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Tumorigenicity and oncogene expression in pediatric cancers
S R Pasquale1, G R Jones, C J Doersen
1Division of Hematology-Oncology, Children's Hospital of Los Angeles, California.
Cancer Research
|May 15, 1988
Summary
Pediatric cancer tumorigenicity appears to be a recessive genetic trait. Hybrid cells formed from adult and pediatric cancer cells lost tumor-forming ability, indicating genetic elements differ between adult and pediatric cancers.
Area of Science:
- Oncology
- Genetics
- Cancer Biology
Background:
- Studies suggest both genetic information loss and oncogene activation contribute to pediatric cancer development.
- Understanding the interplay between genetic elements and oncogene activation is crucial for pediatric cancer research.
Purpose of the Study:
- To investigate the interaction between genetic element loss and oncogene activation in pediatric cancers using somatic cell hybridization.
- To determine if tumorigenicity in pediatric cancers is a dominant or recessive genetic trait.
Main Methods:
- Formation of human-human cell hybrids between a tumorigenic adult carcinoma and tumorigenic pediatric cell lines.
- Assay of tumor-forming ability in nude mice.
- Examination of N-myc, c-myc, and sis oncogene expression in hybrid cells.
Main Results:
- All hybrid cells exhibited suppressed tumor-forming ability, indicating tumorigenicity is a recessive trait in pediatric cancers.
- No correlation was found between the expression of N-myc, c-myc, and sis oncogenes and tumorigenicity in hybrid cells.
- Findings suggest that oncogene expression is not controlled by "tumor suppressor" genes in these hybrid cells.
Conclusions:
- Tumorigenicity in pediatric cancers behaves as a recessive genetic trait.
- Different genetic elements may be lost during the tumor development of adult cancers compared to pediatric cancers.
- Somatic cell hybridization is a valuable model for studying genetic interactions in pediatric cancer.