ArticleCancers2012
Cancer Stem Cells, EMT, and Developmental Pathway Activation in Pancreatic Tumors.
Article in Cancers, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 33 citations in OpenAlex.
- Role of the TGF-β/Smad3 pathway in pancreatic cancer cell growth and stem cell characteristics.Discover oncology · 2025Article
- Waterpipe smoke condensate influences epithelial to mesenchymal transition and interferes with the cytotoxic immune response in non-small cell lung cancer cell lines.Oncology reports · 2021Article
- Oxysterol-Binding Protein 2 Promotes Pancreatic Ductal Adenocarcinoma Progression Through Epithelial-Mesenchymal Transition.Frontiers in oncology · 2021Article
- Epithelial-mesenchymal transition: a hallmark in pancreatic cancer stem cell migration, metastasis formation, and drug resistance.Journal of cancer metastasis and treatment · 2020Article
- Therapeutic Strategies Targeting Cancer Stem Cells and Their Microenvironment.Frontiers in oncology · 2019Review
- Transfection of T-Box Transcription FactorInternational journal of molecular sciences · 2018Article
- Vasohibin 2 promotes malignant behaviors of pancreatic cancer cells by inducing epithelial-mesenchymal transition via Hedgehog signaling pathway.Cancer medicine · 2018Article
- Cellular Phenotype Plasticity in Cancer Dormancy and Metastasis.Frontiers in oncology · 2018Review
- The role of cancer-associated fibroblast MRC-5 in pancreatic cancer.Journal of Cancer · 2018Article
- Neoadjuvant chemotherapy for pancreatic cancer: Effects on cancer tissue and novel perspectives.Oncology letters · 2017Article
- EpCAM+ Liver Cancer Stem-Like Cells Exhibiting Autocrine Wnt Signaling Potentially Originate in Cirrhotic Patients.Stem cells translational medicine · 2017Article
- HES1 Promotes Colorectal Cancer Cell Resistance To 5-Fu by Inducing Of EMT and ABC Transporter Proteins.Journal of Cancer · 2017Article
- 3,6-dihydroxyflavone suppresses the epithelial-mesenchymal transition in breast cancer cells by inhibiting the Notch signaling pathway.Scientific reports · 2016Article
- Activation of anaphase-promoting complex by p53 induces a state of dormancy in cancer cells against chemotherapeutic stress.Oncotarget · 2016Article
- Cancer of the Pancreas: Molecular Pathways and Current Advancement in Treatment.Journal of Cancer · 2016Review
- Hes1 promotes cell proliferation and migration by activating Bmi-1 and PTEN/Akt/GSK3β pathway in human colon cancer.Oncotarget · 2015Article
- Apoptotic and autophagic pathways with relevant small-molecule compounds, in cancer stem cells.Cell proliferation · 2015Review
- Transforming growth factor-β1 regulates epithelial-mesenchymal transition in association with cancer stem-like cells in a breast cancer cell line.International journal of clinical and experimental medicine · 2014Article
- Emerging targets in cancer management: role of the CXCL12/CXCR4 axis.OncoTargets and therapy · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer is a disease with remarkably poor patient survival rates. The frequent presence of metastases and profound chemoresistance pose a severe problem for the treatment of these tumors. Moreover, cross-talk between the tumor and the local micro-environment contributes to tumorigenicity, metastasis and chemoresistance. Compared to bulk tumor cells, cancer stem cells (CSC) have reduced sensitivity to chemotherapy. CSC are tumor cells with stem-like features that possess the ability to self-renew, but can also give rise to more differentiated progeny. CSC can be identified based on increased in vitro spheroid- or colony formation, enhanced in vivo tumor initiating potential, or expression of cell surface markers. Since CSC are thought to be required for the maintenance of a tumor cell population, these cells could possibly serve as a therapeutic target. There appears to be a causal relationship between CSC and epithelial-to-mesenchymal transition (EMT) in pancreatic tumors. The occurrence of EMT in pancreatic cancer cells is often accompanied by re-activation of developmental pathways, such as the Hedgehog, WNT, NOTCH, and Nodal/Activin pathways. Therapeutics based on CSC markers, EMT, developmental pathways, or tumor micro-environment could potentially be used to target pancreatic CSC. This may lead to a reduction of tumor growth, metastatic events, and chemoresistance in pancreatic cancer.
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.