Histopathological and molecular analysis of gastrectomy specimens from hereditary diffuse gastric cancer patients has implications for endoscopic surveillance of individuals at risk

2008 ◽  
Vol 216 (3) ◽  
pp. 286-294 ◽  
Author(s):  
ME Barber ◽  
V Save ◽  
F Carneiro ◽  
S Dwerryhouse ◽  
P Lao-Sirieix ◽  
...  
2013 ◽  
pp. 11-17
Author(s):  
Thi Tuy Ha Nguyen ◽  
Thi Minh Thi Ha

Background: The role of p53 gene in the gastric cancer is still controversial. This study is aimed at determining the rate of the p53 gene codon 72 polymorphisms in gastric cancer patients and evaluating the relationship between these polymorphisms and endoscopic and histopathological features of gastric cancer. Patients and methods: Sixty eight patients with gastric cancer (cases) and one hundred and thirty six patients without gastric cancer (controls) were enrolled. p53 gene codon 72 polymorphisms were determined by PCR-RFLP technique with DNA extracted from samples of gastric tissue. Results: In the group of gastric cancer, Arginine/Argnine, Arginine/Proline and Proline/Proline genotypes were found in 29.4%, 42.7% and 27.9%, respectively. The differences of rates were not statistically significant between cases and controls (p > 0,05). In males, the Proline/Proline genotype was found in 38.1% in patients with gastric cancer and more frequent in patients without gastric cancer (15.7%, p = 0,01). An analysis of ROC curve showed that the cut-off was the age of 52 in the Proline/Proline genotype, but it was 65 years old in the Arginine/Proline genotype. The Proline/Proline genotype was found in 41.9% in Borrmann III/IV gastric cancer, this rate was higher than Borrmann I/II gastric cancer (16.2%, p = 0.037) and also higher than controls (18.4%, p = 0,01). The rate of Proline/Proline genotype was 41.7% in the diffuse gastric cancer, it was higher than in controls (p = 0,023). Conclusion: No significative difference of rate was found in genotypes between gastric cancer group and controls. However, there was the relationship between Proline/Proline genotype and gastric cancer in males, Borrmann types of gastric cancer, the diffuse gastric cancer. Key words: polymorphism, codon 72, p53 gene, PCR - RFLP, gastric cancer.


Endoscopy ◽  
2020 ◽  
Author(s):  
Apostolos Pappas ◽  
Wei Keith Tan ◽  
William Waldock ◽  
Susan Richardson ◽  
Monika Tripathi ◽  
...  

Abstract Background Endoscopic surveillance is recommended in patients with hereditary diffuse gastric cancer (HDGC) who refuse or want to delay surgery. Because early signet-ring cell carcinoma (SRCC) can be inconspicuous, the current surveillance endoscopy protocol entails 30 random biopsies, which are time-consuming. This study aimed to compare single-bite and double-bite techniques in HDGC surveillance. Methods Between October 2017 and December 2018, consecutive patients referred for HDGC surveillance were prospectively randomized to the single- or double-bite arm. The primary outcome was the diagnostic yield for SRCC foci. Secondary outcomes were: procedural time for random biopsies; comfort score; biopsy size; and quality of specimens, the latter assessed by the presence of muscularis mucosa, crush artifact, and proportion usable for diagnostic assessment. Results 25 patients were randomized to the single-bite arm and 23 to the double-bite arm. SRCC foci were detected in three and four patients in the single- and double-bite arms, respectively (P = 0.70). The procedural time for the double-bite arm (12 minutes, interquartile range [IQR] 4) was significantly shorter than for the single-bite arm (15 minute, IQR 6; P = 0.01), but comfort scores were similar. The size of the biopsies in the double-bite arm was significantly smaller than in single-bite arm (2.5 mm vs. 3.0 mm; P < 0.001) but this did not affect the presence of muscularis mucosa (P = 0.73), artifact level (P = 0.11), and diagnostic utility (P = 0.051). Conclusion For patients undergoing HDGC surveillance, the double-bite technique is significantly faster than the single-bite technique. The diagnostic yield for SRCC and the biopsy quality were similar across both groups.


2019 ◽  
Vol 157 (1) ◽  
pp. 87-96 ◽  
Author(s):  
Michelle F. Jacobs ◽  
Henry Dust ◽  
Erika Koeppe ◽  
Sandra Wong ◽  
Michael Mulholland ◽  
...  

2012 ◽  
Vol 36 (11) ◽  
pp. 1709-1717 ◽  
Author(s):  
Hiroshi Fujita ◽  
Jochen K.M. Lennerz ◽  
Daniel C. Chung ◽  
Devanshi Patel ◽  
Vikram Deshpande ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Alexander Desuki ◽  
Frank Staib ◽  
Ines Gockel ◽  
Markus Moehler ◽  
Hauke Lang ◽  
...  

Background. Loss ofLLGL1has been associated with loss of cellular adhesion and dissemination of cells from colorectal cancer and malignant melanoma. Regulation and relevance ofLLGL1were analyzed in gastric cancer patients with lymphatic and distant dissemination. Furthermore,LLGL1expression was analyzed in relation to the cellular adhesion proteinE-cadherin.Methods.LLGL1andE-cadherintranscription levels were evaluated in 56 gastric cancer patients and five gastric cancer cell lines. IHC staining forLLGL1was performed on 39 gastric cancer specimens.LLGL1was stably transfected intoLLGL1negative gastric cancer cell line SNU16 (del(17) (p11.2)) for functionalin vitroassays and a xenograft bioassay.Results. Gastric cancer specimens and cell lines displayedLLGL1andE-cadherinexpression levels with variable intensity. In gastric mucosa,LLGL1exhibited weak cytoplasmic and strong cortical staining. Loss ofLLGL1expression occurred in 65% of gastric cancers and significantly correlated with loss ofE-cadherinexpression (P=0.00009). Loss ofLLGL1expression was associated with the diffuse type of gastric cancer (P=0.029) with peritoneal carcinomatosis (M1; P=0.006) and with female gender (P=0.017). Stable reexpression ofLLGL1in SNU16 cells significantly increased both plastic surface adhesion and extracellular matrix proteins laminin and fibronectin, but had no impact onin vitroproliferation, apoptosis, or invasion or onin vivoproliferation or differentiation in our xenograft bioassay.Conclusion.LLGL1is coexpressed withE-cadherin.Loss of expression of either protein is associated with diffuse gastric cancer and peritoneal metastases.LLGL1does not impact on proliferation or epithelial-mesenchymal transition (EMT) rather increasing cellular adhesion.


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