TABLE 6.
% gin fisha (n) | % wild typeb (n) | |
---|---|---|
Intestinal adenocarcinoma | 10 (5) | 0 |
Pancreatic adenocarcinoma | 2 (1) | 3 (2) |
Cholangiocarcinoma | 8 (4) | 0 |
Testicular neoplasm (invasive) | 6 (2)c | 0 |
Malignant peripheral nerve sheath tumor d | 2 (1) | 0 |
Primitive neuroectodermal tumor d | 2 (1) | 0 |
Poorly differentiated renal cell tumor | 0 | 1.5 (1) |
Total tumors | 14/50 = 28% | 3/67 = 5% |
Adjustment for 5.0% background | (14 − 2) = 12 | |
Adjustment for gin carrier frequency | 12 × 2 = 24 | |
Corrected tumor frequencye | 24/50 = 48% | |
= 9.6-fold increase in tumor incidence, P < 0.001 |
A total of 50 gin-10 family fish were included in this experiment, 32 male and 18 female, between 30 and 34 months of age. These fish were a mixture of gin-10/+ and +/+ genotypes with a predicted distribution of 50% gin carriers.
A total of 67 wild-type fish were included in this experiment, 29 male and 38 female, between 30 and 34 months of age. These fish were also descended from ENU males from which the gin mutants were derived, but had not exhibited mosaic eyes. They were outcrossed to lab stocks for several generations.
This frequency is calculated from the number of males in this group (2/32).
These tumors occurred in gin fish that were known to be carriers.
This is likely an underestimate, since loss of fish at an earlier age is expected to include more tumor-bearing animals (presumed gin carriers) that were undetected than would be seen in wild-type animals.