Ask about this productRelated genes to: Ccnd1 antibody
- Gene:
- CCND1 NIH gene
- Name:
- cyclin D1
- Previous symbol:
- BCL1, D11S287E, PRAD1
- Synonyms:
- U21B31
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-06
- Date modifiied:
- 2019-04-23
Related products to: Ccnd1 antibody
Related articles to: Ccnd1 antibody
- Mantle cell lymphoma (MCL) is a rare, aggressive subtype of B-cell non-Hodgkin lymphoma with rare cutaneous involvement that typically indicates advanced systemic disease. We report a case of indolent MCL in a 56-year-old previously healthy male who presented with a 5-year history of edematous, painful plaques and associated onychodystrophy in the bilateral toes. Histopathology demonstrated a multinodular dermal and subcutaneous infiltrate of atypical lymphocytes. Immunohistochemistry revealed a primary B-cell population diffusely positive for CD20 and BCL2 and focally positive for BCL1. These cells were negative for CD5, SOX-11, BCL6, and LEF1. In situ hybridization demonstrated admixed lambda-restricted plasma cells, indicating plasmacytic differentiation. Fluorescence in situ hybridization testing for an IGH/CCND1 translocation was positive, confirming a diagnosis of MCL. While bone marrow biopsy demonstrated 10%-20% involvement by MCL, staging revealed no lymphadenopathy or visceral disease. No significant peripheral blood laboratory abnormality was noted. To our knowledge, this is the first reported case of cutaneous involvement by MCL confined to the bilateral toes. This case is also notable for its absence of typical markers, namely CD5 and SOX-11, plasmacytic differentiation, and indolent clinical behavior. We discuss the diagnostic and clinical significance of these atypical clinicopathologic features and diagnostic overlap with other cutaneous B-cell lymphomas, emphasizing the importance of comprehensive immunophenotypic and molecular evaluation in atypical presentations. - Source: PubMed
Publication date: 2026/04/23
Sun Q WiltonCruz Sebastian AMenke JoshuaTan BrentRieger Kerri EBulterys Philip L - Precancerous gastric lesions (PLGC) represent a critical transitional stage toward gastric cancer, yet effective interventions to halt progression remain limited. Vitexin, a naturally occurring flavonoid, exhibits anti-cancer potential; however, its molecular targets and mechanisms in PLGC have not been fully defined. This study aimed to elucidate the targets and mechanisms of vitexin against PLGC using an integrative strategy combining network pharmacology, molecular docking/molecular dynamics (MD), and cellular validation. Putative targets of vitexin and PLGC-associated genes were intersected to obtain 33 common targets, followed by protein-protein interaction network construction and pathway enrichment analyses. Molecular docking was performed against core targets, and MD simulations were conducted to assess the stability of the EGFR-vitexin complex. In vitro validation was carried out in MNNG-induced MC cells using cell viability, migration, and invasion assays, phase-contrast imaging, and immunofluorescence staining of EGFR and E-cadherin. Network analysis highlighted CCND1, EGFR, and ABL1 as central nodes and implicated oncogenic programs including cell-cycle regulation and PI3K-Akt signaling pathway. Docking suggested favorable binding of vitexin to the core targets. MD simulations further supported a stable binding mode of vitexin within the EGFR pocket over 100 ns with preserved global compactness; a late-stage conformational adaptation accompanied by hydrogen-bond network reorganization was observed without signs of global unfolding. Functionally, vitexin reduced MC cell viability in a dose-dependent manner, reaching ~ 50% inhibition at 20 μM, and significantly suppressed cell migration and invasion. Immunofluorescence demonstrated decreased EGFR expression and altered membrane localization, together with restored E-cadherin expression and membrane localization, suggesting a shift toward an epithelial phenotype. Vitexin inhibits PLGC-associated malignant phenotypes through multi-target modulation. Among the identified candidates, EGFR may serve as a putative and functionally relevant target, while modulation of EGFR-associated signaling together with restoration of E-cadherin may contribute to the reversal of EMT-related phenotypes. These findings provide mechanistic and structural support for the further preclinical evaluation of vitexin in preventing gastric cancer progression. - Source: PubMed
