Table 3.

Studies correlating PDX treatment results with clinical data

Tumor type (reference)Definition activityStandard agentnRR (%)Clinical correlates
CRCTR > 50%Cetuximab4710N/A
CRC KRAS WT (28)Cetuximab3817
CRC (29)T/C < 10%5-Fluorouracil5213N/A
Oxaliplatin520
Irinotecan4938
Cetuximab5226
HBC (34)Complete responseAC1776Response to treatment in the PDX model was concordant with clinical data in 5/7 patients.
TGI > 50% or T/C GD > 2-foldDocetaxel1747
Trastuzumab250
GnRH antagonist1100
HBC (16)RR > 30%Docetaxel71492% correlation between clinical responses and responses in PDX
Doxorubicin40
Trastuzumab–lapatinib1100
NSCLC (20)Statistically significant decrement in tumor area in treated vs. control tumorsCisplatin–vinorelbine3228PDX models from 6/7 patients with early recurrent disease were resistant to the clinically used regimen.
Cisplatin–docetaxel1942
Cisplatin–gemcitabine1644
NSCLC (21)T/C < 5%Etoposide254N/A
Carboplatin2512
Gemcitabine2512
Paclitaxel2516
Vinorelbine110
Cetuximab2512
Erlotinib251
SCCHN (25)T/C < 20%Cetuximab119%N/A
RCC (15)Statistically significant differences in TGISunitinib8ActiveN/A
SirolimusActive
ErlotinibInactive
PDAC (26)T/C < 20%Gemcitabine1436N/A
Erlotinib0
Temsirolimus0
PDAC (33)TGI > 85%Gemcitabine2317%Response to gemcitabine in the PDX model predicted longer time to progression in patients.

NOTE: This table provides a summary of studies in which PDX models from different cancer types have been treated with agents used in the clinical care of these patients.

Abbreviations: AC, adriamycin–cyclophosphamide; CRC, colorectal cancer; GD, growth delay; GnRH, gonadotrophin-releasing hormone; HBC, human breast cancer; N/A, not available; RR, response rate; TGI, tumor growth inhibition; TR, tumor regression; T/C, treated divided by control; WT, wild-type.