with three different antibodies agree: adding immunotherapy to first chemotherapy for advanced endometrial cancer roughly triples progression-free time in dMMR tumours and helps the rest modestly.

Systemic immunotherapy layered on top of bladder BCG reduced recurrence, at the cost of systemic side effects in a disease usually treated locally.

Pairing a new EGFR antibody with immunotherapy tripled the response rate seen with immunotherapy alone in early trials.

The ADC-immunotherapy pair that doubled survival in advanced disease now also works around surgery, in fit and unfit patients alike.

Adding a FLT3 blocker to standard chemotherapy is the proven way to improve survival in FLT3-mutated AML.

A drug that hits the exact mutation plus a drug that hits every RAS protein, so the tumour cannot escape through a wild-type RAS cousin.

Chemotherapy plus immunotherapy is now the first treatment for advanced bile duct cancer, with a small average gain and a minority of long survivors.

Heated intraperitoneal cisplatin during interval surgery, after neoadjuvant chemotherapy, extends survival in stage III disease.

In colorectal cancer, a KRAS blocker alone barely works because the cell turns EGFR up; adding an EGFR antibody stops that.

An anti-angiogenic pill makes immunotherapy work in endometrial cancers that would otherwise ignore it, at the cost of significant side effects.

Combining the newest leukaemia drug class with the venetoclax backbone is producing remission rates in frontline NPM1 and KMT2A leukaemia that single agents never reached.

An oncolytic virus blows up tumour cells and inflames the tumour; PD-1 blockade then exploits the inflammation.

In prostate cancer, blocking androgen signalling makes cells more dependent on PARP, and PARP inhibition weakens AR signalling in turn.

In tumours with faulty DNA repair, adding olaparib to bevacizumab maintenance roughly doubled progression-free time and improved survival.

Immunotherapy given alongside standard chemotherapy from day one cures more advanced Hodgkin lymphoma with less nerve damage.

Adding pembrolizumab to curative chemoradiation improved survival in high-risk locally advanced cervical cancer (KEYNOTE-A18); durvalumab in a broader population did not (CALLA).

When the tumour shows little PD-L1, immunotherapy alone is weak, but adding chemotherapy makes it work for most patients.

Normalising the tumour's blood vessels lets immune cells in, and VEGF blockade removes an immunosuppressive signal.

The vaccine teaches the immune system what to hunt; PD-1 blockade stops the tumour from switching the hunters off.

Blocking the PI3K growth pathway alongside hormone therapy works only when the tumour carries a mutation in that pathway, and works best early.

DNA-crosslinking chemotherapy is especially effective in tumours that cannot repair double-strand breaks.

Radiation turns the irradiated tumour into a vaccine; immunotherapy spreads the response.

Adding drugs to the catheter procedure keeps intermediate-stage liver cancer under control for longer, though a survival gain is still unproven.

The one regimen proven in a randomised trial to help HER2-positive brain metastases, extending survival in those patients by six months.

Azacitidine primes leukaemia cells for death; venetoclax removes the BCL-2 shield. Together they roughly doubled remissions in older AML.

Venetoclax plus obinutuzumab, one year of a pill plus an antibody, was the first fixed-duration, chemotherapy-free CLL regimen, with half of patients still in remission at six years.

When a BCMA drug stops working, switching to a drug against a different myeloma protein still produces responses in about two-thirds of patients.

When lutetium radioligand therapy stops working, alpha-emitting versions can still control the disease.

After lutetium therapy stops working, an actinium version of the same drug can still produce responses.

Shrink a BRAF-mutant anaplastic thyroid tumour with pills first, then remove what is left; some patients now survive years instead of months.

Chemo-immunotherapy followed by maintenance in small-cell lung cancer gives four cycles of chemotherapy plus immunotherapy, then keeps the immunotherapy going and adds a second drug to hold the disease longer.

Hit Claudin 18.2 twice: first with a plain antibody plus chemotherapy, then with an ADC or engineered cells when the cancer comes back.

Chemotherapy and radiation, then surgery, then a year of immunotherapy if the operation shows cancer was still there. This is the current curative-intent pathway.

If large B-cell lymphoma comes back within a year, CAR-T should come before, not after, a transplant attempt.

After the lung cancer pill stops working, an ADC that does not care which resistance mutation emerged.

For HER2-positive stomach cancer, an antibody-plus-chemotherapy first, then Enhertu when it progresses. Both steps now have phase 3 proof.

In head and neck cancer, immunotherapy works when given before surgery but not when given alongside chemoradiation.

