Table 2.

Genomic and transcriptomic evaluation of breast tumor patient-derived xenografts

	Marangoni et al. [6]; Cottu et al. [21]; Reyal et al. [23]	Bergamaschi et al. [24]	Ding et al. [7]	DeRose et al. [8]	Kabos et al. [20]	Petrillo et al. [22]
Genomic	DNA copy number alterations: 14/18 pairs of tumors shared more than 56% copy number alterations, unsupervised hierarchical clustering showed 16/18 pairs segregated together. Recurrent changes between patient tumors and xenografts showed losses in 176 chromosomal regions and gains in 202 chromosomal regions	CGH array Agilent 244K human genome CGH microarrays. CGH results showed shared alterations between primary and xenograft tumors with more pronounced alterations in engrafted tumors, that is, TP53 patient 1 wild-type allele, xenograft LOH; ER+ tumor gained basal-like alterations	Paired-end sequencing to achieve deep coverage of patient blood, tumor, metastasis, and xenografted tumor Confirmed SNP coverage by Illumina 1M duo arrays. The PDX retained primary tumor mutations and showed enrichment of mutations similar to patient metastasis	Genome-wide SNPs with enhancement of existing aberrations
Microarray-gene expression	Gene expression analysis (GEA)	Agilent GEA High dose E2 supplementation altered gene expression	PAM50 intrinsic subtype classification	Agilent GEA, intrinsic subtype classification, PAM50 confirmation	Agilent GEA, PAM50 intrinsic subtype classification	Agilent GEA, PAM50 intrinsic subtype classification
Intrinsic subtypes represented	Basal-like (5) Luminal A (2) Luminal B (1) [23]	Basal-like (1) Luminal B (1)	Basal-like (1)	Basal-like (4) HER2-like (1) Luminal B (4) Normal-like (1)	Basal-like (1) HER2-like (1) Luminal B (4)	Basal-like (3) Luminal A (1)

CGH, comparative genomic hybridization; ER, estrogen receptor; GEA, gene expression analysis; HER2, human epidermal growth factor receptor-2; LOH, loss of heterozygosity; PDX, patient-derived xenograft.