We assessed HER2 expression in a consecutive series of 211 GBC cases by immunohistochemistry (IHC), paying particular attention to intratumoral heterogeneity.
Deconstructing the epidemiological association between GBC and Salmonella Typhi infection, we show that Salmonella enterica induces malignant transformation in predisposed mice, murine gallbladder organoids, and fibroblasts, with TP53 mutations and c-MYC amplification.
HER2/neu blockade is a promising treatment strategy for gallbladder cancer patients with gene amplification and deserves further exploration in a multi-center study.
BCL-2 and c-Myc expressions gradually increased among CC, XGC and GBC (P = 0.032 and P = 0.020, respectively); while p53 and p21 were similar in the three groups (P = 0.167 and P = 0.122, respectively).
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).
Examining expression of enhanced green fluorecent protein (EGFP), E1A and the target gene P53 in the oncolytic adenovirus system validated that Survivin promoter-regulated oncolytic adenovirus had high proliferation activity and high P53 expression in Survivin-positive gallbladder cancer cells.
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.
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.
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.