Metronomic cyclophosphamide activation of anti-tumor immunity: tumor model, mouse host, and drug schedule dependence of gene responses and their upstream regulators

Table 1 Tumor models, mouse hosts, CPA schedules, gene responses and UPR analysis. RNA-seq was performed on two replicated RNA pools for each condition (Additional file 1: Table S1 legend)

	Responsive tumors				Unresponsive tumors
Tumor	GL261				LLC	B16F10
Mouse host	B6	scid	scid	scid	B6	B6
CPA schedule (days)	6	6	9	6 and 9^a	6	6
Tumor responses to CPA treatment	Complete regression	Major regression with late rebound	Major regression with early rebound	–	Minor growth delay	Moderate growth delay
Up regulated genes	2119	2574	2713	2352	151	663
Down regulated genes	809	1250	1564	1176	70	394
Stringent Upstream Regulators (UPRs)	180	210	218	179	6	93

Shown here is a summary of tumor responses to drug treatment, for GL261(B6) [20], GL261(scid) [18], LLC and B16F10 tumors (Fig. 1), the number of genes up or down regulated at |FC| > 2 and p < 0.001 (Additional file 1: Table S1), and the number of significant UPRs (Additional file 4: Table S3) after filtering of the full set of UPRs output by IPA (Additional file 3: Table S2)
^a, Number of commonly regulated genes and UPRs responding in common between GL261(scid) tumors treated with CPA/6d and GL261(scid) tumors treated with CPA/9d

ISSN: 1471-2407