Molecular analysis of mucinous nonneoplastic cyst of the pancreas

Bing Zhu, Sydney D. Finkelstein, Gong Feng, Rajesh N. Keswani, Xiaoqi Lin*

*Corresponding author for this work

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Although a mucinous nonneoplastic cyst (MNNC) of the pancreas is defined as a benign nonneoplastic lesion with no malignant potential, its histogenesis and etiology are still uncertain. To explore the origin and development of MNNC, we searched for neoplasia-associated mutational change in oncogene and tumor suppressor genes. Specifically, we analyzed KRAS oncogene mutations by polymerase chain reaction/dideoxy DNA (Sanger) sequencing and tumor suppression gene deletion by loss of heterozygosity (LOH) using polymerase chain reaction/capillary gel electrophoresis for a panel of 16 polymorphic microsatellite repeat markers targeting common tumor suppression gene loci at 1p, 3p, 5q, 9p, 10q, 17p, 17q, 18q, 21q, and 22q on DNA isolated from the cystic lining epithelium microdissected from 15 surgically diagnosed MNNCs by microdissection of unstained histologic sections of fixed resection specimens. DNA mutations were demonstrated in 4 of 15 cases: 1 with KRAS mutation at codon 12 glycine (G) substitution by aspartic acid (D) (G12D), 1 with KRAS mutation at 12 glycine (G) substitution by arginine (R) (G12R), 1 with LOH at 10q (PTEN), and 1 with LOH at 17q (RNF43). Therefore, although the genomic mutation rate detected in MNNC is relatively low, our results indicate that MNNCs may acquire genetic alteration similar to low-grade pancreatic intraepithelial neoplasia, furthering debate of the true nature of these lesions.

Original languageEnglish (US)
Pages (from-to)159-163
Number of pages5
JournalHuman pathology
Volume55
DOIs
StatePublished - Sep 1 2016

Fingerprint

Cysts
Pancreas
Loss of Heterozygosity
Mutation
Oncogenes
Microsatellite Repeats
Glycine
Neoplasms
D-Aspartic Acid
Polymerase Chain Reaction
Microdissection
DNA
Gene Deletion
Capillary Electrophoresis
Mutation Rate
Tumor Suppressor Genes
DNA Sequence Analysis
Codon
Arginine
Epithelium

Keywords

  • Histomorphology
  • KRAS
  • Loss of heterozygosity
  • MNNC
  • Molecular analysis

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Zhu, Bing ; Finkelstein, Sydney D. ; Feng, Gong ; Keswani, Rajesh N. ; Lin, Xiaoqi. / Molecular analysis of mucinous nonneoplastic cyst of the pancreas. In: Human pathology. 2016 ; Vol. 55. pp. 159-163.
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Molecular analysis of mucinous nonneoplastic cyst of the pancreas. / Zhu, Bing; Finkelstein, Sydney D.; Feng, Gong; Keswani, Rajesh N.; Lin, Xiaoqi.

In: Human pathology, Vol. 55, 01.09.2016, p. 159-163.

Research output: Contribution to journalArticle

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AU - Zhu, Bing

AU - Finkelstein, Sydney D.

AU - Feng, Gong

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AB - Although a mucinous nonneoplastic cyst (MNNC) of the pancreas is defined as a benign nonneoplastic lesion with no malignant potential, its histogenesis and etiology are still uncertain. To explore the origin and development of MNNC, we searched for neoplasia-associated mutational change in oncogene and tumor suppressor genes. Specifically, we analyzed KRAS oncogene mutations by polymerase chain reaction/dideoxy DNA (Sanger) sequencing and tumor suppression gene deletion by loss of heterozygosity (LOH) using polymerase chain reaction/capillary gel electrophoresis for a panel of 16 polymorphic microsatellite repeat markers targeting common tumor suppression gene loci at 1p, 3p, 5q, 9p, 10q, 17p, 17q, 18q, 21q, and 22q on DNA isolated from the cystic lining epithelium microdissected from 15 surgically diagnosed MNNCs by microdissection of unstained histologic sections of fixed resection specimens. DNA mutations were demonstrated in 4 of 15 cases: 1 with KRAS mutation at codon 12 glycine (G) substitution by aspartic acid (D) (G12D), 1 with KRAS mutation at 12 glycine (G) substitution by arginine (R) (G12R), 1 with LOH at 10q (PTEN), and 1 with LOH at 17q (RNF43). Therefore, although the genomic mutation rate detected in MNNC is relatively low, our results indicate that MNNCs may acquire genetic alteration similar to low-grade pancreatic intraepithelial neoplasia, furthering debate of the true nature of these lesions.

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