WNT3A, Wnt family member 3A, 89780

N. diseases: 141; N. variants: 5
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 AlteredExpression group BEFREE In addition, restoration of Wnt3a expression partially reversed the tumor suppressor action of miR‑485 in RB cells. 30896857 2019
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 Biomarker group BEFREE However, the effect was not attributable to the interruption of T-cell-intrinsic β-catenin signaling, because Wnt3a/β-catenin activation correlated with enhanced, not reduced, T-cell effector functions both <i>ex vivo</i> and <i>in vitro</i> Adoptively transferred CD8<sup>+</sup> T cells, not directly exposed to the anti-Wnt3a antibody but infiltrating previously Wnt3a-neutralized tumors, also showed improved functions. 30018042 2018
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 Biomarker group BEFREE Wnt3a blockade improved the capacity of T naïve cells to differentiate into effector cells <i>in vitro</i> However, Wnt3a blockade did not affect the function and phenotype of differentiated, partially exhausted, tumor-infiltrating T cells <i>ex vivo</i> Taken together, our data suggest that Wnt3a blockade halts the capacity of Wnt/β-catenin signaling to inhibit the differentiation of T naïve cells, but it does not restore the dysfunction of differentiated T cells, in the tumor setting.<i></i>. 30018041 2018
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 Biomarker group BEFREE For this purpose, the profiles (expression/methylation/deletion) of β-catenin, p-β-catenin (Y654), Wnt3a, and APC were studied in disease free normal cervical epithelium (n = 9), adjacent normal cervical epithelium of primary tumors (n = 70), CIN (n = 28), CACX (n = 102) samples, and two CACX cell lines (HeLa and SiHa). 29079964 2018
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 AlteredExpression group BEFREE In this study, we found that Wnt3a and its target gene c‑Myc showed higher expression in tumour tissues than normal liver tissues in HCC patients; 71.8% of the cases studied had high Wnt3a and c‑Myc expression levels (n=32); Wnt3a expression positively correlated with its target genes MMP‑7 and c‑Myc. 28902357 2017
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 AlteredExpression group BEFREE WNT3a was overexpressed at the protein and mRNA levels in malignant astrocytic tumors and cell lines. 26708597 2016
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 AlteredExpression group BEFREE The member 3a of Wingless-type MMTV integration site family (Wnt3a) as an oncogene is overexpressed in many kinds of tumors with a worse outcome. 26577850 2016
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 Biomarker group BEFREE Furthermore, we demonstrated that GPC5 could suppress the Wnt/β-catenin signaling by binding to Wnt3a at the cell surface, which mediated its function as a tumor suppressor. 27157618 2016
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 Biomarker group BEFREE The mouse xenograft model showed that Wnt3a-overexpressing cells grew into larger tumor masses and formed more VM than the control cells. 26266404 2015
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 AlteredExpression group BEFREE Wnt3a expression in primary tumors was significantly associated with lymph node involvement (p = 0.038) and MMP-9 expression in the primary tumor (p = 0.0387), mesenchyme adjacent to tumor (p = 0.022) and metastatic site (p = 0.004). 24564183 2014
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 Biomarker group BEFREE Taken together, our study indicates Wnt/β-catenin signaling pathway as an essential driver of glioma tumorigenesis, recognizing role of Wnt3a as an oncogene and thereby offering novel therapeutic strategies for management of these tumors. 23337036 2013
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 Biomarker group BEFREE Also, core protein increases cell proliferation rate and promotes Wnt3A-induced tumor growth in the xenograft tumor model of human HCC. 22110662 2011