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. 2015 Jun 19;36(Suppl 1):S89–S110. doi: 10.1093/carcin/bgv032

Table 3.

Cross-validation of disruptors

Prototypical disruptors Deregulated metabolism Evasion of antigrowth signaling Angiogenesis Genetic instability Immune system evasion Replicative immortality Sustained proliferative signaling Tissue invasion and metastasis Tumor promoting inflammation Tumor microenvironment
BPA +(319–322) +(152) +(323) +(155,324,325) 0 + +(154) +(326–328) +(329) 0
DBP All via hormone disruption 0 +(165) +(330) 0 0 +(165,166) 0 +(331) 0
Chlorothalonil 0 +(332) 0 +(138,333) 0 0 +(138) 0 +(158) 0
Lindane +(179,180,334) 0 +(335) +(243,336) 0 0 +(199,200) 0 +(155) 0
DDVP +(337) +(338) 0 +(339,340) 0 0 0 0 +(338,341) 0
MXC 0 0 0 +(342,343) 0 0 +(201) 0 +(344,345) 0
Oxyfluorfen +(192) 0 + 0 0 0 +(192) 0 +(192) 0
DEHP +(168,346) +(169) 0 0 0 0 +(167) 0 +(347) 0
Linuronx +(348) 0 0 0 0 0 0 0 +(349,350) 0

Disruptors of resistance to cell death were cross-validated for effects in other cancer hallmark pathways. Disruptors that were found to have opposing actions in a particular hallmark (i.e. anticarcinogenic) were denoted using ‘−’, whereas disruptors that were found to have promoting actions 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 anticarcinogenic potential), the symbol ‘+/−’ were 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’.