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Basal cell carcinomas in mice overexpressing sonic hedgehog
1Howard Hughes Medical Institute, Department of Dermatology, Stanford University School of Medicine, Stanford, CA 94305-5427, USA.
Science (New York, N.Y.)
|May 2, 1997
Summary
Overexpressing Sonic hedgehog (SHH) in mice skin caused basal cell nevus syndrome and basal cell carcinomas, mimicking loss of PATCHED (PTC) gene function. This suggests SHH
Area of Science:
- Developmental biology
- Oncology
- Genetics
Background:
- Mutations in the PATCHED (PTC) tumor suppressor gene are linked to basal cell nevus syndrome (BCNS).
- BCNS is characterized by developmental defects and tumors, notably basal cell carcinomas.
- Fruit fly studies suggest Sonic hedgehog (SHH) overproduction may mimic loss of PTC function.
Purpose of the Study:
- To investigate if Sonic hedgehog (SHH) overproduction is sufficient to induce basal cell carcinomas.
- To determine if SHH overexpression can replicate features of basal cell nevus syndrome.
Main Methods:
- Generation of transgenic mice with skin-specific SHH overexpression.
- Observation and analysis of phenotypic characteristics in the transgenic mice.
Main Results:
- Transgenic mice overexpressing SHH exhibited multiple features of basal cell nevus syndrome.
- The study demonstrated SHH's sufficiency in inducing basal cell carcinomas in mice.
- These findings link SHH signaling to the development of basal cell carcinomas.
Conclusions:
- Sonic hedgehog (SHH) signaling is sufficient to cause basal cell carcinomas.
- SHH may play a significant role in human basal cell carcinoma development.
- This research provides a mouse model for studying BCNS and SHH-driven tumorigenesis.