Ask about this productRelated genes to: Axin1 antibody
- Gene:
- AXIN1 NIH gene
- Name:
- axin 1
- Previous symbol:
- -
- Synonyms:
- PPP1R49
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2015-08-24
Related products to: Axin1 antibody
Related articles to: Axin1 antibody
- Colorectal cancer (CRC) is shaped by inherited genetic susceptibility, metabolic reprogramming, epigenetic regulation, and tumor microenvironment (TME) heterogeneity. Lactylation has recently emerged as an epigenetic mechanism that links lactate accumulation to chromatin remodeling and transcriptional regulation. However, the roles of lactylation-related genes in CRC initiation and progression, particularly from the perspective of SNP-based germline genetic variation, remain to be elucidated. - Source: PubMed
Publication date: 2026/06/17
Sheng BiaoWang Jianwei - Emerging evidence from recent pathological investigations has demonstrated that inflammation plays a critical role in the progression of gastrointestinal diseases. However, the causal relationships between inflammation and gastritis still lack further validation. - Source: PubMed
Publication date: 2026/06/17
Wang TongLin Lu - Cribriform morular thyroid carcinoma (CMTC) is a rare neoplasm more common in young euthyroid females, usually associated with familial adenomatous polyposis (FAP) syndrome, but also presenting as sporadic cases. These tumors result from the activation of the WNT/β-catenin signaling pathway, usually through germline APC gene mutations in FAP-associated disease, while sporadic cases may exhibit somatic mutations in APC, CTNNB1, and AXIN1. Additional possible molecular events include somatic mutations in KRAS, PIK3CA, KMT2C, KMT2D, TERT promoter or RET rearrangements. BRAF mutations do not occur. We describe a sporadic case of high-grade CMTC presented in a 44-year-old female with a large multilobulated, unifocal mass in the right thyroid lobe. The tumor showed the typical cribriform and morular patterns, high grade features (Ki-67 proliferative index of 20% and foci of necrosis), marked vascular invasion and regional lymph node metastases. The tumor cells were immunoreactive for keratin (KRT) clone CKAE1/AE3, KRT7, and TTF1/NKX2, with aberrant (nuclear and cytoplasmic) expression of β-catenin, but negative for thyroglobulin and calcitonin. CDX2 was detected exclusively in the morular structures. The somatic APC p.(Thr621Leufs*9) oncogenic variant and the somatic TERT promoter - 124 (C228T) oncogenic variant were found, in line with the tumor type and tumor grade respectively; but, for the first time, EWSR1 gene rearrangement was also detected, expanding the molecular spectrum of this uncommon entity. - Source: PubMed
Publication date: 2026/06/19
Alorjani Mohammed SayelSobrinho-Simões ManuelAl-Oqaily Ayat NaderAlsinglawi Dania JamalHeis Hussein AliCameselle-Teijeiro José Manuel - Vascular cognitive impairment (VCI) is a syndrome of cognitive dysfunction attributable to vascular risk factors and cerebrovascular diseases, representing a major component of global dementia burden. Dysglycemia, encompassing diabetes mellitus and impaired glucose regulation, is increasingly recognized as a modifiable risk factor for cognitive decline, particularly VCI. Chronic low-grade inflammation mediates the association between metabolic dysfunction and neurodegeneration. The lack of validated diagnostic tools for early VCI detection in high-risk dysglycemic populations highlights the urgent need for robust diagnostic models based on molecular signatures. - Source: PubMed
Publication date: 2026/05/22
Wang YuyingZhao ZhenyuJi LinnaHe HaoyingPeng SisiXu JuanXu ZhipengZhang Junjian - Hepatocellular carcinoma (HCC), accounting for nearly 90% of primary liver cancers, remains a major global health challenge due to late diagnosis and therapy resistance. Up to 50% of cases exhibit aberrant activation of the canonical Wnt/β-catenin pathway, driven by CTNNB1 mutations or inactivating alterations in AXIN1, APC, or ZNRF3, which are mutually exclusive. This hyperactivation has complex implications: it has been associated with drug resistance, larger tumors, epithelial-mesenchymal transition, vascular invasion, cancer stemness, and immune evasion, yet in some contexts, it correlates with a less aggressive, well-differentiated phenotype and improved survival. This heterogeneity highlights the need for further research to clarify its prognostic significance. This review explores recent mechanisms by which aberrant nuclear β-catenin accumulation fosters resistance to frontline tyrosine kinase inhibitors like sorafenib and lenvatinib through ferroptosis evasion, cancer stemness, and β-catenin stabilization. It also highlights how hyperactivated Wnt/β-catenin promotes an immunosuppressive "cold" tumor microenvironment, impairing immunotherapy efficacy. These include cytokine profile alterations, CD8+ T-cell exclusion, dendritic cell repression, and recruitment of immunosuppressive cells such as myeloid-derived suppressor cells, tumor-associated neutrophils, M2 macrophages, and regulatory T cells. Recent preclinical studies show that combining Wnt inhibitors with immunotherapy or tyrosine kinase inhibitors can reprogram the tumor microenvironment, restore ferroptosis sensitivity, eradicate cancer stem cells, enhance CD8+ T-cell infiltration, boost anti-tumor immunity, and overcome resistance with minimal side effects. Targeting the Wnt/β-catenin pathway offers a promising strategy to transform HCC treatment and improve outcomes by exploiting this pathway as a key therapeutic vulnerability. - Source: PubMed
Publication date: 2026/06/04
Park ChangmoWong Tin LokMa Stephanie