TABLE 3.
Incidence, latency, and molecular characterization of SL3-3dm-induced tumors of different types
| Tumor phenotypea | No. of miceb | Mean tumor latency (days) ± SD | No. of clonal ecotropic integrationsc
|
No. of second-site altered proviral enhancer structuresd | |
|---|---|---|---|---|---|
| Range | Avg | ||||
| CD3+, CD3+ CD138+, or CD3− CD4+ | 15 | 266 ± 63 | 0-3 | 1-2 | |
| T-cell lymphomas [TCRβ r, IgH g/r, and Ig(κ) g]e | 7 | 240 ± 72 | 0-3 | 1-2 | 11/13 (5/7) |
| T-cell lymphoblastic lymphoma | 4 | 189 ± 32 | 1-2 | 1-2 | 10/10 (4/4) |
| Small T-cell lymphoma | 2 | 290 ± 19 | 0-3 | 1-2 | 0/2 (0/2) |
| No histologic diagnosis | 1 | 349 | 1 | 1 | 1/1 (1/1) |
| Other CD3+ typesf | 9 | 285 ± 43 | 0-3 | 1-2 | 4/17 (2/9) |
| Mature T-cell lymphoma, not otherwise specified | 3 | 246 ± 16 | 0-2 | 1-2 | 0/7 (0/3) |
| Small T-cell lymphoma | 2 | 339 ± 14 | 0-2 | 1-2 | 4/4 (2/2) |
| Diffuse large B-cell lymphoma, histiocyte-associated | 2 | 313 ± 14 | 2 | 2 | 0/3 (0/2) |
| No histologic diagnosis | 2 | 287 ± 60 | 2-3 | 2-3 | 0/2 (0/1) |
| CD11b+ (Myeloid leukemia with maturation) | 14 | 267 ± 49 | 0-4 | 1-2 | 0/22 (0/14) |
| CD43+ only | 7 | 258 ± 41 | 0-3 | 1-2 | 7/9 (5/7) |
| Erythroid leukemia | 2 | 292 ± 16 | 0-2 | 1-2 | 0/2 (0/2) |
| Myeloid leukemia without maturation | 3 | 232 ± 47 | 0-2 | 1 | 5/5 (3/3) |
| Pre-T-cell lymphoblastic lymphoma | 1 | 288 | 2 | 2 | 1/1 (1/1) |
| No histologic diagnosis | 1 | 242 | 3 | 3 | 1/1 (1/1) |
| CD138+ CD43+ | 1 | 177 | 1 | 1 | 0/1 (0/1) |
| Heterogeneous | 1 | 260 | 1 | 1 | 0/1 (0/1) |
| Total, all types | 37 | 253 ± 53 | 0-4 | 1-2 | |
As determined by three-color flow cytometry and molecular and histopathological analyses.
A few mice had tumors of two different types and, hence, appear twice in the table.
Number of clonal ecotropic provirus integrations in tumors of each phenotypic group, as detected by Southern blot hybridization.
Number of tumors with complex proviral enhancer structures/number of tumors analyzed (number of mice with complex enhancer structures detected/number of mice analyzed), determined by PCR amplification and sequencing of proviral enhancer sequences from genomic tumor DNAs. See Fig. 8 for a schematic presentation of enhancer structures with second-site alterations.
T-cell lymphoma subgroup of tumors with TCRβ clonally rearranged (r), IgH in germline configuration or clonally rearranged (g/r), and Ig(κ) in germline configuration (g), as determined by Southern blot analyses.
CD3+ type tumors not included in the T-cell lymphoma subgroup. Based on histopathological evidence; these cases included mature T-cell lymphomas (not otherwise specified), small T-cell lymphomas without detectable TCRβ rearrangements, and histiocyte-associated diffuse large B-cell lymphomas.