Abstract
The widespread use of FVB/N mice for the establishment of transgenic lines containing active oncogenes suggested the importance of testing the parent FVB/N mice for sensitivity to experimental carcinogenesis. After initiation of mouse skin by a single treatment with 7, 12-dimethylbenz[a]anthracene (DMBA) and promotion by 20 weekly applications of 12-O-tetradecanoylphorbol-13-acetate (TPA), the skin tumor incidence was compared in FVB/N mice, TPA-sensitive (SENCAR and CD-I) and TPA-resistant mice (BALB/c and C57BL/6). Initiation by 25 μg DMBA followed by promotion with a low dose of TPA (2 μg/week) induced one or more papillomas in only 25% of FVB/N mice, compared with 100% in SENCAR, 53% in CD-I, 17% in BALB/c and 0% in C57BL/6 mice. At a more effective dose of TPA (5 /ig/week), FVB/N mice initiated by 5, 25 or 100μg DMBA developed 3.4, 6.9 and 11.8 papillomas per mouse. In contrast, the incidence of squamous cell carcinomas (SCCs) (17-18/30 mice) did not increase with DMBA dose. TPA promotion of non-initiated mice induced only six papillomas, but three progressed to SCCs, a high rate of malignant conversion. Skin tumor induction by 20 weekly treatments with 10 μg DMBA produced few papillomas, but 50.0% of the papillomas progressed to carcinomas in FVB/N mice, compared with 9.15% in SENCAR, 37.5% in CD-I, 23.1% in BALB/c and 15.0% in C57CL/6 mice. The first carcinomas appeared after 14 weeks in FVB/N, 24 weeks in SENCAR, 26 weeks in CD-I and C57BL/6 and 34 weeks in BALB/c mice. Thus, FVB/N mice develop an unusually high incidence of SCCs after treatment with repeated DMBA, DMBA initiation-TPA promotion and even TPA alone.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2353-2358 |
| Number of pages | 6 |
| Journal | Carcinogenesis |
| Volume | 14 |
| Issue number | 11 |
| DOIs | |
| State | Published - Nov 1 1993 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Cancer Research
Cite this
}
Fvb/n mice : An inbred strain sensitive to the chemical induction of squamous cell carcinomas in the skin. / Hennings, Henry; Glick, Adam B.; Lowry, David T.; Krsmanovic, Ljubicka S.; Sly, Linda M.; Yuspa, Stuart H.
In: Carcinogenesis, Vol. 14, No. 11, 01.11.1993, p. 2353-2358.Research output: Contribution to journal › Article
TY - JOUR
T1 - Fvb/n mice
T2 - An inbred strain sensitive to the chemical induction of squamous cell carcinomas in the skin
AU - Hennings, Henry
AU - Glick, Adam B.
AU - Lowry, David T.
AU - Krsmanovic, Ljubicka S.
AU - Sly, Linda M.
AU - Yuspa, Stuart H.
PY - 1993/11/1
Y1 - 1993/11/1
N2 - The widespread use of FVB/N mice for the establishment of transgenic lines containing active oncogenes suggested the importance of testing the parent FVB/N mice for sensitivity to experimental carcinogenesis. After initiation of mouse skin by a single treatment with 7, 12-dimethylbenz[a]anthracene (DMBA) and promotion by 20 weekly applications of 12-O-tetradecanoylphorbol-13-acetate (TPA), the skin tumor incidence was compared in FVB/N mice, TPA-sensitive (SENCAR and CD-I) and TPA-resistant mice (BALB/c and C57BL/6). Initiation by 25 μg DMBA followed by promotion with a low dose of TPA (2 μg/week) induced one or more papillomas in only 25% of FVB/N mice, compared with 100% in SENCAR, 53% in CD-I, 17% in BALB/c and 0% in C57BL/6 mice. At a more effective dose of TPA (5 /ig/week), FVB/N mice initiated by 5, 25 or 100μg DMBA developed 3.4, 6.9 and 11.8 papillomas per mouse. In contrast, the incidence of squamous cell carcinomas (SCCs) (17-18/30 mice) did not increase with DMBA dose. TPA promotion of non-initiated mice induced only six papillomas, but three progressed to SCCs, a high rate of malignant conversion. Skin tumor induction by 20 weekly treatments with 10 μg DMBA produced few papillomas, but 50.0% of the papillomas progressed to carcinomas in FVB/N mice, compared with 9.15% in SENCAR, 37.5% in CD-I, 23.1% in BALB/c and 15.0% in C57CL/6 mice. The first carcinomas appeared after 14 weeks in FVB/N, 24 weeks in SENCAR, 26 weeks in CD-I and C57BL/6 and 34 weeks in BALB/c mice. Thus, FVB/N mice develop an unusually high incidence of SCCs after treatment with repeated DMBA, DMBA initiation-TPA promotion and even TPA alone.
AB - The widespread use of FVB/N mice for the establishment of transgenic lines containing active oncogenes suggested the importance of testing the parent FVB/N mice for sensitivity to experimental carcinogenesis. After initiation of mouse skin by a single treatment with 7, 12-dimethylbenz[a]anthracene (DMBA) and promotion by 20 weekly applications of 12-O-tetradecanoylphorbol-13-acetate (TPA), the skin tumor incidence was compared in FVB/N mice, TPA-sensitive (SENCAR and CD-I) and TPA-resistant mice (BALB/c and C57BL/6). Initiation by 25 μg DMBA followed by promotion with a low dose of TPA (2 μg/week) induced one or more papillomas in only 25% of FVB/N mice, compared with 100% in SENCAR, 53% in CD-I, 17% in BALB/c and 0% in C57BL/6 mice. At a more effective dose of TPA (5 /ig/week), FVB/N mice initiated by 5, 25 or 100μg DMBA developed 3.4, 6.9 and 11.8 papillomas per mouse. In contrast, the incidence of squamous cell carcinomas (SCCs) (17-18/30 mice) did not increase with DMBA dose. TPA promotion of non-initiated mice induced only six papillomas, but three progressed to SCCs, a high rate of malignant conversion. Skin tumor induction by 20 weekly treatments with 10 μg DMBA produced few papillomas, but 50.0% of the papillomas progressed to carcinomas in FVB/N mice, compared with 9.15% in SENCAR, 37.5% in CD-I, 23.1% in BALB/c and 15.0% in C57CL/6 mice. The first carcinomas appeared after 14 weeks in FVB/N, 24 weeks in SENCAR, 26 weeks in CD-I and C57BL/6 and 34 weeks in BALB/c mice. Thus, FVB/N mice develop an unusually high incidence of SCCs after treatment with repeated DMBA, DMBA initiation-TPA promotion and even TPA alone.
UR - http://www.scopus.com/inward/record.url?scp=0027496668&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027496668&partnerID=8YFLogxK
U2 - 10.1093/carcin/14.11.2353
DO - 10.1093/carcin/14.11.2353
M3 - Article
C2 - 8242866
AN - SCOPUS:0027496668
VL - 14
SP - 2353
EP - 2358
JO - Carcinogenesis
JF - Carcinogenesis
SN - 0143-3334
IS - 11
ER -