Table 3.
Stage-specific inhibition of DMBA-induced mammary alveolar lesions (MAL) by 25(OH)D3 in mouse mammary organ culture
| Treatment | Days of treatment | Number of glands with lesions (%incidence) | %inhibition | Significance (P valuea) |
|---|---|---|---|---|
| IPAF control | – | 0/10 | – | – |
| DMBA | – | 13/15 (86.7) | – | – |
| DMBA + 25(OH)D3––250 nM | 0–4 | 8/14 (57.1) | 34.1 | 0.1732 |
| DMBA + 25(OH)D3––250 nM | 4–10 | 3/14 (21.4) | 75.3 | 0.0016 |
| DMBA + 25(OH)D3––250 nM | 0–10 | 1/15 (6.7) | 92.3 | <0.0001 |
| DMBA + 1,25(OH)2D3––100 nM | 4–10 | 0/15 (0) | 100 | <0.0001 |
| DMBA + Aspirin––100 nM | 0–4 | 2/15 (13.3) | 84.7 | 0.0003 |
χ2 test, in comparison with DMBA control
1,25(OH)2D3 served as a positive control for inhibition of promotion of MAL; aspirin served as a positive control for inhibition of initiation of MAL. 25(OH)D3 mainly exhibited inhibition at the promotion stage of DMBA-induced MAL, similar to that of 1,25(OH)2D3. But treatment during day 1–10 with 25(OH)D3 generated best inhibitory effect on MAL development