|
rs121913412
|
|
G |
0.700 |
CausalMutation |
CLINVAR |
|
|
|
|
rs137854578
|
|
T |
0.700 |
CausalMutation |
CLINVAR |
|
|
|
|
rs28931588
|
|
T |
0.700 |
CausalMutation |
CLINVAR |
|
|
|
|
rs28931589
|
|
T |
0.700 |
CausalMutation |
CLINVAR |
|
|
|
|
rs28934573
|
|
A |
0.700 |
CausalMutation |
CLINVAR |
|
|
|
|
rs1042522
|
|
|
0.010 |
GeneticVariation |
BEFREE |
No significant association between the <i>TP53</i> rs1042522 C>G polymorphism and HB susceptibility was detected in the main analysis or in stratification analyses of age, gender, and clinical stages.
|
31293648 |
2019 |
|
rs11655237
|
|
|
0.010 |
GeneticVariation |
BEFREE |
In conclusion, we confirmed that the <i>LINC00673</i> rs11655237 C>T polymorphism may be associated with HB susceptibility.
|
31178901 |
2019 |
|
rs121913400
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Co-expression of S33Y/S45Y-β-catenin and S127A-YAP1 led to activation of Yap and Wnt signaling and development of HB, with 100% mortality by 13 to 14 weeks.
|
30794807 |
2019 |
|
rs121913409
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Finally, using a previously reported 16-gene signature, it was shown that YAP1-ΔN90-β-catenin HB tumors exhibited genetic similarities with more proliferative, less differentiated, GS-negative HB patient tumors, whereas YAP1-S33Y/S45Y-β-catenin HB exhibited heterogeneity and clustered with both well-differentiated GS-positive and proliferative GS-negative patient tumors.
|
30794807 |
2019 |
|
rs762471803
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Co-expression of S33Y/S45Y-β-catenin and S127A-YAP1 led to activation of Yap and Wnt signaling and development of HB, with 100% mortality by 13 to 14 weeks.
|
30794807 |
2019 |
|
rs768298443
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Co-expression of S33Y/S45Y-β-catenin and S127A-YAP1 led to activation of Yap and Wnt signaling and development of HB, with 100% mortality by 13 to 14 weeks.
|
30794807 |
2019 |
|
rs780571021
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Co-expression of S33Y/S45Y-β-catenin and S127A-YAP1 led to activation of Yap and Wnt signaling and development of HB, with 100% mortality by 13 to 14 weeks.
|
30794807 |
2019 |
|
rs137854573
|
|
|
0.010 |
GeneticVariation |
BEFREE |
The mutation of APC (rs137854573, c.C1606T, p.R536X) could result in HB carcinogenesis by activating Wnt signaling.
|
30619485 |
2018 |
|
rs137854574
|
|
|
0.010 |
GeneticVariation |
BEFREE |
The mutation of APC (rs137854573, c.C1606T, p.R536X) could result in HB carcinogenesis by activating Wnt signaling.
|
30619485 |
2018 |
|
rs1389001294
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Sequence analysis of ANXA10S identified a missense mutation (E36K, c.106G>A) in a HB cell line.
|
20461752 |
2010 |
|
rs202128953
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Sequence analysis of ANXA10S identified a missense mutation (E36K, c.106G>A) in a HB cell line.
|
20461752 |
2010 |
|
rs4647924
|
|
|
0.010 |
GeneticVariation |
BEFREE |
We report on a 3-year-old girl, from a 3-generation family with an FGFR3 Pro250Arg mutation, who in addition to craniosynostosis, had a laterality disorder and hepatoblastoma, following a pregnancy complicated by maternal insulin-dependent diabetes.
|
20707699 |
2010 |
|
rs763708092
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Sequence analysis of ANXA10S identified a missense mutation (E36K, c.106G>A) in a HB cell line.
|
20461752 |
2010 |
|
rs781124288
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Sequence analysis of ANXA10S identified a missense mutation (E36K, c.106G>A) in a HB cell line.
|
20461752 |
2010 |
|
rs983496580
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Sequence analysis of ANXA10S identified a missense mutation (E36K, c.106G>A) in a HB cell line.
|
20461752 |
2010 |
|
rs28933386
|
|
|
0.010 |
GeneticVariation |
BEFREE |
We identified hepatoblastoma spreading into bilateral hepatic lobes in a 1-month-old NS patient with a heterozygous PTPN11 mutation (Asn308Asp).
|
18253957 |
2008 |
|
rs28934571
|
|
|
0.010 |
GeneticVariation |
BEFREE |
It includes integration of hepatitis B virus (HBV) DNA, R249S TP53 (tumor protein p53) mutation in aflatoxin B1-exposed patients, KRAS mutations related to vinyl chloride exposure, hepatocyte nuclear factor 1alpha (HNF1alpha) mutations associated to hepatocellular adenomas and adenomatosis polyposis coli (APC) germline mutations predisposing to hepatoblastomas.
|
16799619 |
2006 |