ReviewOncology reports2025
Lactate and lactylation in gastrointestinal cancer: Current progress and perspectives (Review).
Review in Oncology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- LDHC4 drives lung adenocarcinoma progression by inducing lactylation of RB1 at lysine 900 to disrupt the RB1-E2F1 complex.Journal of translational medicine · 2026Article
- Microbiome Signatures in Advanced Gastric Cancer: Emerging Biomarkers for Risk Stratification, Therapy Guidance, and Prognostic Insight.International journal of molecular sciences · 2026Review
- The multifaceted functions of lactate and its translational potentials in cancer.Frontiers in pharmacology · 2026Review
- Histone lactylation: a new target for overcoming immune evasion and therapy resistance.Medical oncology (Northwood, London, England) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrointestinal (GI) cancers, which have notable incidence and mortality, are impacted by metabolic reprogramming, especially the increased production and accumulation of lactate. Lactylation, a post‑translational modification driven by lactate, is a crucial regulator of gene expression and cellular function in GI cancer. The present review aimed to examine advancements in understanding lactate and lactylation in GI cancer. The mechanisms of lactate production, its influence on the tumor microenvironment and the clinical implications of lactate levels as potential biomarkers were explored. Furthermore, lactylation was investigated, including its biochemical foundation, primary targets and functional outcomes. The present review underscored potential therapeutic strategies targeting lactate metabolism and lactylation. Challenges and future directions emphasize the potential of lactate and lactylation as innovative therapeutic targets in GI cancer to improve clinical outcomes.
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.