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Wang et al. [13] also reported 6 (3%) PTPRF mutations in CRCs, 1 (9%) in lung cancer, and 1 (9%) in breast cancer.
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Consistent to this notion, the RB1CC1 locus (8q11.23) is frequently amplified in CRCs [41].
The PIK3CA gene is mutated in approximately 20% of CRCs [21].
Exposure to even a single light pulse synchronizes the CRCs [63].
This suggests that epigenetic mechanisms of PTEN downregulation are frequent in CRCs [13].
In MSI primary CRCs, UPF1 was significantly over-expressed compared to normal adjacent mucosa (P<0.002).
One hundred and twelve CRCs (82%) had stable microsatellites, whereas 25 CRCs (18%) had MSI.
Of 31 CRCs, 23 (74%) cases showed positive immunoreactivity against BRG1.
MSI CRCs have a significantly better prognosis with higher survival rates compared to MSS CRCs 23.
BNIP3 promoter-methylated CRCs less frequently demonstrated BNIP3 protein expression than unmethylated CRCs (25 vs 75%, respectively).
A similar tendency was observed for CLR-positive CRCs (M1 in six out of 29 CLR+ vs 17 out of 45 CLR− CRCs, P=0.13).
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