DDR2 antibody (APC)
- Known as:
- DDR2 (anti-) (Antigen presenting cellular)
- Catalog number:
- orb113099
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- DDR2 antibody (APC)
Related genes to: DDR2 antibody (APC)
- Gene:
- ANAPC1 NIH gene
- Name:
- anaphase promoting complex subunit 1
- Previous symbol:
- -
- Synonyms:
- MCPR, TSG24, APC1
- Chromosome:
- 2q13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2016-10-05
- Gene:
- ANAPC2 NIH gene
- Name:
- anaphase promoting complex subunit 2
- Previous symbol:
- -
- Synonyms:
- APC2, KIAA1406
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-06
- Date modifiied:
- 2015-08-24
- Gene:
- ANAPC4 NIH gene
- Name:
- anaphase promoting complex subunit 4
- Previous symbol:
- -
- Synonyms:
- APC4
- Chromosome:
- 4p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2016-10-05
- Gene:
- ANAPC5 NIH gene
- Name:
- anaphase promoting complex subunit 5
- Previous symbol:
- -
- Synonyms:
- APC5
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-01
- Date modifiied:
- 2014-08-12
- Gene:
- ANAPC7 NIH gene
- Name:
- anaphase promoting complex subunit 7
- Previous symbol:
- -
- Synonyms:
- APC7
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2016-10-05
Related products to: DDR2 antibody (APC)
Related articles to: DDR2 antibody (APC)
- Atypical fibroxanthoma (AFX) and pleomorphic dermal sarcoma (PDS) are rare cutaneous mesenchymal tumours sharing clinical and histopathological features. Compared to AFX, PDS has an increased risk of local recurrence and metastasis. A precise diagnosis is critical to ensure proper clinical management and follow-up. AFX and PDS show a similar genetic background, but also a heterogeneous pattern of different molecular abnormalities still poorly investigated due to the rarity of these tumours. Multiple data from different institutions and geographical areas, facilitate the identification of molecular alteration/s of valuable diagnostic and/or sub-classification power. We investigated the DNA profile of 32 AFX and PDS samples using a custom targeted Next-Generation Sequencing panel including 228 cancer genes. We confirm a common pattern of gene mutations affecting TP53, CDKN2A and NOTCH1. Differences appeared in less frequently detected genes (e.g. TSC2) and in NF2 harbouring novel genetic alterations. Integrating our results with published datasets of AFX and PDS mutation profiles we observed a divergent distribution of alterations in genes signalling through angiogenic pathway (KDR, PDGFRB), DNA damage response (ATR), cellular migration/metastasis (DDR2, CDH1). These differences do not reach statistical significance, and histopathological evaluation remains the diagnostic gold standard, however, they offer valuable insights into the pathogenesis of these tumours. - Source: PubMed
Publication date: 2026/05/03
Caprini ElisabettaScaglione Giovanni LucaScarponi ClaudiaMorelli MartinaMadonna StefaniaMarani CarlaSebastiani ValeriaScala EnricoAlbanesi CristinaRahimi Siavash - Bladder cancer (BC) is a prevalent malignant tumor worldwide, posing a significant public health burden and challenge to human society. Current therapeutic modalities for BC include surgical treatment, radiotherapy, chemotherapy, targeted therapy, and immunosuppressive therapy. However, almost all patients experience disease progression and ultimately succumb to BC. Our study demonstrated that elevated expression of Heat Shock Protein Beta-6 (HSPB6) correlated with higher clinical grades and stages, establishing it as an independent prognostic risk factor for BC. Enrichment analysis indicated that HSPB6 is associated with the extracellular matrix in BC. Experimental validation revealed that HSPB6 overexpression inhibits the proliferation of BC cell line T24. This effect may be achieved by inhibiting the PI3K/Akt signaling pathway, which in turn leads to inhibition of epithelial-mesenchymal transition (EMT). Furthermore, we developed a prognostic risk model that incorporated DDR2, DPYSL3, MFAP5, PDGFRB, and SPOCD1, allowing accurate prediction of patient outcomes based on immunological status. In conclusion, this study highlights that HSPB6 overexpression can restrain the proliferation of BC cells and inhibit EMT, underscoring its potential as a diagnostic marker and therapeutic target in BC. - Source: PubMed
Publication date: 2026/04/20
