Tumor Take Rate Optimization for Colorectal Carcinoma Patient-Derived Xenograft Models

Table 3

(a)

ID	vWA	TH01	TPOX	CSF1 PO	D5S818	D13S317	D7S820	D16S539	Sex
HROC107	16, 17	8, 9	10, 11	10, 12	11, 13	8	10, 11	10, 13	m
HROC131	16	10	8	11	12, 13	12	11, 13	8, 12	f

(b)

ID	Molecular type	Ploidy status	Mutations		K-Ras	N-Ras	H-Ras	PIK3CA	B-Raf	CIMP-number	MSI - status
			p53	APC
HROC107	spStd	Aneuploid	Ex8	mut	G12D	wt	wt	E542K	wt	2	MSS
HROC131	spMSI-H	Aneuploid	n.a.	n.a.	wt	wt	wt	wt	mut	5	MSI-H

(a) Fingerprint analysis of cases HROC107 and HROC131. The alleles of nine classical markers are displayed. No differences were observed between the original tumor and both the PDX models and the tumor cell lines generated from the 24 h PDX models.
(b) The results of the molecular analysis of cases HROC107 and HROC131 (according to [3]) are displayed. Mutations in the CRC-relevant target genes p53, APC, K-, N-, and H-Ras, PIK3CA, and B-Raf were analyzed. Together with the CIMP and MSI analysis results, the underlying molecular type could be identified as spSTD for HROC107 and spMSI-H for HROC131.
ID: pseudonym of case, sex: result of the amelogenin marker analysis, m: male, f: female, sp: sporadic, Std: standard type, Ex8: exon number 8, mut: mutated, wt: wild type, n.a.: not analyzed, CIMP: CpG island methylator phenotype, MSI: microsatellite instability, MSS: microsatellite stable, MSI-H: high grade microsatellite instable.