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Nonrandom structural and numerical chromosome changes in non‐small‐cell lung cancer
Author(s) -
WhangPeng J.,
Knutsen T.,
Gazdar A.,
Steinberg S. M.,
Oie H.,
Linnoila I.,
Mulshine J.,
Nau M.,
Minna J. D.
Publication year - 1991
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.2870030303
Subject(s) - breakpoint , chromosomal translocation , biology , lung cancer , chromosome , cytogenetics , genetics , cancer , pathogenesis , karyotype , cancer research , gene , ploidy , pathology , immunology , medicine
Cytogenetic studies were performed on 27 tumor cell lines (most of which were derived from metastatic lesions) and four fresh malignant pleural and pericardia! effusions from 30 patients with non‐small‐cell lung cancer (non‐SCLC). Many clonal structural (deletions and nonreciprocal translations) and numerical abnormalities were found in each specimen. Statistical analysis revealed these changes were nonrandomly distributed among the chromosomes. A statistically significant number of chromosomal breakpoints were seen in regions 1 q 1, 1 q3, 3p1, 3p2, 3q1, 3q2, 7q1, 13p1, 14p1, 15p1, and 17q1 when the regions were compared to the total haploid complement. In addition, when a given region was compared to other regions within the same chromosome, statistically significant numbers of breakpoints were noted for regions 1q3, 5q1, 7q1, 13p1, 14p1, 15p1, 16q2, 17q1, and 21p1. Specific chromosome bands showing the most frequent involvement in structural abnormalities were (in descending order) 3p 14.2, 3q21, 19q13, 11p15, 1q11, 7q111, 1q21, 3p23, and 3p21. The breakpoints indicate areas to look for new dominant oncogenes activated by translocations, while the areas of deletions and loss of material by nonreciprocal translocations highlight areas to search for recessive oncogenes. These cytogenetic studies represent strong evidence that multiple genetic lesions are associated with the development of metastatic lung cancer, and provide a roadmap to search for new genes involved in the pathogenesis of lung cancer.