Table 2.
Genomic Alterations Series in Pancreatic Acinar Cell Carcinoma
| Study | Genetic Alteration |
|---|---|
| Hoorens et al15 | KRAS (4%) and TP53 (0%) |
| Rigaud et al22 | LOH in chromosomes 1p, 4q, and 17p (>70% of pts); chromosomes 11q, 13q, 15q, and 16q (60%–70% of pts); and chromosomes 3q, 6q, 8q, 18q, and 21q (50%–60% of pts) |
| Taruscio et al23 | Gains in chromosomes 1 (1q21, 66% of pts; 1q42, 50% of pts), 12 (12p11.2, 66% of pts), and X (Xq12–21, 50% of pts) and loss of sequences at chromosomes 16p (16p13.2–p13.1, 50% of pts) and 16q (16q23, 50% of pts) |
| Abraham et al16 | APC/β-catenin pathway 23.5% (4/21 pts); allelic loss of 11p15.5, 50% (6/12 pts); MSI, 23% (3/13 pts) |
| Furlan et al24 | APC loss (48%), methylation (56%), mutations (7%) |
| Liu et al25 | dMMR in 11% (2/18 pts) |
| Bergmann et al19 |
c-MYC amplification (17% of pts) and deleted colon cancer (79% of pts) EGFR (42%), HSP90 (98%), LICAM (72%), loss of MGMT (26%) and KRAS (3%) |
| Jiao et al17 | SMAD4 (26%); JAK1 (17%); TP53, BRAF, RB1 (13% each); GNAS, APC, PTEN GNAS, ARID 1A, MLL2 (9% each); ATM, BRCA2, PALB2, MEN1, RNF 43 (4% each) |
| Furukawa et al18 | BRCA2 (45%); FAT1, FAT3, FAT4 (57%) |
| Dewald et al42 | Gains of CTNNB1 (80%), loss of CTNNB1 (20%), gain of APC (20%), loss of APC (20%), gain of CDKN2A (20%), loss of BRCA2 (40%), gain of EGFR (20%), loss of ERBB2 (20%), loss of TYMS (40%), loss of TYMP (40%) |
Abbreviations: dMMR, DNA mismatch repair deficiency; LOH, loss of heterozygosity; MSI, microsatellite instability; pts, patients.