|1.||Herbst, Uta: 1 article (04/2006)|
|2.||Steinberg, Pablo: 1 article (04/2006)|
|3.||Fuchs, Judith Iris: 1 article (04/2006)|
|4.||Teubner, Wera: 1 article (04/2006)|
10/01/1994 - "These results indicate that Ki-ras and Ha-ras mutations are not involved in the induction of rat mammary tumors by anti-B[c]PhDE. "
10/01/1994 - "Therefore, we analyzed rat mammary tumors and mouse skin tumors induced by anti-B[c]PhDE for mutations at codons 12, 13 and 61 of the Ki-ras and Ha-ras genes. "
04/15/2006 - "Within 6 weeks after injection, eight animals out of eight injected with HCEC(B[c]PhDE) or HCEC(N-OH-PhIP) cells developed tumors at the site of injection, thus demonstrating the high tumorigenic potential of the HCEC(B[c]PhDE) and HCEC(N-OH-PhIP) cell cultures. "
10/01/1996 - "The higher formation of B[c]PhDE-DNA adducts by (+/-)-B[c]Ph-3,4-dihydrodiol correlates with the greater potency of (+/-)-B[c]Ph-3,4-dihydrodiol than of B[c]Ph as a tumor initiator in mouse skin. "
|2.||Breast Neoplasms (Breast Cancer)
05/01/1997 - "In mouse epidermis, the weak ability of B[c]Ph to increase hydrocarbon-metabolizing activity and the increase in mainly P4501A1, leading to formation of the less carcinogenic stereoisomer B[c]PhDE-1, may explain the low carcinogenic activity of B[c]Ph. In a human mammary carcinoma cell line, treatment with B[c]Ph increases mainly P4501B1 and results in formation of a higher proportion of the more carcinogenic B[c]PhDE-2. This indicates that cells in which B[c]Ph treatment increases P4501B1 levels effectively activate B[c]Ph to potent carcinogenic metabolites."
|4.||2- hydroxyamino- 1- methyl- 6- phenylimidazo(4,5- b)pyridine