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Chromosome Preparation From Cultured Cells
Published on: January 28, 2014
Multiple chromosomal aberrations and 11p allelotyping in lung cancer cell lines
1Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
Abstract:
Cytogenetic and molecular genetic studies have implicated many chromosomal aberrations in the pathogenesis of lung cancer. Deletions on 3p and 9p are presently the primary target for positional cloning of putative tumor suppressor genes. We have recently reported frequent loss of heterozygosity in three separate regions (HRAS, D11S12, D11S16) on 11p in freshly resected lung cancer specimens. Here we report cytogenetic and molecular genetic analyses of 26 permanently growing human lung cancer cell lines. Deletions indicating regions which may harbor potential tumor suppressor genes were found in 5/9 cell lines on 2p, 5/9 on 2q, 6/9 on 3p, 7/9 on 3q, 5/9 on 6q, 3/9 on 9p, 5/9 on 11p, and 6/9 on 13q. Reduction to hemizygosity or a statistically significant increase in the frequency of homozygosity on 11p was found for all markers investigated except for ST5 (D11S832E). Eight of twenty-six (31%) cell lines were hemizygous for D11S12 and 9/26 (35%) for D11S16. Seventeen of eighteen (94%) cell lines were homozygous for PTH (expected homozygosity, 53%), 15/15 (100%) for WT1 (expected homozygosity, 55%), and 16/18 (89%) for CAT (expected homozygosity, 50%). These results confirm the notion that 11p harbors several putative tumor suppressor genes which may become inactivated at different stages of tumor development and progression. They also provide a basis for selecting cell lines for genetic complementation specifically targeted at the regions described.
Insights
This study analyzed lung cancer cell lines, identifying deletions on chromosome 11p that suggest the presence of tumor suppressor genes. These findings aid in understanding lung cancer development and selecting cell lines for further genetic research.
Area of Science:
- Oncology
- Human Genetics
- Molecular Biology
Background:
- Chromosomal aberrations are implicated in lung cancer pathogenesis.
- Previous research identified deletions on 3p and 9p as key targets for tumor suppressor gene discovery.
- Frequent loss of heterozygosity on 11p was previously observed in lung cancer specimens.
Purpose of the Study:
- To investigate cytogenetic and molecular genetic alterations in human lung cancer cell lines.
- To identify chromosomal regions harboring potential tumor suppressor genes.
- To analyze alterations on chromosome 11p, specifically focusing on loss of heterozygosity and changes in homozygosity.
Main Methods:
- Cytogenetic and molecular genetic analyses were performed on 26 permanently growing human lung cancer cell lines.
- Microsatellite markers were used to assess deletions and loss of heterozygosity on various chromosomal regions, including 11p.
- Allele frequencies and homozygosity rates were compared to expected values to identify significant alterations.
Main Results:
- Deletions were frequently observed in multiple chromosomal regions, including 2p, 2q, 3p, 3q, 6q, 9p, 11p, and 13q.
- Significant reductions in heterozygosity and increases in homozygosity were detected on 11p for markers D11S12, D11S16, PTH, WT1, and CAT.
- Specific cell lines exhibited high frequencies of hemizygosity for D11S12 (31%) and D11S16 (35%), and homozygosity for PTH (94%), WT1 (100%), and CAT (89%).
Conclusions:
- The findings confirm that chromosome 11p harbors multiple putative tumor suppressor genes.
- These genes may be inactivated at various stages of lung cancer development and progression.
- The study provides a foundation for selecting specific cell lines for genetic complementation studies targeting these regions.
