ReviewBritish journal of cancer2021
Metabolic reprogramming in prostate cancer.
Review in British journal of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 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
150 citing papers in PubMed.
- Trial
- Mechanism-Informed Language Modeling and Oxygenated 3D Screening Identify Berberine-Enzalutamide Synergy in Prostate Cancer Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Decoding the metabolic‑immune crosstalk: The role of glutamine and ammonium reprogramming in prostate cancer immune evasion (Review).Oncology reports · 2026Review
- Oligometastatic prostate cancer - bridging the gap between localized and metastatic disease.Nature reviews. Urology · 2026Review
- Phytoestrogens and related microbial metabolites remodel aberrant prostate transcriptomic profiles generated upon exposure to oxidative stress.Molecular and cellular biochemistry · 2026Article
- Comparative Analysis of Alcohol and Aldehyde Dehydrogenase Activities in Prostate Cancer and Benign Prostatic Hyperplasia.Journal of clinical medicine · 2026Article
- Nutrient deprivation enhances the cytotoxic effects of a sulfonamide-chalcone hybrid in PC-3 prostate cancer cells.Molecular and cellular biochemistry · 2026Article
- Article
- Review
- Article
- Combined Pharmacologic and Nutritional Modulation of High-Fat Diet-Associated Tumor-Supportive Features in Prostate Cancer Models.Biomolecules · 2026Article
- Histone methyltransferase KMT2D promotes castration-resistant prostate cancer progression by reactivating AR through FOXA1.Oncogene · 2026Article
- Review
- Recurrent intra-tumour heterogeneity is a hallmark of metastatic prostate cancer.Nature communications · 2026Article
- SerpinB7 promotes c-Myc-mediated glycolysis by interacting with ANXA2 to facilitate the progression of non-small cell lung cancer.Molecular cancer · 2026Article
- Dysregulation of the urea cycle - potential targets for treatment and diagnosis in prostate cancer.Expert reviews in molecular medicine · 2026Review
- HAAO‑derived quinolinic acid fuels FDPS‑dependent AR signaling and sensitizes prostate cancer to combination therapy.Cell death discovery · 2026Article
- Co-targeting EGFR and SUCLG2 disrupts a nuclear transcriptional program driving neuroendocrine differentiation and TKI resistance in castration-resistant prostate cancer.Cell communication and signaling : CCS · 2026Article
- Integrated multi-omics profiling uncovers the epigenetic, transcriptional, and metabolic landscape of prostate cancer progression.BMC cancer · 2026Article
- USP2 is an androgen-repressed survival factor that stabilises oncoproteins to facilitate therapy resistance in prostate cancer.Cell death & disease · 2026Article
90 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Although low risk localised prostate cancer has an excellent prognosis owing to effective treatments, such as surgery, radiation, cryosurgery and hormone therapy, metastatic prostate cancer remains incurable. Existing therapeutic regimens prolong life; however, they are beset by problems of resistance, resulting in poor outcomes. Treatment resistance arises primarily from tumour heterogeneity, altered genetic signatures and metabolic reprogramming, all of which enable the tumour to serially adapt to drugs during the course of treatment. In this review, we focus on alterations in the metabolism of prostate cancer, including genetic signatures and molecular pathways associated with metabolic reprogramming. Advances in our understanding of prostate cancer metabolism might help to explain many of the adaptive responses that are induced by therapy, which might, in turn, lead to the attainment of more durable therapeutic responses.
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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.