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Updated: Aug 6, 2026
Cell Population Analyses During Skin Carcinogenesis
Published on: August 21, 2013
Multigenic control of skin tumor susceptibility in SENCARA/Pt mice
B A Mock1, D T Lowry, I Rehman
1Laboratory of Genetics, DBS, NCI, National Institutes of Health, Bethesda, MD 20892-4255, USA.
Abstract:
Skin tumors induced in mice by initiation-promotion (2 microg DMBA-2 microg TPA) protocols were found to be under multigenic control. Eighty-one N2 mice from the cross (BALB/cAnPt x SENCARA/Pt)F1 x SENCARA/Pt that were either solidly resistant (no papillomas) or highly susceptible (> or = 7 papillomas/mouse) were subjected to a 'genome scan' using 89 microsatellite markers to check for associations with susceptible and resistant phenotypes. A locus on Chr 5 (Skts4) was found to control the susceptibility of SENCARA/Pt mice and the resistance of BALB/cAnPt mice to papilloma formation. In addition, higher than expected linkage scores were seen for the markers D9Mit271, D11Mit268 and D12Mit56. Further work is required to establish whether genes determining papilloma formation are located in these regions of the genome. In general, no evidence was seen for loss of heterozygosity in microsatellite markers on Chrs 5, 9 and 11 in 17 microdissected papillomas from (BALB/c x SENCARA)F1 hybrid mice.
Insights
Skin tumor development in mice is controlled by multiple genes. A specific genetic locus on chromosome 5 (Skts4) influences susceptibility and resistance to papilloma formation, indicating a multigenic control of skin tumors.
Area of Science:
- Genetics
- Oncology
- Dermatology
Background:
- Skin tumors, such as papillomas, can be induced in mice using chemical carcinogens like DMBA and TPA.
- The development of chemically induced skin tumors is a complex process influenced by genetic factors.
Purpose of the Study:
- To identify genetic loci associated with susceptibility and resistance to chemically induced skin tumors in mice.
- To investigate the genetic basis of multigenic control in skin tumor formation.
Main Methods:
- A genome scan was performed on 81 N2 mice derived from a cross between BALB/cAnPt and SENCARA/Pt strains.
- Eighty-nine microsatellite markers were used to analyze associations between genetic loci and tumor phenotypes (resistant vs. susceptible).
- Loss of heterozygosity analysis was conducted on microdissected papillomas.
Main Results:
- A significant genetic locus on chromosome 5 (Skts4) was identified, controlling both the resistance of BALB/cAnPt mice and the susceptibility of SENCARA/Pt mice to papilloma formation.
- Elevated linkage scores were observed for markers on chromosomes 9 and 11, suggesting potential involvement in tumor development.
- No evidence of loss of heterozygosity was found in the analyzed microsatellite markers on chromosomes 5, 9, and 11 in the examined papillomas.
Conclusions:
- Skin tumor formation is under multigenic control, with a major locus (Skts4) on chromosome 5 playing a key role.
- Further investigation is warranted to confirm the role of genetic regions on chromosomes 9 and 11 in papilloma development.
- The identified genetic locus provides a target for understanding the mechanisms underlying skin tumor susceptibility and resistance.
