Ask about this productRelated genes to: WIF1 antibody
- Gene:
- WIF1 NIH gene
- Name:
- WNT inhibitory factor 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-29
- Date modifiied:
- 2016-10-05
Related products to: WIF1 antibody
Related articles to: WIF1 antibody
- We report a unique case of a primary ovarian neoplasm with morphological and immunohistochemical features identical to a pleomorphic salivary adenoma in a 56-year-old female. Morphologically the tumour was composed of cellular nodules of bland glands lined by a double cell layer of epithelial and myoepithelial cells; cartilaginous elements were also present with focal osseous and bone marrow metaplasia. No teratomatous elements were present. Immunohistochemistry confirmed the presence of a double layer of epithelial and myoepithelial cells (S100, p40, p63, SOX10, calponin and smooth muscle actin positive) and showed diffuse nuclear positivity of both cell types for HMGA2. A HMGA2::WIF1 fusion was identified on molecular testing; this fusion is found in some pleomorphic salivary adenomas. As far as we are aware, this is the first report of a pleomorphic adenoma of salivary gland type within the ovary. We speculate on the histogenesis and review "salivary gland-type" neoplasms arising within the ovary. - Source: PubMed
Publication date: 2026/05/01
Beckett HollyHunt RogerMcCluggage W Glenn - Canalicular adenoma (CA) is a benign salivary gland tumor predominantly affecting the upper lip and is characterized by monomorphic epithelial cells arranged in branching cords within a loose and vascularized stroma. Unlike pleomorphic adenoma (PA), CA lacks a chondroid matrix and exhibits specific histological features, such as high cuboidal to columnar cells arranged in one to two cell layers. A recently identified PA subtype, named 'HMGA2-canalicular-like PA', mimics the morphology of CA but affects major salivary glands, and harbors the HMGA2::WIF1 fusion. Immunohistochemical markers including SOX10 positivity and p40/p63 negativity are shared between these entities, raising questions about their molecular differences. Therefore, the current study aimed to extensively compare the molecular profiles of CAs and HMGA2-canalicular-like PAs to better understand the mechanisms underlying their oncogenesis. In the present study, CAs and the HMGA2-canalicular-like PAs mostly shared similar histology and immunostaining, while the clinical presentations regarding tumor site and transcriptomic profiles were different. A novel finding was the overexpression of SOX2 in patients diagnosed with CA, in comparison to those diagnosed with HMGA2-canalicular-like PA. The CAs displayed significantly higher enrichment of hallmarks for Hedgehog signaling, IL2/STAT5 signaling, and apical surface, and significantly lower enrichment of hallmarks for apoptosis and mitotic spindle. Additionally, Gene Ontology enrichment analysis displayed significant enrichment of biological process for CAs in comparison to HMGA2-canalicular-like PAs for myofibril assembly, muscle filament sliding, actin-myosin filament sliding, and sarcomere organization. CAs and HMGA2-canalicular-like PAs exhibited similar histology and immunostaining but differed significantly in tumor site and transcriptomic profiles. The latter revealed significant activation of muscle-related transcriptional pathways, and overexpression of SOX2 in CAs. © 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: 2026/04/29
Alsugair ZiyadChampagnac AnneFieux MaximePhilouze PierreCeruse PhilippeThamphya BricePissaloux DanielTirode FranckBenzerdjeb Nazim - The rising incidence and mortality of lung adenocarcinoma (LUAD) present a significant public health challenge. Histidine, an essential amino acid, plays a pivotal role in metabolic processes, yet its specific contribution to LUAD pathogenesis remains to be elucidated. This study obtained bulk and single-cell RNA sequencing (scRNA-seq) data for LUAD from UCSC Xena and Code Ocean platforms, respectively. By integrating differential expression analysis, univariate/multivariate Cox analysis, and LASSO regression analysis, prognostic genes for LUAD were identified, and a prognostic risk model was constructed. Algorithms including ESTIMATE, ssGSEA, and CIBERSORT were employed to investigate immune heterogeneity across different groups. Furthermore, molecular subtypes of LUAD were identified through consensus clustering. This study, through the integration of bulk and scRNA-seq data, identified epithelial cells as the key effector cell population in LUAD, which can be further subdivided into four functionally heterogeneous subpopulations. Seven histidine metabolism-related epithelial cell-specific genes with prognostic significance in LUAD were identified (WIF1, GATA2, CD69, ID1, C4BPA, WFDC2, and CCL20), enabling the construction of a robust prognostic risk model. Immune infiltration analysis revealed that low-risk patients exhibited more robust immune infiltration and activity. Furthermore, cross-cancer exploratory evidence suggested potential sensitivity to CTLA-4 and PD-L1 inhibitors in this group. Furthermore, consensus clustering analysis successfully partitioned LUAD into two molecular subtypes exhibiting immune heterogeneity. The prognostic model constructed based on epithelial cell-specific genes associated with histidine metabolism effectively distinguishes LUAD patients and their immune characteristics, revealing epithelial cells as a key cell population regulating LUAD histidine metabolism. - Source: PubMed
Publication date: 2026/04/28
Mao ChaofanZhou Lin - Experimental animal models are essential for understanding the molecular mechanisms of human leukemia and testing potential therapies. Chemical induction using 7,12-dimethylbenz[a]anthracene (DMBA) has shown promise in recapitulating features of leukemogenesis in rodents, but its molecular fidelity to human disease remains underexplored. The aim of this study was to evaluate the transcriptomic landscape of a DMBA-induced leukemia rat model and assess its alignment with known gene expression signatures and oncogenic pathways in human leukemia. - Source: PubMed
Publication date: 2026/04/06
Alsamman KhaldoonEl-Masry Omar S - Epithelial-myoepithelial carcinoma (EMC) is a rare malignant tumor of the salivary glands, often characterized by HRAS mutations. The present study aimed to better define the molecular and transcriptomic landscape of EMC and explore its relationship with other head and neck neoplasms, particularly basal cell adenoma (BCA). We retrospectively analyzed 14 EMC cases using histology, immunohistochemistry, and whole-exome capture RNA sequencing. HRAS mutations were identified in 57.0% (8/14) of EMC, predominantly at p.Gly61Arg. Additional mutations identified included PIK3CA, STAT5B, and NOTCH1, as well as gene fusions such as HMGA2::WIF1 and FBXO32::PLAG1. A comparative analysis with 54 RAS-mutated head and neck tumors revealed that HRAS mutations were not exclusive to EMC, as they were also found in benign entities such as BCAs. Transcriptomic profiling found that EMC and BCA shared significant gene expression similarities, clustering closely. Differential expression analysis found upregulation of GATA3, CHI3L1, GRIA2, and MME in EMC, while BCAs had enrichment of Wnt-beta-catenin signaling. In contrast, EMCs had activation of the Ras-Raf-MAPK and PI3K-Akt pathways, supported by upregulation of E2F and G2-M checkpoint targets. Immunohistochemistry confirmed GATA3 positivity in HRAS-mutated EMCs. The frequent RAS mutations and overlapping transcriptomic profiles raise important diagnostic considerations and highlight the need for integrated molecular analyses to differentiate these entities. The EMCs displayed a recurrent HRAS mutation, also observed in other head and neck tumors, and were partially clustered with the cases of BCA, suggesting potential biological similarities. - Source: PubMed
Publication date: 2026/03/25
Alsugair ZiyadDescotes FrançoiseChampagnac AnneLopez JonathanFieux MaximePhilouse PierreCéruse PhilippeThamphya BricePissaloux DanielTirode FranckBenzerdjeb Nazim