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Comprehensive karyotyping of the HT‐29 colon adenocarcinoma cell line
Author(s) -
Kawai Kanji,
Viars Carrie,
Arden Karen,
Tarin David,
Urquidi Virginia,
Goodison Steve
Publication year - 2002
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.10003
Subject(s) - karyotype , metaphase , biology , derivative chromosome , chromosomal translocation , telomere , chromosome , fluorescence in situ hybridization , marker chromosome , cytogenetics , comparative genomic hybridization , genetics , microbiology and biotechnology , chromosome instability , dna , gene
The tumor cell line HT‐29 was derived from a primary adenocarcinoma of the rectosigmoid colon. HT‐29 is hypertriploid (3n + ) and has accumulated numerous chromosomal structural aberrations. To identify material involved in chromosome rearrangements, we performed a comprehensive cytogenetic analysis using G‐banding, spectral karyotyping (SKY), and fluorescence in situ hybridization (FISH). The combination of molecular cytogenetic techniques enabled us to define the first comprehensive karyotype for HT‐29. Seventeen marker chromosomes were found in 75–100% of metaphase cells, generally in a single copy per cell. We confirmed the composition of eight previously described markers, refined the classification of seven others, and identified two novel marker chromosomes. Notable aberrations included a reciprocal translocation between chromosomes 6 and 14 and an unusual, large derivative chromosome 8 composed entirely of 8q material. The telomere status, evaluated by FISH, revealed telomeric signals at the termini of all chromosomes. No interstitial telomeric sequences were observed in any cell. Although numerous chromosomal aberrations are present in HT‐29, the cell line appears to have retained a high level of genomic stability during passage in culture since undergoing transformation. The excellent resolving power of SKY, coupled with additional information obtained from molecular cytogenetic analyses, will improve our ability to identify genetic lesions characteristic of cancer. © 2002 Wiley‐Liss, Inc.