Table 2.

Cross-validation of disruptors

Tissue invasion and metastasis disruptors	Deregulated metabolism	Replicative immortality	Tumor-promoting inflammation	Resistance to cell death	Genetic instability	Immune system evasion	Angiogenesis	Tumor microenvironment	Evasion of antigrowth signaling	Sustained proliferative signaling
BPA	+ (557–560)	+ (561)	+ (562)	−/+ (563–566)	+ (567)	0	+ (568)	0	+ (563)	+ (569)
Hexachlorobenzene	+ (570–572)	0	+ (510,573)	− (574,575)	+ (576)	0	− (577)	0	+ (578)	+ (579)
Iron	0	−/+ (580–582)	+ (583)	− (584)	+ (585)	+ (586)	+/−	+ (587)	0	+ (413)
SO2	0	0	+ (588,589)	− (590,591)	+ (592)	0	+ Patent application number: 20100080843	0	0 for carcinogenesis but + (593)	+ (593)
Phthalates	+ (594–596)	0	+ (594,596)	−/+ (595,597–600)	+ (601)	0	+ (602)	0	+ (603)	+ (604,605)
Biorhythms	− (606)	0	+ (607)	0	+ (472)	0	− (608)	0	0	+ (609)

Disruptors of tumor invasion and metastasis were cross-validated for effects in other cancer-associated pathways. Disruptors that were found to have opposing actions in a particular pathway (i.e. anticarcinogenic) were denoted using ‘−’ effects, whereas disruptors that were found to have promoting actions in a particular cancer-associated pathway (i.e. carcinogenic) were denoted using ‘+’. In instances where reports on relevant actions in other cancer-associated pathways were mixed (i.e. reports showing both procarcinogenic potential and anticarcinogenic potential), the term ‘−/+’ 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, we documented this as ‘0’.