ReviewInternational journal of molecular sciences2026
The Emerging Role of N-Acetylaspartate in Cancer.
Review in International journal of molecular sciences, 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
5 authors.
Funding
Abstract
N-Acetylaspartate (NAA), historically considered a brain-restricted neuro-metabolite, has emerged as a pivotal regulator in cancer biology. Governed by the biosynthetic enzyme N-acetyltransferase 8-like (NAT8L), the NAA axis exerts notable biological effects in malignancies. This review delineates the NAA axis as a context-dependent metabolic rheostat that is strategically hijacked by malignancies to orchestrate growth and immune evasion. Rather than a passive bystander, the NAA axis functions through distinct, histology-specific paradigms: it either serves as a metabolic reservoir to fuel lipid biomass expansion or is suppressed to redirect aspartate flux toward nucleotide biosynthesis, depending on the tumor's unique genetic and metabolic bottlenecks. Beyond cell-intrinsic reprogramming, tumor-derived NAA is increasingly linked to immune evasion by impairing cytotoxic lymphocyte function and driving pro-tumorigenic M2-like macrophage polarization. By reconciling these disparate oncogenic roles, this review highlights the NAA axis as an important node of metabolic plasticity and evaluates its potential utility as a circulating biomarker and a stratifiable therapeutic target in diverse human malignancies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.