Ask about this productRelated genes to: Wnt10A antibody
- Gene:
- WNT10A NIH gene
- Name:
- Wnt family member 10A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-13
- Date modifiied:
- 2016-03-18
Related products to: Wnt10A antibody
Related articles to: Wnt10A antibody
- Thoracic SMARCA4-deficient undifferentiated tumors (SMARCA4-UT) represent a distinct and highly aggressive malignancy characterized by SMARCA4 deficiency, poor prognosis, and resistance to chemotherapy. The lack of clarity regarding the regulatory mechanisms underlying this disease has hindered the development of standardized treatment guidelines. In this study, we analyzed clinical samples and found significantly elevated levels of cancer stem cell markers, including SOX2, CD34, c-Myc, and EpCam, in thoracic SMARCA4-UT, which were further confirmed in SMARCA4-deficient non-small cell lung cancer (NSCLC) cells. Furthermore, SMARCA4 knockdown in NSCLC cells promoted cell proliferation, migration, invasion, and tumorsphere formation in vitro, as well as enhanced tumor growth in a mouse model in vivo. RNA sequencing analysis of SMARCA4-deficient cells revealed the upregulation of a subset of genes, including Wnt10A, and activation of Wnt signaling. This was validated through SMARCA4-ChIP-seq and SMARCA4-ChIP-PCR analyses, Wnt activity reporter assays, and subcellular distribution analysis of β-catenin. Subsequent studies using a small molecule Wnt inhibitor in SMARCA4-deficient cells and thoracic SMARCA4-UT patient-derived organoids demonstrated induction of apoptosis, inhibition of cell stemness, and suppression of tumor cell growth. These results suggest the potential for developing a novel therapeutic strategy targeting cancer stem cells for the treatment of thoracic SMARCA4-UT. - Source: PubMed
Publication date: 2026/06/30
Xu YanWang LumeiZhang HongjiaLiang LinHan HuiXiao TianyuZhang ChengHe QiyeYu ZuorenGao Jinli - Dear Editor, Genodermatoses are usually diagnosed in early childhood but diagnosis may be delayed in rare cases. Schöpf-Schulz-Passarge syndrome (SSPS) first described in 1971 is a rare type of autosomal recessive ectodermal dysplasia characterized by palmoplantar keratoderma, periocular and eyelid apocrine hidrocystomas, hypodontia, hypotrichosis, and nail dystrophy (1). Fewer than 40 cases have been reported up to 2018 (2) and the number has slightly increased with subsequent case reports. We report here a 73-year-old male patient whose parents were third-degree cousins presented to dermatology clinic for symptomatic palmoplantar hyperkeratosis (Figs 1a-1b) with a 30-years history. Physical examination determining mild alopecia (Fig. 1c), dental loss (Fig. 1d), micronychia (Figs 1e-1f) in association with numerous cystic lesions suggested the diagnosis of SSPS. Remarkably numerous hidrocystomas localized to the eyelids, periocular area, cheeks, nose, forehead, ears, shoulders, supraclavicular and axillary region showed three distinct morphologies; milia-like yellowish (Fig. 2a), bluish dome-shaped (Figs 2a-2b, 2d) and translucent (Fig. 2c) papular lesions. The histopatological examination determining the diagnosis of apocrine hidrocystoma (Figs 2e-2f) was followed by genetic confirmation of SSPS. A homozygous c.391G>A (p.Ala131Thr) variant was identified in WNT10A by Clinical Exome Sequencing. According to American College of Medical Genetics and Genomics criteria (3), this variant was classified as pathogenic (PS4, PM1, PM2, PM5, PP3, PP5). Rarely reported findings of SSPS including facial dysmorphism, loss of body hair (Fig. 2d), localized hyperhidrosis (Fig. 1f), generalized hypohidrosis, and atrophic tongue (Fig. 1d) was also associated. However, other rare supporting features, such as eccrine syringofibroadenoma, rosacea-like facial erythema, hypoplastic areolae and nipple, and ocular involvement were not observed (4-7). The patient had also a basal cell carcinoma on the nose (Fig. 2c) which has been occasionaly reported in SSPS (4). Furthermore, a 9 × 9 cm soft, subcutaneous mass located on the midline of the lumbar region, clinically suggestive of a lipoma, was also noted. In our case, although dental loss was the earliest presenting feature, major manifestations such as periocular and eyelid apocrine hidrocystomas and palmoplantar keratoderma emerged initially after the 5th decade, leading to a delay in diagnosis. Whereas extraocular localizations of apocrine hidrocystoma is described in sporadic cases (8), it has not been highlighted in the context of SSPS. Our