Ask about this productRelated genes to: PDGFRB antibody
- Gene:
- PDGFRB NIH gene
- Name:
- platelet derived growth factor receptor beta
- Previous symbol:
- PDGFR
- Synonyms:
- JTK12, CD140b, PDGFR1
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: PDGFRB antibody
Related articles to: PDGFRB antibody
- Lucitanib is a novel multi-target inhibitor of vascular endothelial growth factor receptor 1-3, fibroblast growth factor receptor 1-3, and platelet-derived growth factor receptor α/β. This open-label, multicenter, single-arm Phase II study evaluated lucitanib plus the anti-programmed cell death 1 (PD-1) antibody toripalimab in patients with advanced solid tumors refractory to standard therapies. Patients received lucitanib (10 mg) once daily plus toripalimab (240 mg) every 3 weeks until progression or unacceptable toxicity. The primary endpoint was investigator-assessed objective response rate (ORR) and secondary endpoints included disease control rate, duration of response, progression-free survival (PFS), overall survival, and safety. Among 131 patients across four cohorts (PD-1-treated recurrent/metastatic nasopharyngeal carcinoma [NPC], PD-1-naïve NPC, recurrent/metastatic endometrial cancer [EC], and other tumors), ORR was 34.1%, 45.8%, 38.5%, and 13.5%, respectively. Median PFS was 4.2 months (95% confidence interval [CI], 4.1-5.6), 6.5 months (95% CI, 4.0-not estimable [NE]), 5.6 months (95% CI, 2.78-11.21), and 9.7 months (95% CI, 5.4-NE). The most common Grade ≥ 3 treatment-related adverse events were hypertension (37.4%), proteinuria (10.7%), and thrombocytopenia (10.7%). Lucitanib plus toripalimab showed encouraging antitumor activity with manageable safety in heavily pretreated advanced solid tumors, supporting further randomized evaluation, particularly in NPC and EC. : Chinese Clinical Trial Registry Identifier: ChiCTR2400087935. - Source: PubMed
Publication date: 2026/03/11
Zhou TingSun HaishuangChen GangZhang GuopingWu JinshengQu ShenhongHan YaqianHu DeshengLing YangZheng YulongLiu JianLin LizhuLi YongshengPan JianjiLiu YanyanWang CuiyingFu GuohongFeng JianShi JianhuaCai HuimingLi MengLi FugenWang YinbinZhang LiYang Yunpeng - 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 - Cancer-related lymphedema (CRL), the most common type of secondary lymphedema, seriously reduces the life quality of cancer patients. In-depth studies on the pathogenesis of CRL are limited, impeding the development of therapeutic approaches. In this study, an analysis of intercellular heterogeneity reveals a trend towards fibrosis in skin cell subpopulations and identifies the phenomenon of T-cell mesenchymal transition (TcMT). T cells with a mesenchymal phenotype-fibroblast-like (Fib-like) T cells and myofibroblast-like (Myofibro-like) T cells-exhibit a unique fibrotic phenotype and impaired immune function. Furthermore, PDGFRB expression by Fib-like T cells in the affected skin is likely to influence disease severity by regulating TcMT. Additionally, we observe the manifestation of the fibrotic phenotype of T cells in single-cell data from the stromal vascular fraction (SVF) of CRL patients, suggesting that TcMT may be a pathological feature and potential therapeutic target of CRL and providing deep insights into disease pathophysiology. - Source: PubMed
Publication date: 2026/04/20
Wang LiangliangChen JunzheWei MiaomiaoLiu ZhiyuanZhou YanChen YuezhongDeng YapingXiao ShuneXu GuangchaoQi FangWei ZairongMin PeiruZhang YixinDeng Chengliang - Excessive fibrogenesis is associated with adverse cardiac remodeling and heart failure. Myofibroblast, primarily derived resident fibroblast, is the effector cell type in cardiac fibrosis. The mechanism whereby fibroblast-myofibroblast transition is driven remains incompletely understood. In the present study, we investigated the role and targetability of vascular adhesion protein 1 (VAP1) in cardiac fibrosis. Transcriptomic screening identified VAP1 as a direct target for megakaryocytic leukemia 1 (MKL1), a master regulator of tissue fibrosis. VAP1 silencing in primary cardiac fibroblasts down-regulated expression of myofibroblast markers and weakened cell proliferation/migration/contraction when exposed to transforming growth factor-β, whereas VAP1 over-expression exerted the opposite effects. Importantly, VAP1 deletion in quiescent fibroblasts or activated fibroblasts (myofibroblasts), achieved through the Col1a2-Cre driver and the Postn-Cre driver, respectively, dampened cardiac fibrosis and rescued heart function in mice subjected to the transverse aortic constriction procedure. Data obtained from multi-omics techniques indicated that VAP1 influenced fibroblast-myofibroblast transition by directly interacting with platelet-derived growth factor receptor-beta to enable signal transduction. Finally, small-molecule VAP1 inhibitors attenuated cardiac fibrosis and improved heart function in mice. In conclusion, our data support a role for VAP1 in driving fibroblast activation and cardiac fibrosis. Therefore, targeting VAP1 can be considered as a reasonable approach for the intervention of heart failure. - Source: PubMed
Publication date: 2026/04/20
Huang ShanZhao QianwenShao TinghuiZhu ChenghaoXue YujiaChen NaxiaZhang YueXu HuihuiKong MingWang Rui - Axillary LNs (ALNs) initiate immune responses in breast cancer (BC) but how and when ALNs become dysfunctional, facilitating metastasis, is unclear. The fibroblastic reticular cell (FRC) network within ALNs provides structural support and mediates immune homeostasis, but we have yet to elucidate whether this network changes during BC progression. An unbiased computational approach was used to quantify features of the immunolabelled FRC network in ALNs derived from patients with BC. Platelet-derived growth factor receptor β (PDGFRβ) was identified as a robust immunomarker for human FRC and used to quantify how FRC network topology changes during BC progression and after treatment. Formalin-fixed paraffin-embedded ALNs (n = 331) from 179 patients with BC and 23 benign reactive controls were assessed for FRC network metrics, including lacunarity and branchpoints, alongside de-identified clinico-pathological data. These data were then integrated using multivariate, principal component and survival analyses. In node-negative, treatment-naïve triple-negative BC, denser FRC networks in uninvolved nodes significantly improved survival (p = 0.0365). Conversely, similar changes seen in node-positive BC significantly worsened survival (p = 0.0407), regardless of BC subtype or treatment. In metastatic ALNs, FRC network disruption grew proportionately to axillary tumour burden, and this significantly correlated with poorer outcomes (p = 0.043). Interestingly, increased FRC alignment within these metastases significantly improved survival (p = 0.0205). This study showed that changes in human ALN FRC network topology predicts BC prognosis. This could improve how we risk stratify patients in future, and provide a new avenue for mechanistic, translational research. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/04/20
Llewellyn Amy MD'Costa Sharon LLam Cheun YrGore Jasmine ALachina VeronikaShewring Daniel JActon Sophie ENaidoo Kalnisha