Transcriptome instability in colorectal cancer identified by exon microarray analyses: Associations with splicing factor expression levels and patient survival

Table 1 Clinicopathological and molecular characteristics of the two independent colorectal cancer study populations

	Test series (n= 83)	Validation series (n= 77)
Age at diagnosis (mean ± SD)	66.0 ± 11.7	72.7 ± 13.5
Sex (male; female)	40; 43	33; 44
Stage (II; III)	46; 37	44; 33
Location (right; left; rectum)	26; 25; 32	46; 20; 11
Mean follow-up, years (minimum; maximum)	6.7 (0.7; 10.0)	3.5 (0.2; 5.0)
Number of events (deaths from CRC)	41	10
MSI	13	24
sTIN^a	12 (15%)	24 (31%)
oTIN^b	14 (17%)	30 (39%)
Either sTIN, oTIN, or both	24 (29%)	43 (56%)
Both TIN phenotypes	2 (2%)	11 (14%)

^asTIN, skewed transcriptome instability; preferential exon inclusion or skipping (difference in relative amounts of aberrant exon skipping and inclusion greater than ± 0.7). ^boTIN, overall transcriptome instability; total relative amounts of aberrant splicing greater than ± 1.0. SD, standard deviation; TIN, transcriptome instability.

ISSN: 1756-994X