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Analysis of LKB1 mutations and other molecular alterations in pancreatic acinar cell carcinoma. | LitMetric

AI Article Synopsis

  • - Acinar cell carcinoma is a rare type of pancreatic cancer that lacks clearly defined genetic characteristics; recent studies focused on the LKB1 gene due to its involvement in some cases.
  • - In a study of five sporadic cases, researchers found no mutations or altered expression of the LKB1 gene, but identified significant changes like amplifications on certain chromosomes and hypermethylation of tumor suppressor genes in a majority of the samples.
  • - The findings suggest that the molecular mechanisms of acinar cell carcinoma differ from those of ductal pancreatic cancers, highlighting a need for further research to uncover the underlying causes and develop potential treatment options.

Article Abstract

Acinar cell carcinoma is a rare non-ductal neoplasm of the pancreas with poorly defined molecular genetic features. Recently, biallelic inactivation of LKB1 was described in an acinar cell carcinoma of a Peutz-Jeghers patient carrying a heterozygous germline LKB1 mutation, and inhibition of mTOR signaling resulted in partial remission of the tumor. To explore the potential of mTOR inhibitors in sporadic acinar cell carcinoma, the LKB1 gene was investigated in five sporadic acinar cell carcinomas by sequence analysis, methylation analysis and mRNA expression. In addition, microsatellite instability and methylation of a number of tumor suppressor genes were investigated and KRAS, TP53, CDKN1A, SMAD4 and CTNNB1 were studied by mutation analysis and immunohistochemistry. No mutations, deletions or promoter hypermethylation of LKB1 were found in any of the sporadic acinar cell carcinomas, and mRNA expression of LKB1 was not altered. Amplifications at chromosome 20q and 19p were found in 100 and 80% of the cases, respectively. In addition, hypermethylation of one or more tumor suppressor genes was found in 80% of cases. One case harbored a TP53 mutation, and expression of SMAD4 and CTNNB1 was altered in one case each. No KRAS mutations or microsatellite instability were found. To conclude, no evidence for a role for LKB1 in tumorigenesis of sporadic pancreatic acinar cell carcinoma was found. However, copy number variations and hypermethylation were found in a majority of cases. Molecular pathways involved in acinar cell carcinoma-tumorigenesis differ from those involved in ductal pancreatic neoplasms. Further studies are needed to increase our understanding of molecular pathogenesis of acinar cell carcinoma, which may eventually result in development of new therapeutic targets.

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Source
http://dx.doi.org/10.1038/modpathol.2011.83DOI Listing

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