Figure 1.
Amplified/deleteted regions observed in this study's CRC tissue samples.
Amplifications (mean CN≥2.5) are shown in red, and deletions (mean CN≤1.5) are shown in blue. The horizontal size of the bar representation how many samples (at least 9 samples, 10%) exhibited the amplification/deletion.
Table 1.
Patient and tumor characteristics of 86 cases of CRC stratified by MSI status.
Figure 2.
Mosaic monoallelic amplification and deletion in chromosome 8 for CRC tissue sample C10_T.
In 8q (where BAF = 0.34, 0.66 and CN = 2.9), approximately 90% of cells have monoallelic amplifications (AAB or ABB). In 8p (where BAF = 0.35, 0.65 and CN = 1.55), approximately 40% of cells have monoallelic deletions (A_ or B_).
Figure 3.
Mosaic biallelic amplification in chromosome 8q for CRC tissue sample C1_T.
BAF = 0.5 and CN = 2.6. Approximately 30% of cells have biallelic amplification (ABAB).
Figure 4.
Mosaic monoallelic deletion in chromosome 8p for CRC tissue sample C1_T.
BAF = 0.17, 0.83 and CN = 1.2. Approximately 80% cells have mono-allelic deletion (A_ or B_).
Figure 5.
Mosaic monoallelic amplification and deletion in chromosome 8 for CRC tissue sample C21_T.
In 8q (where BAF = 0.38, 0.62 and CN = 2.65), approximately 65% of cells have monoallelic amplifications (AAB or ABB). In 8p (where BAF = 0.26, 0.74 and CN = 1.35), approximately 65% of cells have monoallelic deletions (A_ or B_).
Figure 6.
Mosaic cnLOH in chromosome 17 for CRC tissue sample C17_T.
Note that 17p shows the normal heterozygote pattern in all cells (BAF = 0.5 and CN = 2) but approximately 50% of cells show cnLOH (AA or BB) in 17q (BAF = 0.25, 0.75 and CN = 2).
Figure 7.
Mosaic isotrisomy in chromosome 20q of CRC tissue sample C22_T.
Table 2.
Interpretation of CN and BAF in autosomes for possible underlying mechanism of chromosomal abnormality.
Figure 8.
Regions of cnLOH found in this study's CRC samples.
Each vertical green line shows the occurrence copy-neutral LOH in one sample.
Figure 9.
Mosaic cnLOH in chromosome 6 of CRC tissue sample C46_T.
The cnLOH occurs in the entire chromosome.
Figure 10.
Mosaic cnLOH in chromosome 4 of CRC tissue sample C50_T.
The cnLOH occurs in all of 4p and parts of 4q where BAF = 0.25, 0.75 and CN = 2. The portion of 4q where BAF = 0.5 and CN = 2 shows normal heterozygote patterns in all cells.
Figure 11.
Mosaic cnLOH in chromosome 6 of CRC tissue sample C42_T.
The cnLOH occurs in 6p where BAF = 0.25, 0.75 and CN = 2. The portion of 6q where CN = 1 is mosaic monosomy.
Figure 12.
Genomic regions where the frequency of amplification or deletion is significantly different between MSI and MSS CRC samples.
Amplification regions are shown in red; deletion regions are shown in blue; regions with no significant change are shown in green. Each column represents a single sample.
Table 3.
Association of Chromosomal copy number changes with clinico-histopathological findings in MSS CRC cases (n = 62).
Table 4.
Association of Chromosomal copy number changes with clinico-histopathological findings in MSI CRC cases (n = 24).
Figure 13.
Common regions of amplification/deletion in this study and previous studies of other solid cancers.
(a) Regions of amplification in our study (red circle) were also found in previous studies of other solid cancers (green circle); several are also known to be down-regulated by drugs that are approved or in development (blue circle). (b) Locations of the common regions of amplification in our study and previous studies of other solid cancers (intersection of red and green circles in Fig. 13a) are shown. (c) Regions of deletion in our study (red circle) were also found in previous studies of other solid cancers (green circle); several are also known to be up-regulated by drugs that are approved or in development (blue circle). (d) Locations of the common regions of deletion in our study and previous studies of other solid cancers (intersection of red and green circles in Fig. 13d) are shown.
Table 5.
Approved antibody, antagonist, inhibitor drugs targeted against genes in amplified regions in CRC.
Table 6.
Approved agonist, activator and inducer drugs targeted against genes in deleted regions in CRC.