Publication date: 2026/04/23
Liu JiayingLiu NanYe YitingYe ZhandongJiang DongxuHuang Song - This study aimed to investigate the efficacy of focused ultrasound (FU) for vulvar lichen simplex chronicus (VLSC) and its effect on Cyclin D1 and cyclin-dependent kinase 4 (CDK4) expression. - Source: PubMed
Publication date: 2026/04/20
Liu Hua-MeiZhang FanPi Meng-YuanLv Yu-Mei - Pyrethroid insecticides are widely used globally, but their potential nephrotoxicity has gained increasing attention. Although previous studies suggest pyrethroids may induce acute kidney injury (AKI), the underlying mechanisms remain unclear. This study employed a network toxicology approach to elucidate the molecular mechanisms of pyrethroid-induced AKI. Eight commonly used pyrethroids were analyzed individually. A total of 3203 AKI-related genes were retrieved from public databases, and intersection analysis identified 157-196 common targets for each pyrethroid. Protein-protein interaction (PPI) network integration further identified 18 shared hub targets across the eight pyrethroids, among which 15 were further supported by GEO validation in AKI samples. Notably, 7 targets - SRC, CASP3, ESR1, CCND1, MMP9, BCL2, and HSP90AA1-were consistently shared across all compounds and were therefore considered as core targets. Enrichment analyses indicated that these targets were mainly involved in oxidative stress-, inflammation- and apoptosis-related processes. GEO validation further suggested that these alterations were particularly prominent in renal tubular cells and endothelial cells. Molecular docking supported potential interactions between pyrethroids and the core targets. The findings suggested that pyrethroid-induced AKI may involve processes related to oxidative stress, inflammation, and apoptosis, accompanied by impaired repair responses, ultimately disrupting the balance between injury and regeneration in renal tubular epithelial cells. - Source: PubMed
Publication date: 2026/04/19
Xue XuhangWu YuqingSheng PeiGeng LianyiTang YuxinZhu XinlongWang XufangAn XiaofeiGao Kun - Alzheimer's disease (AD) involves progressive neurodegeneration, with abnormal receptor signaling and disrupted cell-cycle activity leading to neuronal loss. Here, we identify a previously unknown mechanism linking β-amyloid (Aβ) exposure to the nuclear translocation of the Insulin-like Growth Factor 1 Receptor (IGF1R) in differentiated SH-SY5Y neuronal cells. The differentiated cholinergic model induced by retinoic acid and BDNF expresses acetylcholinesterase (AChE) and indicates that under amyloidogenic stress, IGF1R may transition from homeostatic membrane and vesicular signaling to a nuclear-centric function. We show that prolonged Aβ treatment causes phosphorylation-dependent nuclear import of IGF1R, confirmed by confocal imaging and biochemical fractionation. IGF1R is conventionally located in the membrane and vesicular membranes; however, under amyloidogenic stress, we show here that it is imported to the nucleus and exerts transcriptional control. The buildup of nuclear IGF1R coincided with increased Cyclin D1 levels and redistribution of neurons into S and G₂ phases, indicating abnormal cell-cycle re-entry. Chromatin immunoprecipitation demonstrated increased IGF1R binding at the CCND1 and JUN promoters after Aβ exposure, suggesting a direct role in gene transcription. Pharmacological blockade of IGF1R phosphorylation by PPP or SUMOylation by Ginkgolic acid significantly reduced Cyclin D1 elevation, implying that both post-translational modifications are involved in receptor nuclear trafficking. Co-immunoprecipitation and confocal imaging identified Nucleophosmin (NPM1) as a putative IGF1R interacting partner, potentially contributing to its nuclear transport and stabilizing receptor-chromatin complexes. These results establish IGF1R as a signaling-transcription connector linking extracellular amyloid stress to nuclear gene regulation, providing a mechanistic explanation for faulty neuronal cell-cycle re-entry in AD. We suggest that abnormal IGF1R-NPM1 interactions contribute to receptor mislocalization and cell-cycle failure, highlighting new targets for therapeutic intervention aimed at receptor trafficking and neuroprotection in Alzheimer's disease. - Source: PubMed
Publication date: 2026/04/15
Sengupta PriyankaMukhopadhyay Debashis