ReviewDiscover oncology2025
Emerging strategies and translational advancements of DDR1 in oncology.
Review in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- DDR1 sustains ferroptosis resistance in pancreatic ductal adenocarcinoma via SLC40A1-mediated iron homeostasis.Oncogene · 2026Article
- Dual targeting of chemoresistance and ferroptosis in gastric cancer: DDR1/VEGFR2 inhibitor K-13 synergizes with docetaxel from preclinical models to phase Ib/II clinical trial.Cell death and differentiation · 2026Article
- DDR2-COL11A1 Transcriptional Coupling as a Candidate Therapeutic Target in Colorectal Cancer: Integrative Transcriptomic and Deep Learning Validation.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Discoidin domain receptor 1 (DDR1) has emerged as a promising therapeutic target in oncology due to its unique role in tumor-stroma interactions and its involvement in key signaling pathways that drive cancer progression. DDR1 is homologous to the transmembrane receptor tyrosine kinase (RTK) family and uniquely requires binding to collagen for its activation. It regulates several cellular processes related to tumor cell proliferation, metabolism, migration, stromal remodeling, and epithelial-mesenchymal transition (EMT), ultimately influencing patient survival. Dysregulation of DDR1 may contribute to cancer progression, neurodegenerative diseases, fibrotic conditions, and atherosclerosis. Moreover, DDR1 has been shown to affect a wide variety of cancers, including lung, breast, stomach, colon, ovarian, and pancreatic cancers, underscoring its potential as a therapeutic target. Various small-molecule tyrosine kinase inhibitors aimed at DDR1 have been developed and have demonstrated significant effectiveness in reducing tumor growth. This review focuses on the structure, function, and mechanism of DDR1, as well as its involvement in cancer progression. Additionally, it examines the development and therapeutic potential of DDR1 inhibitors, offering a comprehensive overview of their application in cancer treatment. By synthesizing current knowledge, this article provides valuable insights to guide future research and innovation in targeting DDR1 for clinical therapeutic advancement.
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.