In BRAF-mutant melanoma, start with immunotherapy and keep the targeted pills in reserve; the reverse order costs lives.

Six weeks of cheap chemotherapy before chemoradiation cut deaths by 40% (INTERLACE), while chemotherapy after chemoradiation did nothing (OUTBACK). Order matters.

A short course of a MEK or BRAF pill can coax iodine-resistant thyroid cancer into taking up iodine again, letting radioactive iodine work once more.

Treat before surgery, look at the removed tumour, and only continue treatment if the response was incomplete.

When an ESR1 mutation appears, swap the aromatase inhibitor for an oral SERD and keep the CDK4/6 inhibitor going.

When checkpoint blockade fails in melanoma, harvesting and expanding the patient's own tumour-reactive T cells still works in a third of patients.

If a lung cancer has a targetable mutation, give the pill first; immunotherapy works poorly in these tumours and raises the risk of severe side effects when a pill follows.

Two new relapsed-disease options with different targets and mechanisms. Which comes first, and whether one works after the other, is unknown.

An AI reading of the biopsy slide says whether adding hormone therapy to radiation will help.

A blood test that reads which resistance mutation a GIST has acquired, so the second drug can be chosen to fit it.

A ctDNA MRD blood test after surgery decides who gets more treatment and who is spared it.

A PET scan after two cycles of antibodies alone identifies women who can be cured without chemotherapy.

A gene test on the tumour decides who can skip chemotherapy without losing protection.

A blood test for inherited BRCA mutations unlocks a year of olaparib after surgery, which improves survival.

Reading the faint end of the HER2 stain decides who gets Enhertu.

Read the tumour type under the microscope first: non-epithelioid tumours should get immunotherapy up front; epithelioid tumours can reasonably get either immunotherapy or chemo-immunotherapy.

A simple clinical score decides between two immunotherapies together or one immunotherapy with a targeted pill.

Test the tumour for a broken DNA spell-checker; if it has one, immunotherapy before surgery melts most tumours and in the rectum can replace surgery altogether.

The scan shows whether the target is there; the treatment uses the same address. Only patients whose tumours light up are treated.

SSTR PET followed by PRRT is the original theranostic pair: the scan with the diagnostic isotope decides who gets the same molecule with the therapeutic isotope.

Proposed: a TROP2 PET scan to choose between three TROP2 ADCs and predict who will respond, since tissue staining has not worked.

Immunotherapy plus bevacizumab is standard in liver cancer, but the anti-VEGF part can cause fatal bleeding from swollen veins in the oesophagus unless they are checked first.

Bleomycin scars the lungs; combining it with brentuximab was fatal in early trials, and PET-adapted therapy now lets most patients skip it.

Immunotherapy added to first-line chemotherapy has failed to extend survival in ovarian cancer in every large trial so far; its only win is in PD-L1-positive platinum-resistant disease.

Chemotherapy-based regimens barely work when the p53 gene is lost; these patients need BTK inhibitors or venetoclax from the start.

Every dose of doxorubicin adds to a lifetime total; above roughly 450 mg/m2 heart failure risk rises steeply, so sarcoma and lymphoma regimens are capped and hearts are monitored.

Being HPV-positive is not enough to justify less radiation; trials that tried it saw more relapses.

Enhertu and its DXd cousins can inflame the lungs; combining them with immunotherapy, radiation, or mTOR inhibitors stacks that risk.

Ibrutinib raises the risk of irregular heart rhythm, high blood pressure, and sudden cardiac events; second-generation BTK inhibitors are safer choices for patients with heart disease.

Interleukin-2 was part of the original immunotherapy package but a large European trial showed it adds toxicity and no benefit, so it has been dropped.

The CD22 ADC is an excellent bridge to transplant, but too many cycles or the wrong conditioning can cause severe liver damage after the transplant.

LAG-3 blockers helped in measurable melanoma with one drug pairing, but failed as adjuvant therapy and with a different PD-1 partner.

Keyhole radical hysterectomy, though less painful, led to more recurrences and deaths than open surgery in the LACC trial. Open surgery is the standard until protective techniques are proven.

Restarting immunotherapy alongside a targeted pill after immunotherapy has already failed adds side effects and no benefit.

Myeloma bispecifics and CAR-T suppress antibody production so profoundly that infections, not the cancer, became a leading cause of death in early trials.

Adding a TIGIT blocker to PD-1/PD-L1 blockade looked good in phase 2 and then failed repeatedly in phase 3.

Giving a second ADC with the same kind of payload straight after the first often does not work well.