The high proportion of shared amplifications in the Indonesian DD2 sample is mainly due to the strong signal derived from the PfMDR1 locus.
Likewise in the above comparison, the high proportion of shared amplifications in DD2 laboratory strain also results from hits in the PfMDR1 locus.
Regions of shared change (amplification of 5p15.33-p13.13, loss of 3p26.3-p13) and several regions of difference (SCC: gains at 3q12.1-q28 and 12p13.33-p12.1, losses of chromosome 4 (4pter-4qter); AC: gains of 6p25.1-p21.31, losses of 6q13-27, and a greater magnitude of change in several regions of shared loss (9p, 13q, 17p, 18q, 19p, 19q and 22q) or gain (7p, 7q, 8q)) were identified.
Both samples shared focal amplifications at 8p11.21, which encompasses IKBKB, a node in the NF-κB pathway.
First of all, all three models share an amplification loop of TE growth.
Interestingly, T-47D and the two ERBB2-overexpressing lines, BT-474 and SK-BR-3, share amplifications at five gene loci: MAP2K6, CHN2, PRKCA, LIMK1 and c- MYC.
The segments were considered a "Shared segment" when amplification or deletion was found in samples from any two clusters.
Both amplifications shared the same forward primer 5′-ATTACAACAGGTCGTACAATTATGGC-3′, and differed in the reverse primer.
Although the grade II sample also shared the 12q13.3-q14.1 amplification, the entire 4q-arm was amplified in this sample.
It is notable that 6 tumors in TCGA show focal amplification of both PDGFRA and another RTK: four cases sharing focal co-amplification of EGFR, and two cases sharing focal co-amplifications of PDGFRA and MET.
