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. 2015 Jun 19;36(Suppl 1):S160–S183. doi: 10.1093/carcin/bgv035

Table 4.

Cross-validation of disruptors

Tumor microenvironment prototypical disruptors Deregulated metabolism Evasion of anti-growth signaling Angiogenesis Genetic instability Immune system evasion Resistance to cell death Replicative immortality Sustained proliferative signaling Tissue invasion and metastasis Tumor- promoting inflammation
Nickel + Not known + (30) + (253) + (254) 0 +/− (255,256) − (257,258) + (259) + (260) + (261)
BPA + (262) + (92) + (227) + (263) 0 +/− (264,265) + (266) + (267) + Not known + (268)
Butyltins (such as TBT) + (269) + (270) 0 + (271) 0 − (272,273) 0 − (274) 0 + (95)
MeHg + (275) + (276,277) − (278) + (279) 0 − (280–283) 0 + (284) 0 + (285,286)
Paraquat +, 0 + (287) 0 + (288) 0 − (289,290) 0 − (225) 0 + (291)

(+): Targets and chemicals those were not only relevant for tumor microenvironment but also relevant for other areas of cancer biology (i.e. pro-carcinogenic). (−): Targets and chemicals that were found to have opposing actions (i.e. anti-carcinogenic). (+/−): Instances where reports on relevant actions in other aspects of cancer biology were mixed (i.e., reports showing both pro-carcinogenic potential and anti-carcinogenic potential). (0): Instances where no literature support was found to document the relevance of a target site or chemical in a particular aspect of cancer biology.