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. 2002 Mar;160(3):953–962. doi: 10.1016/s0002-9440(10)64917-6

Table 1.

Genetic Alterations in Pancreatic Acinar Cell Carcinomas

Case Age/sex p53 accumulation Dpc4 loss MSI Nuclear β-catenin β-catenin mutation APC mutation 11p LOH
A1 15 /F MSS Wild-type Wild-type
A2 21 /F MSS Wild-type 1444X
A3 32 /F MSS Wild-type Wild-type
A4 73 /F MSI-L Wild-type Wild-type +
A5 51 /M MSI-L 50% Wild-type Wild-type
A6 55 /F MSS Wild-type Wild-type N/I
A7 2 /F MSS Wild-type Wild-type +
A8 70 /M MSS Wild-type Wild-type
A9 76 /M MSS Wild-type Wild-type +
A10 58 /M MSS Wild-type Wild-type
A11 31 /M MSS Wild-type Wild-type +
A12 80 /M MSS Wild-type Wild-type +
A13 31 /M N/N 20% T41I Wild-type N/N
A14 61 /M N/A N/A N/A N/A N/A N/A N/A
A15 63 /M N/A N/A N/A N/A
A16 76 /M N/N 60% Wild-type 1554–1556FS N/N
A17 54 /M N/A N/A N/A N/A
A18 60 /M N/N Wild-type 1554–1556FS N/N
A19 75 /M MSI-H Wild-type Wild-type +
A20 74 /M N/A N/A N/A N/A
A21 79 /M N/N Wild-type Wild-type N/N

Locations of somatic mutations in β-catenin and APC are shown by codon.

Nuclear β-catenin accumulation was evaluated based on the percentage of strongly staining tumor cell nuclei.

FS, frameshift mutation; LOH, loss of heterozygosity; MSI-H, microsatellite instability-high; MSI-L, microsatellite instability-low; MSS, microsatellite stable; N/A, DNA did not amplify or immunohistochemistry failed; N/I, non-informative for allelic loss; N/N, no corresponding normal tissue for evaluation of allelic loss or MSI assays.