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Mutations of KRAS and DDR2 were found in large cell carcinoma (LCC) and squamous cell carcinoma (SCC) subtypes, respectively, whereas mutations of TP53 were seen in SCC and lung adenocarcinoma subtypes with higher frequencies and LCC subtype with lower frequency in Iranian patients.
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Our data indicate that DDR2 is a potent biomarker that can be used as an effective therapeutic target for treating oral squamous cell carcinoma patients with lymph node metastasis.
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DDR2 localisation is independent of integrin activation and the key DDR2 signalling effector SHC1. Structure-function analysis reveals that DDR2 mutants defective for collagen binding or kinase activity are unable to localise to the cell surface, demonstrating for the first time that both collagen binding and kinase functions are required for spatial localisation of DDR2.
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report the identification and characterization of a selective, extracellularly acting small molecule inhibitor (WRG-28) of DDR2 that uniquely inhibits receptor-ligand interactions via allosteric modulation of the receptor. By targeting DDR2, WRG-28 inhibits tumor invasion and migration
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Our results suggest that a mutation in DDR2 occurs naturally with a frequency of about 2% in Korean lung SCC patients. In addition, we showed that each of the novel DDR2 mutations were located in a kinase domain and induced an increase in cell proliferation rate.
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Overexpression of DDR2 might contribute to tumor progression in lung SQCC. The overexpression of DDR2 could be potential molecular target of lung SQCC.
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DDR2 overexpression is independently associated with tumor progression and poor survival rates in urothelial carcinoma patients.
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The DDR2 E655K mutation can play a role in cancer progression.
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collagen II-activated phosphorylated-DDR2 induces CYR61 through activation of transcription factor activator protein 1 (AP-1). The elevated CYR61, in turn, accelerates MMP1 production via ETS1 (ETS proto-oncogene 1).
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these data suggest that biological collagen aging could increase tumor cell proliferation by reducing the activation of the key matrix sensor DDR2
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Female ddr2-deficient mice homozygous for the slie mutation show inefficient spontaneous BC metastasis.
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This study suggested that DDR1 and DDR2 knockdown alters brain immunity and significantly reduces the level of triggering receptor expressed on myeloid cells (TREM)-2 and microglia.
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This work identifies DDR2 as a potential therapeutic target that controls breast cancer metastases through its action in both tumor cells and tumor-stromal cells at the primary tumor site.
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The group of patients with colorectal cancer with high DDR2 expression had significantly higher frequencies of T4, lymph node metastasis, and peritoneal dissemination compared to the group with low DDR2 expression.
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DDR2 showed high expression in gastric cancer tissues and cells. In xenograft models, DDR2 overexpression promoted tumor formation. Furthermore, DDR2 expression impacted on the invasion and motility of GC cells, accompanied by changes in EMT marker expression. Finally, our results revealed that DDR2 facilitates GC cell invasion and EMT through mTORC2 activation and AKT phosphorylation.
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DDR2 mediates collagen-induced activation of MT1-MMP in human fibroblasts
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Study strongly suggests that during pulmonary fibrosis, DDR2 not only participates in both the initiation and maintenance of fibrotic reaction, but also affects both ECM production and angiogenesis.
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signaling pathway, effectively suppressed peritoneal dissemination. DDR2 was identified as a driver gene for Gastric Cancer dissemination from the combined expression signature and can potentially serve as a novel therapeutic target for inhibiting Gastric Cancer peritoneal dissemination.
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Ang II induces cardiac fibrosis by enhancing DDR2 expression in cardiac fibroblasts via p38 MAPK-mediated activation of NF-kappaB.
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DDR2 Missense mutation is associated with spondylo-meta-epiphyseal dysplasia, short limb-abnormal calcification type.
