ReviewCell death discovery2026
Amino acid metabolic reprogramming: future prospects for cholangiocarcinoma therapy.
Review in Cell death discovery, 2026. 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.
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- mTOR signaling in cholangiocarcinoma: mechanistic insights and therapeutic opportunities.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Cholangiocarcinoma (CCA) is a highly heterogeneous disease with a poor prognosis and a 5-year survival rate of less than 20% due to late diagnosis and limited therapeutic options, and the current problems in the treatment of CCA can be mainly attributed to the low rate of early diagnosis, the limited availability of targeted drugs, and the gradual increase in chemoresistance. Metabolic reprogramming in CCA causes the accumulation of large amounts of lactic acid and glycolytic intermediates, exacerbating hypoxia and the formation of an acidic environment at the tumor site, which further reduces the effectiveness of therapeutic drugs. Amino acid metabolic reprogramming promotes the proliferation, metastasis, spreading, and tumor angiogenesis of CCA cells, and some amino acid metabolites, in turn, regulate the metabolic state and gene expression of cells, which in turn regulates the cellular phenotype. Abnormal metabolism of amino acids negatively affects the progression of CCA. In the amino acid metabolism of CCA, the PI3K/AKT/mTOR and AMPK/Nrf2 pathways are two key pathways, and c-Myc plays an important role in glutamine metabolism as a transcription factor. Future studies should design targeted drugs around the abnormal accumulation process of glutamine, arginine and other amino acids to disrupt the amino acid uptake dominance in malignant tumors, as well as design novel drugs according to the changes in the tumor microenvironment.
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.