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. 2001 Nov;159(5):1619–1627. doi: 10.1016/s0002-9440(10)63008-8

Table 1.

Clinicopathological Findings and Genetic Alterations in Pancreatoblastomas

Case Age/sex K-ras p53 Accumulation Dpc4 loss Nuclear β-catenin accumulation, % β-Catenin APC alterations 11p LOH
P1 5 /M Wild type 25 N32H N/E
P2 3 /M N/A 15 Wild type N/A N/A
P3 4 /M Wild type N/A 25 S33F N/E N/I
P4 45 /F Wild type + (diffuse) 90 S37F N/E +
P5 51 /F Wild type + (focal) 40 Wild type Germline + LOH +
P6 6 /M Wild type Wild type Wild type +
P7 13 /F Wild type Wild type Wild type +
P8 5 /F Wild type 90 G34R N/E +
P9 3.5 /F Wild type 40 N32H N/E +

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

Nuclear β-catenin accumulation was evaluated based on the percentage of strongly staining tumor cell nuclei. Cytoplasmic accumulation was found to mirror nuclear staining in pancreatoblastomas.

LOH, loss of heterozygosity; N/A, DNA did not amplify or immunohistochemistry failed; N/E, not evaluated due to the presence of mutation detected elsewhere; N/I, noninformative for allelic loss assays.