| First Author | Yamamoto M | Year | 2002 |
| Journal | Cancer Lett | Volume | 179 |
| Issue | 2 | Pages | 121-32 |
| PubMed ID | 11888666 | Mgi Jnum | J:75233 |
| Mgi Id | MGI:2176116 | Doi | 10.1016/s0304-3835(02)00013-7 |
| Citation | Yamamoto M, et al. (2002) Independent variation in susceptibilities of six different mouse strains to induction of pepsinogen-altered pyloric glands and gastric tumor intestinalization by N-methyl-N-nitrosourea. Cancer Lett 179(2):121-32 |
| abstractText | Strain differences in susceptibility regarding stomach carcinogenesis due to N-methyl-N-nitrosourea were examined in males of six strains of mice: BALB/cA (BALB), C57BL/6N (C57BL6), CBA/JN (CBA), C3H/HeN (C3H), DBA/2N (DBA/2), and CD-1 (ICR). The frequency of pepsinogen-altered pyloric glands (PAPGs), putative precancerous lesions, was highest (19.6plus minus9.9%) in the BALB and lowest in the ICR (12.3plus minus5.7%) mice (P<0.05). Incidences of adenocarcinomas at week 52 were 59.3% (16 of 27) and 18.5% (5 of 27), respectively (P<0.005). Invasion also tended to be deepest in BALB compared with the other strains. Intestinal alkaline phosphatase-positive intestinal type cells were observed heterogeneously in some hyperplasias, adenomas and adenocarcinomas consisting of gastric type cells. Thus, intestinalization appeared to occur at random in both non-neoplastic and monoclonal neoplastic lesions, making it unlikely that IAP-positive cells could be precursors of gastric tumors. In contrast, the data suggest a direct histogenetic role for the PAPG, a useful preneoplastic marker lesion in mouse strains. |
