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Trials recruiting now, the landmark trials, the trials held by this cancer's subtypes, the key papers and what they mean, the latest literature, and the milestones year by year.
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168 trials on record are attached to one of the types below rather than to Non-small-cell lung cancer itself. They are grouped by the type that holds them, so someone still working out which type they have can see the whole field from here.
The 48 most recent of 142 papers; see them all →
Late-stage lung cancer is rarely curable, so the authors look for ways to act before a cancer becomes invasive. This paper points to two things that could move the fight earlier. First, a blood signal: immune cells that suppress the response to the tumour rise as precancerous airway lesions progress, which could one day help decide which screen-detected nodules or lesions need treatment now. Second, a target: in mice, blocking the PI3K-delta signal these cells use prevented the immune changes and reduced tumours. Neither is a test or a treatment yet; both need trials in people at high risk.
The survival benefit first reported in 2023 has held five years after the last dose of adjuvant osimertinib, which answers the worry that a three-year course only delays relapse. Patients with an exon 19 deletion gained most; the L858R estimate crosses one and is less certain. Nothing here changes the recommendation, which already rests on the 2023 analysis, but it tightens the case for testing every resected non-squamous tumour for EGFR mutations.
Residual disease testing is prognostic after EGFR lung cancer surgery, but in this trial it did not pick out who benefits from icotinib, since both groups did.
Enrichment may make parts-per-million testing possible on small sequencers, though only eight patients were studied.
For a patient weighing the FLAURA2 regimen against osimertinib alone, the extra toxicity is front-loaded: the hardest months are the four induction cycles, and once pemetrexed stops the profile returns to that of osimertinib by itself. Kidney function deserves watching during pemetrexed maintenance.
Useful for a patient offered adagrasib after chemotherapy or immunotherapy who wants the trial explained without jargon. It adds no new data; the primary KRYSTAL-12 publication and the trial page remain the reference for the numbers.
Every insured Korean adult from 40 is offered a stomach endoscopy every two years, and people at high risk of liver cancer an ultrasound and blood test every six months. This review, by the researchers who run the programme, sets out how that came about.
A domestically developed checkpoint antibody has now produced a positive phase 3 overall-survival result in lung cancer, which is the strongest evidence yet that Russian oncology can supply its own immunotherapy rather than import it. The trial ran in Russia with sites in China, Hungary and Slovakia and has not been reviewed by the European Medicines Agency or the United States Food and Drug Administration.
Query for this cancer: (TITLE:"Non-small-cell lung cancer" OR ABSTRACT:"Non-small-cell lung cancer" OR TITLE:"LUAD" OR ABSTRACT:"LUAD" OR TITLE:"LUSC" OR ABSTRACT:"LUSC" OR TITLE:"LSCC" OR ABSTRACT:"LSCC" OR TITLE:"TCGA-LUAD" OR ABSTRACT:"TCGA-LUAD" OR TITLE:"TCGA-LUSC" OR ABSTRACT:"TCGA-LUSC") AND (treatment OR therapy OR trial OR survival OR diagnosis). Results are unfiltered search hits about Non-small-cell lung cancer, not a curated reading list.
Lynch, Paez, and Pao identify activating EGFR mutations; the birth of lung cancer precision medicine.
EGFR T790M is found in a patient relapsing after two years on gefitinib, and independently in progressing tumours that had not carried it before treatment. It becomes the most studied resistance mutation in cancer.
Soda et al.; crizotinib approved 2011.
MET amplification restores the growth signal through ERBB3 in 4 of 18 lung cancers resistant to an EGFR inhibitor, defining bypass resistance as a category.
Focal FGFR1 amplification in 22% of squamous cell lung cancers, with selective killing of amplified cell lines by FGFR inhibition.
TP53 mutated in nearly all of 178 squamous tumours, with the NFE2L2 and KEAP1 pathway altered in 34%, squamous differentiation genes in 44% and CDKN2A with RB1 in 72%; ROS1 rearrangements are defined as a class in 1,073 screened patients.
Rebiopsy of 155 patients: T790M in 63%, MET amplification in 5%, HER2 amplification in 13% and small-cell transformation in 3%, making rebiopsy at progression standard.
Two hundred and thirty adenocarcinomas profiled on every platform add RIT1 and MGA to the driver list and show that NF1, MET, ERBB2 and RIT1 drive the tumours with no other oncogene; the Lung Cancer Mutation Consortium finds a driver in 64% of 733 patients and longer survival where treatment matched it.
CheckMate 017/057; pembrolizumab first line for PD-L1 ≥50% follows (KEYNOTE-024, 2016).
Biallelic TP53 and RB1 loss in nearly all of 110 small-cell genomes, with NOTCH inactivation in 25%; in the same year, non-synonymous mutation burden is shown to predict response to PD-1 blockade in lung cancer, and KRAS-mutant disease is split into immune-poor and inflamed subsets by its co-mutations.
Across 103 repeat biopsies, each ALK inhibitor is shown to select its own spectrum of resistance mutations, with G1202R rising after second-generation treatment and the presence of a mutation predicting benefit from the third generation.
The Blueprint comparison shows three PD-L1 assays agree on tumour cells and SP142 does not. Of 860 patients with metastatic lung adenocarcinoma sequenced prospectively, 37.1% received a matched therapy, and the limiting factor was the evidence behind each alteration rather than detection; transformation to small-cell carcinoma is shown to branch from the adenocarcinoma clone before treatment begins.
STK11 and KEAP1 are tied to poor immunotherapy outcomes in KRAS-mutant disease; the College of American Pathologists, the International Association for the Study of Lung Cancer and the Association for Molecular Pathology require ROS1 testing for all adenocarcinomas and allow plasma to rule a mutation in but not out.
Transcription factor expression splits small-cell disease into four subtypes; in parallel, cell-free DNA is shown to be non-inferior to tissue genotyping at diagnosis and six days faster.
Whole genomes of 232 never-smoker lung cancers find no tobacco signature and three copy-number subtypes, one of them slow-growing with driver progenitor cells dating back many years.
In the trials of pembrolizumab with chemotherapy, continuous tissue mutational burden predicts nothing in either histology, and neither do STK11, KEAP1 or KRAS status.