Skip to main content
. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: Semin Cancer Biol. 2015 Dec;35(Suppl):S276–S304. doi: 10.1016/j.semcancer.2015.09.007

Table 1.

Prioritized targets with summary of information from cross-validation tables.

Hallmark1,2 Target (action on
target)
Contrary Controversial Complementary None
known
AP, RI, TPI Akt (inhbit) 0 0 11 0
SPS Androgen receptor signaling (suppress) 0 2 8 1
TIM AP-1 (inhibit) 1 RI 0 7 3
EAG ARID1A (activate) 1 TIM 0 5 5
AP Bcl-2 (inhibit) 0 1 9 1
RI CDK 1/2/5/9 (inhibit) 1 TME 0 9 1
RI CDK 4/6 (inhibit) 1 GI 1 8 1
SPS Cell cycle (CDKs/cyclins) (attenuate) 2 IS, TIM 0 9 0
GI Centrosome clustering (block) 0 0 8 3
TME Cholesterol metabolites (inhibit) 0 0 7 4
TME Cholesterol synthesis (inhibit) 0 1 8 2
TPI COX-2 (inhibit) 1 AN 0 10 0
TPI CXC chemokine (inhibit) 0 3 5 3
AN Disturbed circadian rhythms (normalize) 0 2 9 0
GI DNA damage (prevent) 1 TPI 3 5 2
GI DNA repair (enhance) 1 TPI 3 5 2
EAG, TIM E-cadherin (restore) 1 AN 4 4 2
EAG E2F (inactivate) 1 TME 0 7 3
AP EGFR (inhibit) 0 0 10 1
AN Elevated interstitial fluid pressure (reduce) 0 0 9 2
TME Endoglin (inhibit) 0 1 5 5
AN Endothelial cell migration/tip cell formation (inhibit) 0 0 7 4
AP Enox (inhibit) (AP) 0 0 5 6
SPS ER signaling (suppress) 1 TIM 3 7 0
EAG ER stress (induce) 2 AN, TIM 1 7 1
TIM FAK signaling (inhibit) 0 0 9 2
TME Fibrosis (inhibit) 0 0 6 5
EAG Growth differentiation factor 15 (induce) 1 GI 0 5 5
SPS HIF-1 signaling (inhibit) 0 0 9 2
AP Hsp90 (inhibit) (AP) 1 TIM 0 8 2
RI hTERT (inhibit) 0 1 8 2
AN Hypoxia (reduce) 0 1 10 0
TME IDO (inhibit) 0 1 7 3
EAG, SPS IGF-1R (inhibit) 0 0 9 2
IE IL-12 (induce) 1 AP 0 5 5
TME IL-6 (inhibit) 0 3 7 1
TPI iNOS (block) 1 AN 1 6 3
TME JAK (inhibit) 0 0 10 1
AN Lymphangiogenesis (impede) 0 1 4 6
TME M2 macrophage conversion (inhibit) 0 0 7 4
IE Macrophages (activate) 2 SPS, TIM 2 3 4
AP Mcl-1 (inhibit) 0 0 10 1
TPI MIF (block) 0 0 9 2
TIM MMP-9 (suppress) 0 1 7 3
RI mTOR (inhibit) 0 2 8 1
SPS, TIM, TPI NF-KB signaling (inhibit) 0 2 8 1
IE NK cell activity (promote) 0 0 7 4
EAG NOTCH (block) 1 AN 0 8 2
AP Nuclear exporter CRM1 (inhibit) 0 0 6 5
RI PI3K (inhibit) 0 0 11 0
EAG, SPS, TIM PI3K/Akt signaling (inhibit) 0 0 11 0
AN Poor perfusion (improve) 0 1 7 3
AP Proteasome (inhibit) 0 0 10 1
TME ROS (inhibit) 0 2 7 2
AN Structural abnormalities of vessel walls (inhibit) 0 0 7 4
GI Target deficient DNA repair 1 TPI 2 5 3
GI, RI Telomerase (inhibit) 0 0 10 1
TIM TGF-β (inhibit) 1 RI 2 7 1
IE Th1 response (promote) 1 TPI 0 5 5
TIM Tight junctions (promote) 1 AN 0 6 4
TPI TNF-α (block) 1 IE 1 8 1
IE Treg lymphocytes (inhibit) 0 1 6 4
AP Tumor autophagy (activate) 1 TPI 4 4 2
AN Tumor cell metabolism/acidosis (normalize) 0 0 9 2
AP Tumor necrosis (activate) 2 AN, TME 3 5 1
AN Tumor-promoting fibro-blasts (deactivate) 0 0 9 2
AN Tumor-promoting inflammation (suppress) 0 0 7 4
TIM Urokinase plasminogen activator (suppress) 1 RI 0 7 3
TME VEGF (inhibit) 0 3 8 0
EAG Wildtype p53 (upregulate) 0 0 10 1
SPS Wnt (B-catenin) (inhibit) 0 3 7 1
EAG YAP/TEAD activity (inhibit) 0 0 6 5
TIM β-catenin/ZEB1 (inactivate) 0 0 7 4
IE γδ T-cell activity (promote) 2 TPI, AN 0 4 5
Totals: 32 62 543 177
Percentages: 3.93% 7.62% 66.71% 21.74%
1

For each target, the following items are shown: the hallmark(s) for which it was selected, and the number of other hallmarks with which it has complementary relationships, contrary relationships, no known relationships and controversial relationships. For targets that have contrary relationships, the conflicted hallmark(s) are shown. Totals and percentages of each type of relationship are shown at the end of the table.

2

AN = Angiogenesis, AP = Resistance to Apoptosis, DM = Dysregulated Metabolism, EAG = Evasion of Anti-Growth Signaling, GI = Genomic Instability, IE = Immune Evasion, RI = Replicative Immortality, SPS = Sustained Proliferative Signaling, TIM = Tissue Invasion and Metastasis, TME = Tumor Microenvironment, TPI = Tumor Promoting Inflammation.