ReviewFrontiers in physiology2018
GDNF and the RET Receptor in Cancer: New Insights and Therapeutic Potential.
Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Downregulation of hsa-microRNA-204-5p and identification of its potential regulatory network in non-small cell lung cancer: RT-qPCR, bioinformatic- and meta-analyses.Respiratory research · 2020Pooled it
- Review
- Molecular mechanisms and therapeutic targets in lung cancer-nerve crosstalk.Chinese medical journal pulmonary and critical care medicine · 2026Review
- RET signaling as a mediator of estrogen receptor positive breast cancer brain metastasis.Communications biology · 2026Article
- RET Signaling Pathway in Human Cancer: Oncogenic Mechanisms, Selective Inhibitors, and Emerging Resistance Strategies.International journal of molecular sciences · 2026Review
- How to manage medullary thyroid carcinoma: current treatment strategies.Drugs in context · 2026Review
- Integrative multi-cohort analysis of DNA methylation profiles for pancreatic ductal adenocarcinoma biomarker discovery and prognosis.Frontiers in bioinformatics · 2026Article
- Transcriptome study exploring the mechanisms linking pollutants and breast cancer aggressiveness.Scientific reports · 2025Article
- IGSF10 is a RET antagonist regulating Ewing sarcoma growth and GnRH neuron migration.Cell reports · 2025Article
- Inhibition of GDNF-Driven Macrophage-to-Myofibroblast Transition Protects Against Colitis-Associated Intestinal Fibrosis.Inflammation · 2025Article
- Neurturin gene IVSI-663 polymorphism but not RET variants is associated with increased risk for breast cancer.Laboratory medicine · 2025Article
- The fusion characteristics of RET fusion in pan-cancer among the Chinese population: A comprehensive genomic analysis.Translational oncology · 2025Article
- Article
- Beyond Hormone Receptors: liquid biopsy tools to unveil new clinical meanings and empower therapeutic decision-making in Luminal-like metastatic breast cancer.Breast (Edinburgh, Scotland) · 2025Review
- Dual PI3K and HDAC inhibitor, CUDC-907, effectively inhibits endometrial cancer growthFrontiers in oncology · 2025Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Loss of tumor suppressor TMEM127 drives RET-mediated transformation through disrupted membrane dynamics.eLife · 2024Article
- Fibroblasts in the Aged Pancreas Drive Pancreatic Cancer Progression.Cancer research · 2024Article
- Loss of Tumour Suppressor TMEM127 Drives RET-mediated Transformation Through Disrupted Membrane Dynamics.bioRxiv : the preprint server for biology · 2024Article
- Hallmarks of perineural invasion in pancreatic ductal adenocarcinoma: new biological dimensions.Frontiers in oncology · 2024Review
18 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Glial cell line-derived neurotrophic Family Ligands (GFL) are soluble neurotrophic factors that are required for development of multiple human tissues, but which are also important contributors to human cancers. GFL signaling occurs through the transmembrane RET receptor tyrosine kinase, a well-characterized oncogene. GFL-independent RET activation, through rearrangement or point mutations occurs in thyroid and lung cancers. However, GFL-mediated activation of wildtype RET is an increasingly recognized mechanism promoting tumor growth and dissemination of a much broader group of cancers. RET and GFL expression have been implicated in metastasis or invasion in diverse human cancers including breast, pancreatic, and prostate tumors, where they are linked to poorer patient prognosis. In addition to directly inducing tumor growth in these diseases, GFL-RET signaling promotes changes in the tumor microenvironment that alter the surrounding stroma and cellular composition to enhance tumor invasion and metastasis. As such, GFL RET signaling is an important target for novel therapeutic approaches to limit tumor growth and spread and improve disease outcomes.
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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.