One additional tumor showed high level gain restricted to 2p13 consistent with n-myc amplification.
Fluorescence in situ hybridization for c-myc showed amplification in 4 of 11 cases of the LC/A phenotype and 1 additional case of high level gain at 8q24 was disclosed by comparative genomic hybridization.
These measures included: the number of copy number changes i.e. gains, losses, higher level gains (>0.6 log2 amplitude) and total number of segments; the percentage of the genome targeted by copy number change (gain, loss and high level gain); and a "Hicks index" as described [31] for gains, losses and both.
Red identifies a high level gain or amplification; blue a loss.
Small clonal foci of cancer containing high level gain of the androgen receptor (AR) -gene develop before hormone deprivation therapy.
For example high level gain was observed at 20q where AURKA is located, frequent gain at 16p (PLK1), and loss at 4q (MAP9) in a number of colorectal tumors.
For this purpose, the thresholds were as used in Nexus 6.0 analysis (high level gain: 0.485, gain, 0.138, loss -0.153, homozygous copy loss -0.153.
High level gain (CGH ratio >1.5 : 1) was infrequent, and mostly implied gain of several copies of the whole, or most of, a chromosome arm.
Data matrices were generated, containing the imbalance status ("1" = gain, "-1" = loss, "2" = high level gain) for each of 862 chromosomal bands (UCSC Genome Bioinformatics [ 35], Golden Path mapping, May 2004 edition), or subsets thereof.
Analysis settings for data segmentation and calling were the following: significant threshold for Rank Segmentation algorithm: 0.005, Max Continuous Probe Spacing: 6000, Min number of probes per segment: 6, high level gain: 0.485, gain, 0.138, loss -0.153, homozygous copy loss -0.153
Both high level gain in chromosome X (⩾4 fold; n=4, 0.7%) and locus-specific amplification of the AR-gene (n=6, 1%) were detected at low frequencies in HNPCa TMAs.
