These results suggest that the Val allele of CYP1A1 Ile462Val polymorphism and the Pro allele of TP53Arg72Pro polymorphism contribute to an increased risk of GBC among Japanese women and men, respectively.
Spontaneous apoptosis in gallbladder carcinoma. Relationships with clinicopathologic factors, expression of E-cadherin, bcl-2 protooncogene, and p53 oncosuppressor gene.
Fifty-three cases of advanced gallbladder carcinoma (45 primary tumors and 8 metastases) were analyzed, p53 protein expression was determined by immunohistochemistry, DNA content was measured by cytophotometric techniques.
We aimed to examine the associations of cytochrome P450 1A1 (CYP1A1), glutathione S-transferase class mu (GSTM1), and tumor protein p53 (TP53) polymorphisms with the risk of GBC in Chilean women.
HER2/neu blockade is a promising treatment strategy for gallbladder cancer patients with gene amplification and deserves further exploration in a multi-center study.
Ectopic expression of ERBB2/ERBB3 mutants upregulated PD-L1 expression in GBC cells, effectively suppressed normal T-cell-mediated cytotoxicity in vitro through activation of the PI3K/Akt signalling pathway and contributed to the growth and progression of GBC in vivo.
Consistent with STYK1 gene knockdown, AKT specific inhibitor MK2206 abrogated tumor promoting action induced by STYK1, suggesting that PI3K/AKT pathway is essential for the oncogenic role of STYK1 in GBC.
This study performed a TP53 gene investigation by PCR-SSCP and direct sequencing using both bile supernatants and tissue samples from cholecystectomy specimens lacking gallbladder cancer, in order to investigate gallbladder carcinogenesis.
Over-expression of p53 was seen in 56.25% of GBC cases and was not seen in chronic cholecystitis or in control gallbladders. p53 expression in gallbladder cancer was significantly higher than in inflammatory or control gallbladders (P < 0.0001). p53 expression increased with increasing tumor grade (P = 0.039).
The high incidence of p53 overexpression in gallbladder carcinoma and its presence in dysplasia, even in specimens without invasive carcinomas, suggests that this abnormality is an important and early event in the pathogenesis of the tumor.
Frequent mutations were identified in tumor protein 53 (<i>TP53</i>) (14/27), SMAD family member 4 (<i>SMAD4</i>) (6/27), phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (<i>PIK3CA</i>) (6/27), and Kirsten rat sarcoma (<i>KRAS</i>) (6/27); no significant differences were identified between EBDC and GBC tissues.