When we compared the relative levels of phosphorylated Atg1 peptides under nutrient-rich conditions and starvation conditions, we found that most of the sites identified from the mass spectrometry analysis, including T226, S343, S356, S515, S621, T685 and S769, were phosphorylated at significantly higher levels (ratio of IR in starvation medium/IR in full medium >2) when autophagy occurs (Fig. 1D).
For all monogenomic and polygenomic tumours analysed, aberrations were seen at the level of large-scale structural aberrations such as gains or losses of whole chromosomes or chromosome arms as well as at the level of more focal events including high-level (log ratio >1) amplifications and homozygous(log ratio < −3) deletions.
High-level gains (ratio > 1.5) were seen only on 8q, 13q, 20 and X, and only in DNA aneuploid tumours.
Blue, high-level hypersusceptibility (MIC ratio ≤0.25).
In addition, a high-level amplification (locus/centromere ratio ⩾2) of all three genes was found in MDA436 and PC-3 cancer cell lines.
Thresholds for copy gains were set at gene/centromere ratio of more than 1.5 and high-level amplification at a ratio of more than 2.5.
A region of gain or loss was defined as two or more consecutive clones showing an absolute log2 ratio ≥ 0.2 and high-level amplifications as a log2 ratio ≥ 1.5.
Here we report two cases of MET inhibitor sensitive NSCLC harboring high-level MET amplification (MET/CEP7 ratio ≥5) without coincident exon 14 alterations, suggesting that these two methods of MET activation can produce independent MET-addicted states in NSCLC.
The other patient had high-level amplification with a ratio of more than 3 in the primary tumour (10 to 20/2 to 4), in contrast with a ratio of 1.83 (3 to 6/2 to 3) in the metastasis.
There was high-level HER2 amplification (HER2/CEP17 ratios > 5) in six cancer cases (6/33 = 18.2%), including the five cases with HER2 overexpression.
