Frequent codeletion of p16/MTS1 and p15/MTS2 and genetic alterations in p16/MTS1 in pancreatic tumors

Naumann, Michael; Савицкая, Н. Г.; Eilert, Christina; Schramm, Alexander; Kalthoff, Holger; Schmiegel, Wolff

doi:10.1053/gast.1996.v110.pm8613012

Cited by 116 publications

(63 citation statements)

References 4 publications

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“…Capan2 is a well-characterized human pancreatic ductal adenocarcinoma cell line derived from the primary pancreatic tumor of a 56-year-old caucasian (Kalthoff et al, 1993;Berrozpe et al, 1994;Lohr et al, 1994;Naumann et al, 1996;Sipos et al, 2003). Capan2 was chosen as this cell line inherently expresses very low levels of CEACAM6 (Gardner-Thorpe et al, 2002;Duxbury et al, 2004).…”

Section: Ceacam6 Overexpression Increases Igf-i-stimulated Cellular Imentioning

confidence: 99%

Overexpression of CEACAM6 promotes insulin-like growth factor I-induced pancreatic adenocarcinoma cellular invasiveness

et al. 2004

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Section: Ceacam6 Overexpression Increases Igf-i-stimulated Cellular Imentioning

confidence: 99%

Overexpression of CEACAM6 promotes insulin-like growth factor I-induced pancreatic adenocarcinoma cellular invasiveness

et al. 2004

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“…The tumour suppressor genes p53 and p16 are frequently mutated with loss of function in pancreatic cancer. Up to 80% of cancers have no detectable p16 protein 5,6 due to homozygous deletion, mutation or promoter methylation. p53 is present in a mutated form in up to 60% of pancreatic cancers.…”

Section: Introductionmentioning

confidence: 99%

Adenovirus-mediated transfer of p53 and p16INK4a results in pancreatic cancer regression in vitro and in vivo

et al. 2001

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Pancreatic cancer has a very poor prognosis. Current chemotherapy and radiotherapy regimens are only moderately successful. The tumour suppressor genes p53 and p16INK4a encode cell cycle regulatory proteins that are important candidates for gene replacement therapy. Over 80% of pancreatic adenocarcinoma cases lack detectable p16 protein while over 60% contain mutated p53 protein. We used replication-deficient recombinant adenoviruses to reintroduce wild-type p16 and p53 into pancreatic cancer cells in vitro and into subcutaneous pancreatic tumours in an animal model to determine the effect on tumour growth. Significant growth inhibition was observed in all five human pancreatic cell lines with these viruses (P Ͻ 0.002) compared with simi-

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“…Less information is available regarding alterations of p16 and DPC4 in primary PDC and the only two available reports suggested that alterations in these two genes occur less frequently in primary PDC than in derived cell lines (Huang et al, 1996;Bartsch et al, 1999a). Studies on xenografts and cell lines have shown that homozygous deletions may account for up to half of all instances of inactivation of these genes Hahn et al, 1996;Naumann et al, 1996;Villanueva et al, 1998) although this phenomenon is difficult to demonstrate in primary PDC due to the high admixture of nonneoplastic cells in these tissues. In addition, the p16 gene may also be silenced by promoter methylation , an epigenetic event not yet examined in a series of primary PDC.…”

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confidence: 99%

Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis

et al. 2001

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Summary Alterations of K-ras, p53, p16 and DPC4/Smad4 characterize pancreatic ductal cancer (PDC). Reports of inactivation of these latter two genes in pancreatic endocrine tumours (PET) suggest that common molecular pathways are involved in the tumorigenesis of pancreatic exocrine and endocrine epithelia. We characterized 112 primary pancreatic tumours for alterations in p16 and DPC4 and immunohistochemical expression of DPC4. The cases included 34 PDC, 10 intraductal papillary-mucinous tumours (IPMT), 6 acinar carcinomas (PAC), 5 solid-pseudopapillary tumours (SPT), 16 ampulla of Vater cancers (AVC) and 41 PET. All tumours were also presently or previously analysed for K-ras and p53 mutations and allelic loss at 9p, 17p and 18q. Alterations in K-ras, p53, p16 and DPC4 were found in 82%, 53%, 38% and 9% of PDC, respectively and in 47%, 60%, 25% and 6% of AVC. Alterations in these genes were virtually absent in PET, PAC or SPT, while in IPMT only K-ras mutations were present (30%). Positive immunostaining confirmed the absence of DPC4 alterations in all IPMT, SPT, PAC and PET, while 47% of PDC and 38% of AVC were immunonegative. These data suggest that pancreatic exocrine and endocrine tumourigenesis involves different genetic targets and that among exocrine pancreatic neoplasms, only ductal and ampullary cancers share common molecular events.

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Frequent codeletion of p16/MTS1 and p15/MTS2 and genetic alterations in p16/MTS1 in pancreatic tumors

Cited by 116 publications

References 4 publications

Overexpression of CEACAM6 promotes insulin-like growth factor I-induced pancreatic adenocarcinoma cellular invasiveness

Overexpression of CEACAM6 promotes insulin-like growth factor I-induced pancreatic adenocarcinoma cellular invasiveness

Adenovirus-mediated transfer of p53 and p16INK4a results in pancreatic cancer regression in vitro and in vivo

Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis

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