Portal:CPTAC/Hallmarks

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Current revision (18:59, 5 October 2017) (view source)
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|width=100px; style="text-align:center;"|[[Portal:CPTAC/Hallmark/Avoiding|<big><u><b>Avoiding immune destruction</b></u></big>]] {{ #pathwayOfTheDay: {{LOCALDAYNAME}} {{LOCALDAY}} {{LOCALMONTHNAME}} {{LOCALYEAR}} | Portal:CPTAC/Hallmark/Avoiding}}
|width=100px; style="text-align:center;"|[[Portal:CPTAC/Hallmark/Avoiding|<big><u><b>Avoiding immune destruction</b></u></big>]] {{ #pathwayOfTheDay: {{LOCALDAYNAME}} {{LOCALDAY}} {{LOCALMONTHNAME}} {{LOCALYEAR}} | Portal:CPTAC/Hallmark/Avoiding}}
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|width=100px; style="text-align:center;"|[[Portal:CPTAC/Hallmark/Therapeutics|<big><u><b>Therapeutics</b></u></big>]] {{ #pathwayOfTheDay: {{LOCALDAYNAME}} {{LOCALDAY}} {{LOCALMONTHNAME}} {{LOCALYEAR}} | Portal:CPTAC/Hallmark/Therapeutics}}
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Current revision

Sustaining proliferative signaling

Translation inhibitors in chronically activated PDGFRA cells (Homo sapiens)

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Translation inhibitors in chronically activated PDGFRA cells
Evading growth suppressors

G1 to S cell cycle control (Homo sapiens)

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G1 to S cell cycle control
Activating invasion and metastasis

Focal adhesion: PI3K-Akt-mTOR-signaling (Homo sapiens)

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Focal adhesion: PI3K-Akt-mTOR-signaling
Enabling replicative immortality

Notch signaling (Homo sapiens)

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Notch signaling
Inducing angiogenesis

Angiogenesis (Homo sapiens)

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Angiogenesis
Resisting cell death

Target of rapamycin signaling (Homo sapiens)

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Target of rapamycin signaling
Deregulating cellular energetics

Glycolysis and gluconeogenesis (Homo sapiens)

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Glycolysis and gluconeogenesis
Genome instability and mutation

Nucleotide excision repair (Homo sapiens)

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Nucleotide excision repair
Tumor promoting inflammation

IL6 signaling (Homo sapiens)

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IL6 signaling
Avoiding immune destruction

Interferon type I signaling (Homo sapiens)

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Interferon type I signaling
Therapeutics

MFAP5 effect on permeability and motility of endothelial cells via cytoskeleton rearrangement (Homo sapiens)

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MFAP5 effect on permeability and motility of endothelial cells via cytoskeleton rearrangement