ArticleOncology letters2018
c-Met affects gemcitabine resistance during carcinogenesis in a mouse model of pancreatic cancer.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 17 citations in OpenAlex.
- PP2A complex disruptor SET prompts widespread hypertranscription of growth-essential genes in the pancreatic cancer cells.Science advances · 2024Article
- New insights into the role of adipocytes in pancreatic cancer progression: paving the way towards novel therapeutic targets.Theranostics · 2023Review
- Recent progress in the imaging of c-Met aberrant cancers with positron emission tomography.Medicinal research reviews · 2022Review
- Resistance to Gemcitabine in Pancreatic Ductal Adenocarcinoma: A Physiopathologic and Pharmacologic Review.Cancers · 2022Review
- Targeting the complement system in pancreatic cancer drug resistance: a novel therapeutic approach.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Combinational blockade of MET and PD-L1 improves pancreatic cancer immunotherapeutic efficacy.Journal of experimental & clinical cancer research : CR · 2021Article
- The tumor microenvironment in pancreatic ductal adenocarcinoma: current perspectives and future directions.Cancer metastasis reviews · 2021Review
- The plasticity of pancreatic cancer stem cells: implications in therapeutic resistance.Cancer metastasis reviews · 2021Review
- Targeting HGF/c-MET Axis in Pancreatic Cancer.International journal of molecular sciences · 2020Review
- Application ofOncotarget · 2019Article
- MET/HGF Co-Targeting in Pancreatic Cancer: A Tool to Provide Insight into the Tumor/Stroma Crosstalk.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic adenocarcinoma is thought to develop from histologically identifiable intraductal lesions known as pancreatic intraepithelial neoplasias (PanINs), which exhibit similar morphological and genetic features to pancreatic ductal adenocarcinoma (PDAC). Therefore, a better understanding of the biological features underlying the progression of PanIN is essential to development more effective therapeutic interventions for PDAC. In recent years, numerous studies have reported that MET proto-oncogene receptor tyrosine kinase (c-MET) is a potential marker of pancreatic cancer stem cells (CSCs). CSCs have been revealed to initiate and propagate tumors
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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.