ReviewCells, tissues, organs2017
Therapeutic Targeting of Epithelial Plasticity Programs: Focus on the Epithelial-Mesenchymal Transition.
Review in Cells, tissues, organs, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 36 citations in OpenAlex.
- Do Metastatic Cells Arise from PD-L1International journal of molecular sciences · 2026Review
- EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025Review
- The impact of epithelial-mesenchymal transition (EMT) induced by metabolic processes and intracellular signaling pathways on chemo-resistance, metastasis, and recurrence in solid tumors.Cell communication and signaling : CCS · 2024Review
- Epithelial-to-mesenchymal transition in cancer progression: unraveling the immunosuppressive module driving therapy resistance.Cancer metastasis reviews · 2024Review
- Loss of Key EMT-Regulating miRNAs Highlight the Role of ZEB1 in EGFR Tyrosine Kinase Inhibitor-Resistant NSCLC.International journal of molecular sciences · 2023Article
- Therapeutic targeting approach on epithelial-mesenchymal plasticity to combat cancer metastasis.Medical oncology (Northwood, London, England) · 2023Review
- WNT Pathway Mutations in Metachronous Oligometastatic Castration-Sensitive Prostate Cancer.International journal of radiation oncology, biology, physics · 2023Article
- LncRNA SNHG4 Modulates EMT Signal and Antitumor Effects in Endometrial Cancer through Transcription Factor SP-1.Biomedicines · 2023Article
- Review article epithelial to mesenchymal transition‑associated microRNAs in breast cancer.Molecular biology reports · 2022Review
- Metastasis prevention: targeting causes and roots.Clinical & experimental metastasis · 2022Review
- Drug resistance in cancer therapy: the Pandora's Box of cancer stem cells.Stem cell research & therapy · 2022Review
- Review
- Review
- Cancer drug resistance induced by EMT: novel therapeutic strategies.Archives of toxicology · 2021Review
- Epithelial to Mesenchymal Transition History: From Embryonic Development to Cancers.Biomolecules · 2021Review
- Controversies around epithelial-mesenchymal plasticity in cancer metastasis.Nature reviews. Cancer · 2019Review
- Contribution of Epithelial Plasticity to Therapy Resistance.Journal of clinical medicine · 2019Review
- Exosomes in esophageal cancer: A review on tumorigenesis, diagnosis and therapeutic potential.World journal of clinical cases · 2019Review
- How apoptosis and epithelial-to-mesenchymal transition are nested in EGFR inhibitors resistance in lung cancer.Journal of thoracic disease · 2019Article
- O-GlcNAcylation is required for mutant KRAS-induced lung tumorigenesis.The Journal of clinical investigation · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mounting data points to epithelial plasticity programs such as the epithelial-mesenchymal transition (EMT) as clinically relevant therapeutic targets for the treatment of malignant tumors. In addition to the widely realized role of EMT in increasing cancer cell invasiveness during cancer metastasis, the EMT has also been implicated in allowing cancer cells to avoid tumor suppressor pathways during early tumorigenesis. In addition, data linking EMT to innate and acquired treatment resistance further points towards the desire to develop pharmacological therapies to target epithelial plasticity in cancer. In this review we organized our discussion on pathways and agents that can be used to target the EMT in cancer into 3 groups: (1) extracellular inducers of EMT, (2) the transcription factors that orchestrate the EMT transcriptome, and (3) the downstream effectors of EMT. We highlight only briefly specific canonical pathways known to be involved in EMT, such as the signal transduction pathways TGFβ, EFGR, and Axl-Gas6. We emphasize in more detail pathways that we believe are emerging novel pathways and therapeutic targets such as epigenetic therapies, glycosylation pathways, and immunotherapy. The heterogeneity of tumors and the dynamic nature of epithelial plasticity in cancer cells make it likely that targeting only 1 EMT-related process will be unsuccessful or only transiently successful. We suggest that with greater understanding of epithelial plasticity regulation, such as with the EMT, a more systematic targeting of multiple EMT regulatory networks will be the best path forward to improve cancer outcomes.
Indexed as
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.