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Comparative cytogenetics of mouse and human lung adenocarcinoma.

Authors
Sargent-LM; Ensell-MX; Senft-JR; Lowry-DT; Jefferson-AM; Kashon-ML; Tyson-FL; Reynolds-SH
Source
Proceedings of the abstracts of the 7th World Congress on Advances in Oncology and 5th International Symposium on Molecular Medicine: 10-12 October, 2002, Hersonissos, Crete, Greece. Spandidos D, ed., Hersonissos, Crete, Greece: University of Crete, 2002 Oct; :409
Link
NIOSHTIC No.
20033762
Abstract
Although lung cancer is the leading cause of cancer death in the United States, the genetic changes associated with progression of the disease are not well understood. As powerful tools to detect molecular changes associated with primary and invasive mouse lung adenocarcinoma cells, we used Spectral Karyotyping, mapping with fluorescently labeled genomic clones and comparative genomic hybridization on a BAC array to analyze 15 primary adenocarcinoma and 9 pairs of high and low invasive tumor cell cultures. Gain of entire copies of chromosomes 1, 2, 6, 12, 15 and 19 were observed. Loss of entire copies of chromosomes 7, 8, and 14 were significant in the primary tumor cell cultures. Loss of the distal portion and duplication of the proximal region of chromosome 4 were observed in the primary tumor cell cultures. Investigations of the minimal region of alteration of chromosome 4 by fluorescent in situ hybridization (FISH) and BAC array demonstrated the deletion of a 3 centimorgan region in the middle portion of the chromosome. In addition, FISH demonstrated a 20 centimorgan duplication on chromosome 4. The duplication of chromosome 1 and 15 were associated with the ability of cells to invade a gel matrix. Mapping with FISH and CGH array further narrowed the region of duplication of chromosome 1 to five centimorgans. The minimal region of chromosomal alteration of chromosomes 1, 2, 4, 6, 7, 8, 12 and 15 contain putative susceptibility loci for mouse lung cancer. These same linkage groups are altered in human lung cancer. In addition, the chromosomal loci associated with invasion are amplified in both mouse and human lung cancer. The alteration of the same linkage groups in mouse and human indicates that the mouse is a valid model for human lung adenocarcinoma.
Keywords
Adenocarcinomas; Animal-studies; Lung-cancer; Gene-mutation; Tumors; Humans; Respiratory-system-disorders; Pulmonary-system-disorders
Publication Date
20021001
Document Type
Abstract
Fiscal Year
2003
NTIS Accession No.
NTIS Price
NIOSH Division
HELD
Source Name
Proceedings of the abstracts of the 7th World Congress on Advances in Oncology and 5th International Symposium on Molecular Medicine: 10-12 October, 2002, Hersonissos, Crete, Greece
State
WV
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