Wang Jian-SheQiu Yi-FanZhang LuJi BoLiang SenWang Ya-XuanZhu Hai-Xia - Glioblastoma (GBM) is a highly aggressive brain tumor with a poor prognosis, and its etiology involves both genetic and environmental factors. Triphenyl phosphate (TPHP), an organophosphorus flame retardant widely used in various consumer products, has raised public health concerns due to its environmental prevalence and detection in human samples. However, its potential role in GBM pathogenesis remains unclear. This study combined machine learning and molecular simulation docking technology to investigate the effects of TPHP on the pathogenesis and related molecular mechanisms of glioma. - Source: PubMed
Publication date: 2026/03/24
Wang ZiyuCui KaiWang JialinMa RongWang Yanyang - Osteoarthritis (OA) is a common degenerative joint disease characterized by cartilage degradation and abnormal bone remodeling. Discoidin Domain Receptor 2 (DDR2) has emerged as a critical mediator of OA pathogenesis by disrupting extracellular matrix (ECM) homeostasis. This study investigates the therapeutic potential of DDR2 inhibition via selective allosteric inhibitor WRG-28. To evaluate its in vivo efficacy, an OA rat model was established, followed by intra-articular injections of WRG-28. The therapeutic effects were assessed using μCT, Safranin O/Fast Green staining, immunohistochemistry, and gait analysis. Furthermore, primary chondrocytes were stimulated with Type II collagen (Col II) in vitro, followed by immunofluorescence and qPCR to elucidate the underlying molecular mechanisms. Results showed that WRG-28 significantly attenuated osteophyte formation and cartilage degradation in vivo. Treated OA cartilage exhibited preserved Col II content, alongside suppressed DDR2 activation and reduced expression of matrix metalloproteinase 13 (MMP13). Consistent with these findings, in vitro experiments showed that WRG-28 effectively inhibited DDR2 activation in chondrocytes, leading to downregulated MMP expression and restored levels of cartilage matrix-related genes. Additionally, WRG-28 treatment prevented abnormal chondrocyte calcification. In summary, this study concludes that WRG-28 prevents cartilage degradation and inhibits abnormal chondrocyte calcification by targeting DDR2 activation, offering a novel approach to alleviate the progression of OA. - Source: PubMed
Publication date: 2026/04/01
Zong GaoyangLi XiangyangSun YueWei LiangliangXia ZhihaoYin ZhanhaiZhang YanLi Haopeng - High-grade urothelial carcinoma (HGUC) shows marked morphologic plasticity with many recognized histologic subtypes that may coexist within the same tumor. These pose a diagnostic challenge and should be distinguished from collision tumors, defined by the coexistence of morphologically and genotypically distinct tumors at the same anatomic site. Herein, we present the first case report of HGUC with malignant prostatic differentiation mimicking a collision tumor in a bladder diverticulum. The patient was a 68-year-old male patient who presented with gross hematuria and was found to have a 2.2 cm tumor in a posterior bladder diverticulum. Initial transurethral resection (TUR) suggested HGUC, while re-TUR showed a component resembling prostatic ductal adenocarcinoma. Subsequent diverticulectomy specimen revealed two morphologically and immunohistochemically distinct tumor components: 1) a papillary component associated with urothelial carcinoma in situ, positive for keratin 34BE12 and GATA3, and compatible with HGUC of the bladder, and 2) a distinct abutting and focally admixed malignant glandular component, which was GATA3 negative, but positive for markers of prostatic differentiation such as NKX3.1, PSA and PSAP and displayed prostatic ductal adenocarcinoma features. These findings raised the possibility of a collision tumor between urothelial carcinoma and metastatic prostatic adenocarcinoma. However, the patient's PSA level was normal and magnetic resonance imaging of the prostate was unremarkable. To render an accurate diagnosis and guide patient management, these two tumor components were macrodissected and subjected to targeted massively parallel sequencing. Disease-associated variants in , , , and were identified and were identical and shared among the two histologically distinct components. These findings suggest that the two components are part of the same neoplastic process and, given the presence of urothelial carcinoma in situ, possibly represent the first reported example of urothelial carcinoma with divergent prostatic differentiation. Awareness of divergent differentiation in urothelial carcinomas has important diagnostic, prognostic and therapeutic implications and can be resolved with the use of ancillary molecular studies. - Source: PubMed
Publication date: 2026/03/31
Budina AnnaVergara NorgeNavarro Farah El-SharkawyMorrissette Jennifer J DNayak Anupma