ReviewInternational journal of molecular medicine2025
L‑type amino acid transporter 1 in enhancing boron neutron capture therapy: Mechanisms, challenges and future directions (Review).
Review in International journal of molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Synthesis of Gd-DOTA-BMTP and its application in gadolinium neutron capture therapy for osteosarcoma.Journal of cancer research and clinical oncology · 2026Article
- Boron neutron capture therapy plus bevacizumab versus bevacizumab alone in recurrent glioblastoma: A propensity score-matched analysis.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
L‑type amino acid transporter 1 (LAT1) has emerged as a critical molecular target for advancing boron neutron capture therapy (BNCT), a promising treatment that leverages selective boron accumulation and neutron irradiation to eradicate cancer cells. The frequent upregulation of LAT1 in aggressive tumors (such as gliomas and specific subtypes of lung and breast cancer) underpins its essential role as the principal mediator of tumor‑selective boron compound uptake in BNCT. The present review comprehensively examines the structure and function of LAT1, the mechanistic principles of boron transport (including LAT1 mediation) and the key regulatory pathways governing BNCT efficacy. Building on this and given the role of LAT1 in reprogramming tumor metabolism through amino acid transport, advanced metabolomics tools, particularly liquid chromatography‑mass spectrometry and nuclear magnetic resonance, offer a novel approach for clarifying the contribution of LAT1 to BNCT. These techniques hold significant potential to map metabolic profiles altered by LAT1‑mediated boron compound uptake, thereby elucidating downstream biochemical consequences relevant to the therapeutic efficacy and resistance mechanisms. Synthesizing the dual role of LAT1 as both a vulnerability and therapeutic target in BNCT, the present review systematizes key challenges, including the need for selective boron compounds, resistance mechanisms and off‑target effects, while mapping actionable pathways to unlock its potential via refined regulation strategies, next‑generation delivery agents and personalized approaches. By addressing these knowledge gaps, this synthesis provides a foundational framework to harness LAT1‑targeted BNCT, offering potential to advance precision oncology paradigms and improve clinical outcomes for patients with LAT1‑enriched tumors.
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.