Table 3.

Cross-validation of disruptors

Prototypical disruptors	Sustained proliferative signalling
	Deregulated metabolism	Evasion of anti-growth signalling	Angiogenesis	Genetic instability	Resistance to cell death	Replicative immortality	Tissue invasion and metastasis	Tumor promoting inflammation	Tumor microenvironment
Benzo(a)pyrene	+ (218)	+ (219)	− (220)	+ (219)	+ (219)	+ (219)	+ (221)	+ (222)	+ (223)
TPA	+ (224)	+ (225,226)	0	0	0	− (227,228)	+ (229)	+ (230,231)	+ (232)
BPA	+ (233,234)	+ (235)	+ (236)	+ (237)	± (235,238–240)	+ (241,242)	0	+ (243)	0
PFOS	0	+ (244)	+ (245)	+ (246)	− (247,248)	0	0	+ (249,250)	0
Lactofen	0	0	0	0	+ (251)	0	0	+ (252)	0
Imazalil	+ (253)	0	− (254)	+ (255)	0	0	0	+ (256)	0
Phosalone	0	0	− (257)	0	0	0	0	+ (258)	0

Disruptors of sustained proliferative signalling were cross-validated for effects in other cancer hallmark pathways. Disruptors that were found to have opposing actions in a particular hallmark (i.e. anti-carcinogenic) were denoted using ‘−’, whereas disruptors that were found to have in a particular hallmark (i.e. carcinogenic) were denoted using ‘+’. In instances where reports on relevant actions in other hallmarks were mixed (i.e. reports showing both pro-carcinogenic potential and anti-carcinogenic potential), the symbol ‘±’ was used. Finally, in instances where no literature support was found to document the relevance of a chemical in a particular aspect of cancer’s biology were denoted using ‘0’. BPA, bisphenol A; PFOS, perfluorooctane sulfonate; TPA, 12-O-tetradecanoylphorbol-13-acetate.