ReviewAmerican journal of clinical and experimental urology2024
Impact of cell plasticity on prostate tumor heterogeneity and therapeutic response.
Review in American journal of clinical and experimental urology, 2024. 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.
- Progress in targeted therapy for prostate cancer via cell surface proteins (Review).Biomedical reports · 2026Review
- Rutin Suppresses EMT and Induces Mitochondrial BiogenesisCancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is a dynamic process of lineage plasticity in which epithelial cancer cells acquire mesenchymal traits, enabling them to metastasize to distant organs. This review explores the current understanding of how lineage plasticity and phenotypic reprogramming drive prostate cancer progression to lethal stages, contribute to therapeutic resistance, and highlight strategies to overcome the EMT phenotype within the prostate tumor microenvironment (TME). Emerging evidence reveals that prostate tumor cells can undergo lineage switching, adopting alternative growth pathways in response to anti-androgen therapies and taxane-based chemotherapy. These adaptive mechanisms support tumor survival and growth, underscoring the need for deeper insights into the processes driving prostate cancer differentiation, including neuroendocrine differentiation and lineage plasticity. A comprehensive understanding of these mechanisms will pave the way for innovative therapeutic strategies. Effectively targeting prostate cancer cells with heightened plasticity and therapeutic vulnerability holds promise for overcoming treatment resistance and preventing tumor recurrence. Such advancements are critical for developing effective approaches to prostate cancer treatment and improving patient survival outcomes.
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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.