Table 1.

Relationships between resistance to apoptosis targets and cancer hallmarks.

Targets related to resistance to apoptosis	Inhibit Bcl-2		Inhibit Mcl-1		Activate tumor autophagy		Activate tumor necrosis		Inhibit hsp90		Inhibit proteasome		Inhibit nuclear exporter CRM1
Other cancer hallmarks
Genomic instability	0		0		0		0		0		0		0
Sustained proliferative signaling	+	[360,361]	+	[32,362]	+/−	[363,364]	+/−	[365,366]	+	[367,368]	+	[369,370]	+
													[141]
Tumor promoting inflammation	+	[371,372]	+	[373,374]	−	[375,376]	+/−	[377,378]	+	[379,380]	+	[381–383]	0
Evasion of Anti–growth Signaling	+	[384–386]	+	[237,387]	+	[388]	+	[389]	+	[390,391]	+	[392,393]	+
Replicative immortality	+/−	[395,396]	+	[362]	+/−	[397–399]	+/−	[400]	+	[401,402]	+	[403,404]	[394]
Dysregulated metabolism	+	[405–407]	+	[408–410]	+	[411–413]	+	[414–417]	+	[418–420]	+	[421]	0
Immune system evasion	+	[422]	+	[423]	0		+	[424]	0		+	[425–427]	0
Angiogenesis	+	[428]	+	[429]	+/−	[430]	−	[431]	+	[432]	+	[433]	+
													[434]
Tissue invasion and metastasis	+	[435]	+	[436]	+	[437,438]	+	[439]	-	[440,441]	+	[442]	+
													[443]
Tumor microenvironment	+	[444,445]	+	[444]	+/−	[446,447]	−	[448]	+	[449]	+	[450]	+
													[451]

Prioritized targets were evaluated for known effects in other cancer hallmark areas. Targets that were found to have complementary, anti-carcinogenic actions reported in another hallmark area were indicated with “+”, while targets that were found to have pro-carcinogenic actions in another hallmark area were indicated with “-”. In instances where reports on relevant actions in other hallmark areas were mixed (i.e., reports showing both anti-carcinogenic potential and pro-carcinogenic potential), the symbol “+/−” was used. Finally, in instances where no literature support was found to document the relevance of a target in a particular aspect of cancer‘s biology, we documented this as “0”. These cross-hallmark relationships are reported in the upper rows of the table.