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Telomeric structure in cells with chromosome end associations
D Saltman1, R Morgan, M L Cleary
1Department of Molecular Genetics, Genelabs Incorporated, Redwood City, CA 94063.
Chromosoma
|January 1, 1993
Summary
Chromosome end associations in tumors may stem from shortened telomeres. However, this study found severely shortened telomeres in some cells without functional compromise, suggesting telomere length isn't the sole factor in chromosome fusion.
Area of Science:
- Genetics and Molecular Biology
- Cell Biology
- Oncology
Background:
- End-to-end chromosome associations are observed in human tumors, aging cells, and chromosome instability syndromes.
- Shortened telomeres in tumor cells and aging tissues have led to the hypothesis that telomere attrition causes chromosome end associations.
Purpose of the Study:
- To investigate the molecular structure of telomeres in human tumor cell lines exhibiting frequent end-to-end chromosome associations.
- To determine the relationship between telomere length and the fusigenic behavior of human telomeres in cancer.
Main Methods:
- Analysis of telomere molecular structure in two human tumor cell lines with frequent metaphase chromosome end-to-end associations.
- Comparison of telomere length in these cell lines with other human cells possessing functional telomeres.
Main Results:
- The telomeres of the studied tumor cell lines with end-to-end associations were found to be severely reduced in length.
- Two additional cell lines with significantly shortened telomeres were identified, yet their telomere function was not detectably compromised.
Conclusions:
- Telomere length reduction is not the sole determinant of end-to-end chromosome associations (fusigenic behavior) in human tumor cells.
- Other factors likely contribute to the observed chromosome end fusions in cancer cells, even in the presence of shortened telomeres.