Tags

Type your tag names separated by a space and hit enter

Tumor-suppressing pathways in cystic pancreatic tumors.
Pancreas 2003; 26(1):42-8P

Abstract

INTRODUCTION AND AIMS

Serous and mucinous cystic pancreatic tumors have different clinical behavior. We evaluated whether they also have genotypic differences by analyses of the tumor suppressor genes, p16INK4a, p53, and DPC4.

METHODOLOGY

Seven serous cystadenomas (SCA) and seven malignant mucinous cystadenocarcinomas (MCC) were analyzed for alterations in the tumor suppressor genes p16INK4a, p53, and DPC4 by single-strand conformational variant analysis, direct sequencing, and immunohistochemical analysis. Methylation-specific polymerase chain reaction analysis was performed to identify p16INK4a promoter hypermethylation. Clinical data were compared with genetic data.

RESULTS

None of the seven patients with SCAs but five of the seven patients with MCCs died of the tumor after a median follow-up of 44.5 months (range, 4-169 months). All seven MCCs had alterations in at least one tumor suppressor gene compared with none of the seven SCAs. Of the seven MCCs, three had inactivating p16INK4a promoter hypermethylation, five had p53 alterations, and three had DPC4 mutations.

CONCLUSIONS

The tumor suppressor genes p16INK4a, p53, and appear to play an important role in the tumorigenesis of MCCs but not SCAs. These molecular data underscore the clinical and histologic differences of serous and mucinous cystic pancreatic tumors.

Authors+Show Affiliations

Department of General Surgery, Philipps University of Marburg, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

12499916

Citation

Gerdes, Berthold, et al. "Tumor-suppressing Pathways in Cystic Pancreatic Tumors." Pancreas, vol. 26, no. 1, 2003, pp. 42-8.
Gerdes B, Wild A, Wittenberg J, et al. Tumor-suppressing pathways in cystic pancreatic tumors. Pancreas. 2003;26(1):42-8.
Gerdes, B., Wild, A., Wittenberg, J., Barth, P., Ramaswamy, A., Kersting, M., ... Bartsch, D. K. (2003). Tumor-suppressing pathways in cystic pancreatic tumors. Pancreas, 26(1), pp. 42-8.
Gerdes B, et al. Tumor-suppressing Pathways in Cystic Pancreatic Tumors. Pancreas. 2003;26(1):42-8. PubMed PMID: 12499916.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tumor-suppressing pathways in cystic pancreatic tumors. AU - Gerdes,Berthold, AU - Wild,Anja, AU - Wittenberg,Judith, AU - Barth,Peter, AU - Ramaswamy,Annette, AU - Kersting,Michael, AU - Lüttges,Jutta, AU - Klöppel,Günter, AU - Bartsch,Detlef K, PY - 2002/12/25/pubmed PY - 2003/1/9/medline PY - 2002/12/25/entrez SP - 42 EP - 8 JF - Pancreas JO - Pancreas VL - 26 IS - 1 N2 - INTRODUCTION AND AIMS: Serous and mucinous cystic pancreatic tumors have different clinical behavior. We evaluated whether they also have genotypic differences by analyses of the tumor suppressor genes, p16INK4a, p53, and DPC4. METHODOLOGY: Seven serous cystadenomas (SCA) and seven malignant mucinous cystadenocarcinomas (MCC) were analyzed for alterations in the tumor suppressor genes p16INK4a, p53, and DPC4 by single-strand conformational variant analysis, direct sequencing, and immunohistochemical analysis. Methylation-specific polymerase chain reaction analysis was performed to identify p16INK4a promoter hypermethylation. Clinical data were compared with genetic data. RESULTS: None of the seven patients with SCAs but five of the seven patients with MCCs died of the tumor after a median follow-up of 44.5 months (range, 4-169 months). All seven MCCs had alterations in at least one tumor suppressor gene compared with none of the seven SCAs. Of the seven MCCs, three had inactivating p16INK4a promoter hypermethylation, five had p53 alterations, and three had DPC4 mutations. CONCLUSIONS: The tumor suppressor genes p16INK4a, p53, and appear to play an important role in the tumorigenesis of MCCs but not SCAs. These molecular data underscore the clinical and histologic differences of serous and mucinous cystic pancreatic tumors. SN - 1536-4828 UR - https://www.unboundmedicine.com/medline/citation/12499916/Tumor_suppressing_pathways_in_cystic_pancreatic_tumors_ L2 - http://dx.doi.org/10.1097/00006676-200301000-00008 DB - PRIME DP - Unbound Medicine ER -