ArticleAnnual review of cancer biology2018
Lineage Plasticity in Cancer Progression and Treatment.
Article in Annual review of cancer biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed.
- A forward genetic screen identifies Sirtuin1 as a driver of neuroendocrine prostate cancer.The Journal of experimental medicine · 2026Article
- Game of clones: decipher lineage plasticity in hormone-driven cancers.Cellular and molecular life sciences : CMLS · 2026Review
- Role of Janus kinase-signal transducer and activator of transcription signaling pathway in hormonal cancer therapeutic resistance and lineage plasticity.Endocrinology · 2026Review
- Article
- Dysregulated Cell Signaling Pathways in Prostate Tumoral Plasticity-Checkpoints.Oncology research · 2026Article
- RoundupFrontiers in endocrinology · 2026Article
- Transcriptomic and epigenetic profiling of neuroblastoma states in response to RBM39 degrader.Scientific data · 2025Article
- Structural basis of DNA-dependent coactivator recruitment by the tuft cell master regulator POU2F3.Cell reports · 2025Article
- F-box proteins in cancer: from cancer cells to the tumor microenvironment.Cell communication and signaling : CCS · 2025Review
- Patient-Derived Tumor Organoids to Model Cancer Cell Plasticity and Overcome Therapeutic Resistance.Cells · 2025Review
- RBM39 degrader invigorates innate immunity to eradicate neuroblastoma despite cancer cell plasticity.Nature communications · 2025Article
- Cell reprogramming in cancer: Interplay of genetic, epigenetic mechanisms, and the tumor microenvironment in carcinogenesis and metastasis.World journal of clinical oncology · 2025Review
- TAF7 directly targets SAA1 to enhance triple-negative breast cancer metastasis via phosphorylating E-cadherin and N-cadherin.iScience · 2025Article
- Glucose Metabolism and Tumor Microenvironment: Mechanistic Insights and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Integrated analysis of single-cell and bulk transcriptomes uncovers clinically relevant molecular subtypes in human prostate cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- Exploring the prognostic significance and therapeutic potential of SUCLG2 in prostate cancer.Frontiers in genetics · 2025Article
- Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025Review
- Article
- Nucleotide depletion promotes cell fate transitions by inducing DNA replication stress.Developmental cell · 2024Article
- Decoding the basis of histological variation in human cancer.Nature reviews. Cancer · 2024Review
2 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
Historically, it has been widely presumed that differentiated cells are determined during development and become irreversibly committed to their designated fates. In certain circumstances, however, differentiated cells can display plasticity by changing their identity, either by dedifferentiation to a progenitor-like state or by transdifferentiation to an alternative differentiated cell type. Such cellular plasticity can be triggered by physiological or oncogenic stress, or it can be experimentally induced through cellular reprogramming. Notably, physiological stresses that promote plasticity, such as severe tissue damage, inflammation, or senescence, also represent hallmarks of cancer. Furthermore, key drivers of cellular plasticity include major oncogenic and tumor suppressor pathways and can be exacerbated by drug treatment. Thus, plasticity may help cancer cells evade detection and treatment. We propose that cancer can be considered as a disease of excess plasticity, a notion that has important implications for intervention and treatment.
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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.