ReviewTrends in cancer2019
Clonal Evolution and Epithelial Plasticity in the Emergence of AR-Independent Prostate Carcinoma.
Review in Trends in cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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
29 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The positive relationship between androgen receptor splice variant-7 expression and the risk of castration-resistant prostate cancer: A cumulative analysis.Frontiers in oncology · 2023Pooled it
- 3D chromatin dynamics in cellular neuroendocrine transformation.Protein & cell · 2026Article
- Deciphering double-negative prostate cancer: from aggressive subtype to novel therapeutic paradigms.Cell communication and signaling : CCS · 2026Review
- The role of growth hormone in metastasis and angiogenesis of breast cancer.Bioscience reports · 2026Review
- E2F1-mediated PKMYT1 upregulation promotes prostate cancer progression by inhibiting the PPAR signaling pathway.Scientific reports · 2025Article
- Clinical significance of stratifying prostate cancer patients through specific circulating genes.Molecular oncology · 2025Article
- The role of transcription factors in prostate cancer progression.Molecules and cells · 2025Review
- Pre-existing cell subpopulations in primary prostate cancer tumors display surface fingerprints of docetaxel-resistant cells.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Deciphering the Tumor Microenvironment in Prostate Cancer: A Focus on the Stromal Component.Cancers · 2024Review
- Prostate Cancer: A Review of Genetics, Current Biomarkers and Personalised Treatments.Cancer reports (Hoboken, N.J.) · 2024Review
- Immunosuppressive role of BDNF in therapy-induced neuroendocrine prostate cancer.Molecular oncology · 2024Article
- Nuclear receptor NURR1 functions to promote stemness and epithelial-mesenchymal transition in prostate cancer via its targeting of Wnt/β-catenin signaling pathway.Cell death & disease · 2024Article
- Tissue-Based Diagnostic Biomarkers of Aggressive Variant Prostate Cancer: A Narrative Review.Cancers · 2024Review
- Exosomal miR-222-3p contributes to castration-resistant prostate cancer by activating mTOR signaling.Cancer science · 2023Article
- Prostate cancer cell heterogeneity and plasticity: Insights from studies of genetically-engineered mouse models.Seminars in cancer biology · 2022Review
- MIRO2 Regulates Prostate Cancer Cell Growth via GCN1-Dependent Stress Signaling.Molecular cancer research : MCR · 2022Article
- RelB upregulates PD-L1 and exacerbates prostate cancer immune evasion.Journal of experimental & clinical cancer research : CR · 2022Article
- Retinoblastoma Protein Paralogs and Tumor Suppression.Frontiers in genetics · 2022Review
- Circulating Tumour Cells Indicate the Presence of Residual Disease Post-Castration in Prostate Cancer Patient-Derived Xenograft Models.Frontiers in cell and developmental biology · 2022Article
- Key promoters of tumor hallmarks.International journal of clinical oncology · 2022Review
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
In spite of an initial clinical response to androgen deprivation therapy (ADT), the majority of prostate cancer patients eventually develop castration-resistant prostate cancer (CRPC). Recent studies have highlighted the role of epithelial plasticity, including transdifferentiation and epithelial-to-mesenchymal transition (EMT), in the development of AR pathway-negative CRPC, a form of the disease that has increased in incidence after the introduction of potent AR inhibitors. In this review, we will discuss the switches between different cell fates that occur in response to AR blockade or acquisition of specific oncogenic mutations, such as those in TP53 and RB1, during the evolution to CRPC. We highlight the urgent need to dissect the mechanistic underpinnings of these transitions and identify novel vulnerabilities that can be targeted therapeutically.
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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.