ArticleWorld journal of gastroenterology2007
Two distinct pathways of p16 gene inactivation in gallbladder cancer.
Article in World journal of gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- Global gene expression landscape of gallbladder cancer and advances in targeted therapeutic strategies.World journal of clinical oncology · 2025Review
- Early detection of gallbladder cancer: Current status and future perspectives.World journal of clinical oncology · 2025Review
- Gallbladder Cancer: Current Insights in Genetic Alterations and Their Possible Therapeutic Implications.Cancers · 2021Review
- Expression of Human epidermal growth factor receptor 2, Survivin, Enhancer of zeste homolog -2, Cyclooxygenase-2, p53 and p16 molecular markers in Gall bladder carcinoma.Journal of carcinogenesis · 2021Article
- Modified CDKN2B (p15) and CDKN2A (p16) DNA methylation profiles in urban pesticide applicators.Environmental science and pollution research international · 2019Article
- Long-term survivors of pancreatic adenocarcinoma show low rates of genetic alterations in KRAS, TP53 and SMAD4.Cancer biomarkers : section A of Disease markers · 2018Article
- Emerging role of precision medicine in biliary tract cancers.NPJ precision oncology · 2018Review
- Gallbladder cancer epidemiology, pathogenesis and molecular genetics: Recent update.World journal of gastroenterology · 2017Review
- Mutational frequency ofEcancermedicalscience · 2017Article
- Global and gene-specific DNA methylation pattern discriminates cholecystitis from gallbladder cancer patients in Chile.Future oncology (London, England) · 2015Article
- Gastrointestinal stromal tumor with synchronous gallbladder adenocarcinoma.Journal of gastrointestinal cancer · 2014Article
- Expression of cell cycle-related proteins, p16, p53 and p63 as important prognostic markers in gallbladder adenocarcinoma.Pathology oncology research : POR · 2014Article
- Integrated genomic characterization reveals novel, therapeutically relevant drug targets in FGFR and EGFR pathways in sporadic intrahepatic cholangiocarcinoma.PLoS genetics · 2014Article
- Analysis of the methylation patterns of the p16 INK4A, p15 INK4B, and APC genes in gastric adenocarcinoma patients from a Brazilian population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- DNA promoter methylation as a diagnostic and therapeutic biomarker in gallbladder cancer.Clinical epigenetics · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo examine the mechanism of inactivation of the p16 gene in gallbladder cancer, and to investigate p16 alterations and their correlation with clinicopathological features.
methodsSpecimens were collected surgically from 51 patients with gallbladder cancer. We evaluated the status of protein expression, loss of heterozygosity (LOH), homozygous deletion and promoter hypermethylation using immunohistochemistry, microsatellite analysis, quantitative real-time polymerase chain reaction (PCR) and methylation-specific PCR, respectively. In addition, mutations were examined by direct DNA sequencing.
resultsHomozygous deletions of the p16 gene exon2, LOH at 9p21-22, p16 promoter hypermethylation, and loss of p16 protein expression were detected in 26.0% (13/50), 56.9% (29/51), 72.5% (37/51) and 62.7% (32/51), respectively. No mutations were found. LOH at 9p21 correlated with the loss of p16 protein expression (P < 0.05). Homozygous deletion of the p16 gene, a combination LOH and promoter hypermethylation, and multiple LOH at 9p21 were significantly correlated with the loss of p16 protein expression (P < 0.05). LOH at 9p21 and promoter hypermethylation of the p16 gene were detected in 15.4% (2/13) and 92.3% (12/13) of the tumors with homozygous deletion of the p16 gene, respectively. P16 alterations were not associated with clinicopathological features.
conclusionOur results suggest that LOH and homozygous deletion may be two distinct pathways in the inactivation of the p16 gene. Homozygous deletion, a combination of LOH and promoter hypermethylation, and multiple LOH are major mechanisms of p16 inactivation in gallbladder cancer.
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