Skip to main content
. 2002 Apr;160(4):1361–1369. doi: 10.1016/s0002-9440(10)62563-1

Table 2.

Genetic Alterations in Pancreatic Solid-Pseudopapillary Tumors

Case β-catenin mutation Nuclear β-catenin, % Nuclear cyclin D1, % K-ras mutation p53 accumulation Dpc4 loss
S1 G34V >90 50 Wild-type Intact
S2 S37F >90 30 Wild-type Intact
S3 D32Y >90 40 Wild-type Intact
S4 G34V >90 50 Wild-type Intact
S5 S37F >90 70 Wild-type Intact
S6 G34V >90 10 Wild-type + (Patchy) Intact
S7 S33A >90 20 Wild-type Intact
S8 S37F >90 10 Wild-type Intact
S9 D32V >90 10 Wild-type Intact
S10 Wild-type >90 Wild-type Intact
S11 D32N 20 Wild-type N/A
S12 S37F 30 Wild-type Intact
S13 S37F >90 15 Wild-type Intact
S14 Wild-type >90 Wild-type 40% Intact
S15 G34R >90 10 Wild-type Intact
S16 S37F >90 30 Wild-type Intact
S17 D32Y >90 30 Wild-type N/A
S18 D32N >90 Wild-type Intact
S19 D32Y >90 10 Wild-type + (Patchy) N/A
S20 G34R N/A N/A Wild-type N/A N/A

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

Nuclear β-catenin, cyclin D1, and p53 accumulation were evaluated based on the percentage of labeled tumor cell nuclei.

N/A, immunohistochemistry failed.