patient, however, exhibited numerous lesions in multiple additional sites including the nose, cheeks, forehead, external ears, upper trunk and axillae, broadening the recognized clinical distribution of this hallmark finding. A noteworthy finding in this patient was the concurrent presence of three morphologically distinct types of facial apocrine hidrocystomas. While a review of previously reported cases revealed that lesions with different morphologies can coexist in individual patients (2), this phenotypic diversity has rarely been explicitly highlighted in the literature. WNT10A mutations, inherited in an autosomal recessive manner, have been documented in both homozygous and compound heterozygous states (7, 9). These mutations can result in a wide phenotypic spectrum, ranging from isolated hypodontia and oligodontia to more complex ectodermal dysplasia syndromes such as odonto-onycho-dermal dysplasia (OODD) and SSPS (5, 6, 9). On the other hand some authors suggest that these two conditions may represent phenotypic variations of the same underlying genetic defect rather than distinct entities (10). While our patient exhibited overlapping features with OODD, including hypodontia, palmoplantar hyperkeratosis, hypotrichosis, and nail dystrophy, the presence of numerous apocrine hidrocystomas was distinctive for SSPS (5)D. In conclusion, SSPS can be recognized even decades after onset of the mild dermatological manifestations (2). Awareness of the rich clinical spectrum of apocrine hidrocystomas as they are not limited to eyelids or periocular area and present with papulonodules in different size and color may be crucial (5)D. Although a therapeutic option for SSPS still does not exist timely recognition may prevent unnecessary diagnostic and therapeutic interventions and enable appropriate genetic counseling of the family members. - Source: PubMed
Baykal CanDuymaz Süleyman HilmiGezdirici AlperAydoğdu İbrahim HalilTürk Sultan BuseSarı Şule Öztürk - This study investigates the genetic basis of congenital tooth agenesis (CTA) using an omics approach. Whole exome sequencing (WES) identified novel variants, which were further analyzed in combination with RNA expression data to uncover genes associated with CTA, molecular mechanisms, and systemic disease links. - Source: PubMed
Publication date: 2026/06/23
Ranjan PrashantDevi ChandraVerma NehaBansal RajeshSrivastava Vinay KumarKumari RimjhimDas Parimal - Vertical facial discrepancies (VFD) are common craniofacial conditions influenced by genetic and environmental factors. This study investigated whether single-nucleotide polymorphisms (SNPs) in the WNT10A and WNT11 genes are associated with VFD in Brazilian children and adolescents. - Source: PubMed
Publication date: 2026/06/07
Reis Gustavo Henrique MarçalSilva Alissa TamaraCruz Isabelle SoaresPedreira Fernanda Rafaelly de OliveiraCruvinel Bianka Jurca da MottaGollino SaraStuani Maria Bernadete SassoKüchler Erika CalvanoKirschneck ChristianAlmeida-Júnior Luciano Aparecido dede Oliveira Daniela Silva BarrosoReis Caio Luiz Bitencourt - Precise orchestration of stem and progenitor cells is essential for tissue homeostasis and regeneration but becomes dysregulated during aging. Despite the known markers, the age-related dynamics of esophageal epithelial cell lineages remain unclear. Using single-cell single cell transcriptomics, we analyzed human esophageal epithelia across different age groups. We identified two stem cell populations: quiescent (qeSCs) and proliferative (peSCs) esophageal stem cells. qeSCs from young donors showed higher expression and Wnt signaling activity. Analysis of cell lineage trajectories combined with cell plastic potentials showed stronger connectivity between peSCs and differentiated cells in younger tissues, indicating more efficient and rapid epithelial turnover and homeostatic maintenance. Cell-cell interaction analysis further demonstrated that NOTCH signaling is more prominent within peSCs and qeSCs in younger esophagi, whereas in older tissues, NOTCH activity is preferentially retained in differentiated cells. Additionally, the inflammatory signaling, Interleukin-1 pathway, is more active in younger esophagi but is largely restricted to differentiated cells. Our findings suggest that age-related decline in esophageal homeostasis is primarily driven by impaired differentiation dynamics rather than by alterations in stem cell self-renewal capacity. - Source: PubMed
Publication date: 2026/05/20
Jang JinhoZhang JiePark Amy SJun SoheePark Jae-IlKo Kyung-Pil