Rearrangement of chromosome band 11q13 in HeLa cells.
Previous somatic cell genetic and molecular genetic studies have localized the Hela cell tumor suppressor gene to the long arm of chromosome 11. To determine if loss of heterozygosity has occurred for the inactivation of the tumor suppressor gene, we investigated the molecular status of chromosome 11 in the HeLa cells. The restriction fragment length polymorphic (RFLP) analysis of four different HeLa sublines showed retention of heterozygosity for the long and short arm specific probes in three of the sublines. Fluorescence in situ hybridization (FISH) studies using whole chromosome painting probes identified 11 material in a marker chromosome in addition to the two normal appearing 11's in these three cell lines. The fourth cell line contained only two 11's. This cell line had lost the 11 material from the marker chromosome. Both molecular and karyotypic analyses indicated q13 as the common site of rearrangement in the derivation of these marker chromosomes. We therefore conclude that 11q13 rearrangement could contribute to the abnormal growth behaviour of HeLa cells in vivo and/or in vitro.
Jesudasan
R A
RA
Department of Surgery, UCLA School of Medicine, VA Medical Center, Wadsworth Division 90073.
Slovak
M L
ML
Sen
S
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Srivatsan
E S
ES
D000483:Alleles; D002871:Chromosome Banding; D002880:Chromosomes, Human, Pair 11; D015342:DNA Probes; D004273:DNA, Neoplasm / Q000235:genetics; D015321:Gene Rearrangement; D005819:Genetic Markers; D006367:HeLa Cells / Q000502:physiology / Q000648:ultrastructure*; D006579:Heterozygote; D006801:Humans; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length
D015342:DNA Probes; D004273:DNA, Neoplasm; D005819:Genetic Markers