Nonrandom chromosomal imbalances in esophageal squamous cell carcinoma cell lines: Possible involvement of the ATF3 and CENPF genes in the 1q32 amplicon

Using comparative genomic hybridization (CGH), we investigated copy number aberrations in 29 esophageal squamous cell carcinoma (ESC) cell lines. All lines displayed numerous chromosome imbalances. The most frequent losses we re observed on chromosome 18q (65.5%), Xp (48.3%), 3p (44.8%), 49 (44.8%), 8p (41.4%), 11923-25 (34.5%) and 4p (27.6%), whereas the most common copy n umber gains were noted at 8q (86.2%), 3q (82.8%), 5p (69%), 7p (69%), 20q ( 65.5%), 9q (55.2%), 11q (55.2%), 1q (48.3%), Xq (44.8%) and 18p (37.9%). Hi gh-level gains (HLGs) were detected at 39q26 (9 cases), 8q23 (6 cases), 5p1 4-15 (6 cases), 18p11.2-11.3 (6 cases), 3q27-28 (5 cases), 5p13 (3 cases), 7p14-15 (3 cases), 20q12-13 (3 cases), 11q13 (3 cases), 14q21 (2 cases), 20 p11.2 (2 cases), 13q32 (2 case), and 1q32 (1 case). Among them, HLGs of 1q3 2 have been reported in other types of cancer, including glioblastoma and b reast cancers. We successfully narrowed down the smallest common amplicon i nvolving 1q-gain to the genomic segment between D1S414 and D1S2860 by fluor escence in situ hybridization (FISH). Southern and northern blot analysis c learly demonstrated that ATF3, human activating transcription factor-3 and CENPF, centromere protein F,mapped within this region, were significantly a mplified and over-expressed in 1q32 amplicon.