April 17–22, 2026 · San Diego · 2418 items
Over 22,000 attendees and more than 7,400 abstracts, including a record 265 clinical trial abstracts. This section collects on-site analysis across fifteen signal directions, plus late-breaking, clinical-trial and new-drug abstracts.
Open a cell to read the chapter. The number on the cell is how many people were still on that topic; the chapter is background, records, and judgment.
KRAS is one of the most common cancer drivers, and for years it was undruggable: the first inhibitors only caught one subtype (G12C) in its off state, then resistance arrived. AACR 2026 is where that story changed — one chemistry can now hit several KRAS forms, and there is a Phase 3 survival readout.
Key readoutdaraxonrasib · mOS 13.2 vs 6.7 mo, HR 0.40
198 people · 232 posts · 15 topics
PD-1 takes the brake off T cells; VEGF grows tumor vessels and also suppresses immunity. Combining the two drugs already worked in liver and kidney cancer. A bispecific puts both arms on one molecule, so the drug is pinned in the tumor vasculature and T-cell activation and vessel normalization happen together.
An ADC is an antibody as the courier and a toxin as the letter. The first three generations argued about linker stability and how toxic the payload was. This meeting argued about what the letter is: degraders, targeted drugs, dual payloads, even enzymes — not only cytotoxics.
CAR-T already has seven approvals in blood cancers and has struggled in solid tumors: messy targets, a microenvironment that traps T cells, short persistence. Personalized mRNA vaccines are the other path — a shot built on a patient’s own mutations, teaching the immune system the tumor.
After surgery or drugs, can you still find tumor DNA in the blood? That is MRD / ctDNA. It used to mean “is anything left.” This meeting put it in a plenary: people who clear it have ~70% pathologic complete response; people who do not, ~0%. The test is becoming a gate on whether to keep treating.
This is not a racetrack. It is the tool layer: spatial omics to see how cells sit together, molecular glues to trick “undruggable” proteins into degradation, AI to turn a slide from a glance into a measurement. Low hallway heat is not a demotion — the things nobody is posting are often the next five years of infrastructure.
KRAS is so bright it hides the other small molecules. This chapter is early chemistry off that spine: CDK2, WEE1, macrocycles, PARP with an ADC. Most of it is still Phase 1. It should not vanish from the topic list for lack of heat.
Breast cancer this year is not “another HER2 drug.” Three things happened at once: first-line treatment dropping chemo (or swapping in an ADC), using tumor DNA in blood to decide whether to intensify after surgery, and new escape switches in triple-negative disease.
Lung cancer is still the meeting’s public square: perioperative immunotherapy, KRAS, and lung adenocarcinoma in never-smokers, three lines in one week. KRAS drug readouts live in direction 1. This chapter is how the tumor type uses those drugs, and how immunotherapy is moving from late disease into the months around surgery.
The nine chapters above are the written recap. This cell is what they did not claim, but people were still posting: ovarian, head and neck, GBM, prostate, liver, gastroesophageal, plus MYC and TP53.