SynthesisBJS open2026
Influence of KRAS mutation subtypes on response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer: meta-analysis.
Synthesis in BJS open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundKRAS mutations are common in colorectal cancer, but the impact of KRAS mutation subtypes on treatment response remains poorly understood. This research aimed to investigate whether different KRAS mutations influence pathological complete response (pCR) rates after neoadjuvant chemoradiotherapy in locally advanced rectal cancer (LARC).
methodsA systematic review and meta-analysis of studies describing genetic determinants of response to neoadjuvant chemoradiotherapy in LARC was conducted, searching for manuscripts published up to March 2026. The primary outcome of interest was the odds ratio for KRAS mutations and pCR. A random-effects model estimated the pooled effect size of KRAS mutations within and outside exon 2 on pCR. Genomic data sets were analysed to investigate the molecular characteristics of KRAS exon 2 and non-exon 2 mutant rectal cancers and their impact on overall and disease-free survival. Finally, a transcriptomic data set was analysed to elucidate the underlying response mechanisms.
resultsOut of 11 537 manuscripts identified, 15 studies (3354 patients) were included in the meta-analysis. The odds ratio for any KRAS mutation and pCR was 0.48 (95% confidence interval 0.32 to 0.70), indicating reduced odds of pCR in KRAS-mutant LARC. Subgroup analysis revealed that KRAS mutations in exon 2 accounted for this effect, whereas variants outside exon 2 had no influence (odds ratio 0.96, 95% confidence interval 0.11 to 8.49). Analysis confirmed poorer disease-free survival in patients with exon 2 alterations (P = 0.019) as well as poorer overall survival (P = 0.047). Transcriptomic analysis revealed that non-exon 2 KRAS-mutant tumours were enriched for inflammatory signalling pathways, suggesting that these tumours represent a subgroup with high immune infiltration.
conclusionThe presence of KRAS mutations adversely affects pCR odds after neoadjuvant chemoradiotherapy in LARC, but this effect is specific to exon 2 mutations.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.