Oncology pathway explorer
Pathways
Signalling
PI3K/AKT
PI3K phosphorylates PIP2 to PIP3, recruiting AKT. AKT supports growth, survival, glucose uptake and mTORC1 input. Pathway activation is common via PIK3CA mutation, PTEN loss or receptor-tyrosine-kinase signalling.
Signalling
mTOR
mTORC1 integrates growth-factor and nutrient signals to drive protein synthesis, lipid synthesis and autophagy suppression. It sits downstream of PI3K/AKT and amino-acid sensing.
Signalling
MAPK/ERK
The RAS–RAF–MEK–ERK cascade transmits mitogenic RTK signals to transcription programmes for proliferation and differentiation.
Signalling
RAS/RAF
RAS GTPases and RAF kinases are frequent oncogenic nodes. KRAS, NRAS and BRAF mutations lock mitogenic signalling on in a ligand-independent way in many tumours.
Metabolism
AMPK
AMP-activated protein kinase senses AMP:ATP ratio, restraining anabolic mTOR signalling and favouring catabolic programmes including fatty-acid oxidation.
Signalling
MYC
MYC transcription factors coordinate biomass accumulation, ribosome biogenesis, glycolysis and glutamine use. Amplification or pathway activation is common.
Signalling
Wnt/β-catenin
Canonical Wnt signalling stabilizes β-catenin, driving TCF/LEF transcription. APC loss is a classic colorectal initiating event; the pathway also contributes to stemness in several tissues.
Stemness
Hedgehog
Hedgehog–GLI signalling patterns development and can support basal-cell and some stromal/stem-like tumour programmes. Ligand-dependent stromal Hedgehog is distinct from mutation-driven ligand-independent activation.
Stemness
Notch
Notch receptors undergo ligand-induced cleavage to NICD, altering lineage and stem/progenitor decisions. Context determines oncogenic versus tumour-suppressive roles.
Signalling
JAK/STAT
Cytokine receptors signal through JAKs to STATs. STAT3 in particular supports survival, invasion and inflammatory gene programmes in many solid and hematologic tumours.
Immune
NF-κB
NF-κB transcription factors link inflammatory cytokines and innate sensors to survival, cytokine production and sometimes therapy resistance.
Microenvironment / fibrosis
TGF-β
TGF-β is cytostatic in intact epithelium but later supports EMT, immune suppression and stromal fibrosis. Context switches its role during progression.
Angiogenesis / hypoxia
HIF-1α
Hypoxia-inducible factors stabilize when oxygen is low, shifting transcription toward glycolysis, angiogenesis and survival.
Angiogenesis / hypoxia
VEGF
VEGF family ligands drive endothelial sprouting and vascular permeability, a canonical tumour angiogenesis axis.
Signalling
EGFR
EGFR is an ERBB-family receptor tyrosine kinase. Ligand activation or mutation (notably NSCLC exon 19/L858R) drives MAPK and PI3K signalling.
Signalling
HER2
HER2/ERBB2 amplification or overexpression produces ligand-independent ERBB signalling, classically in a subset of breast and gastroesophageal cancers and rarely in colorectal cancer.
Signalling
Androgen receptor
AR is a nuclear receptor transcription factor required for most prostate adenocarcinoma growth. Resistance can occur through AR amplification, splice variants, or lineage plasticity.
Signalling
Estrogen receptor
ERα (ESR1) drives a large fraction of breast cancers via genomic and non-genomic signalling. ESR1 mutations and growth-factor crosstalk contribute to endocrine resistance.
Epigenetic / DNA repair
PARP / DNA repair
Homologous-recombination defects (BRCA1/2 and related) create dependence on PARP-mediated repair. Mismatch-repair deficiency creates hypermutation and immune visibility.
Death / survival
p53
TP53 encodes a stress-responsive transcription factor controlling cell-cycle arrest, apoptosis and metabolic adaptation. Loss or mutation is among the most common cancer events.
Death / survival
BCL-2 family
BCL-2, BCL-XL, MCL-1 and BAX/BAK control mitochondrial outer-membrane permeabilization, a core apoptosis checkpoint frequently skewed toward survival in lymphoid and solid tumours.
Death / survival
Apoptosis
Intrinsic and extrinsic apoptotic programmes remove damaged cells. Evasion of apoptosis is a hallmark, via BCL-2 family imbalance, death-receptor decoys, or p53 loss.
Death / survival
Autophagy
Autophagy recycles organelles and can support survival under nutrient or therapy stress. Context determines tumour-suppressive versus therapy-protective roles.
Death / survival
Ferroptosis
Ferroptosis is iron-dependent lipid-peroxidation cell death opposed by GPX4 and cystine/GSH supply. Some therapy-resistant and mesenchymal states show altered ferroptosis sensitivity.
Metabolism
Glycolysis
Aerobic glycolysis (Warburg metabolism) supports ATP, biomass and redox buffering even when oxygen is available. Hexokinase, PKM2 and lactate export are frequent nodes.
Metabolism
Glutaminolysis
Glutamine supplies nitrogen and anaplerotic carbon via glutaminase and glutamate dehydrogenase, supporting nucleotide synthesis and TCA replenishment in MYC-driven and other tumours.
Metabolism
Fatty-acid metabolism
De novo lipogenesis, fatty-acid oxidation and lipid uptake are rewired in a tumour-type-specific way, especially in hypoxic, obese-host, or OXPHOS-dependent subsets.
Metabolism
Mitochondrial oxidative phosphorylation
Despite Warburg metabolism, many tumours retain or upregulate OXPHOS, including residual disease, CSC-like fractions and some oncogene-driven subsets.
Metabolism
Lactate metabolism
Lactate export acidifies the extracellular space and can fuel oxidative tumour or stromal compartments (metabolic symbiosis). MCT transporters are central.
Metabolism
Oxidative stress
Reactive oxygen species are both signalling molecules and sources of damage. Tumours often upregulate antioxidant programmes to live with higher ROS set-points.
Metabolism
NRF2
NRF2/KEAP1 controls antioxidant and detoxification transcription. KEAP1 or NFE2L2 mutations in lung and other cancers stabilize NRF2 and can confer therapy resilience.
Immune
COX / inflammatory signalling
COX-2–PGE2 signalling can promote angiogenesis, immune suppression and epithelial proliferation, notably in colorectal neoplasia.
Immune
PD-1 / PD-L1
PD-1 on T cells engaging PD-L1/PD-L2 restrains cytotoxic function. Tumour or myeloid PD-L1 is a canonical adaptive immune-evasion axis.
Immune
CTLA-4
CTLA-4 competes with CD28 for B7 ligands, restraining priming of T cells mainly in lymphoid tissues and Tregs.
Immune
Immune suppression
Tumours recruit Tregs, MDSCs and M2-like macrophages, and secrete TGF-β, IL-10, adenosine and IDO-related metabolites to blunt effector immunity.
Angiogenesis / hypoxia
Angiogenesis
New vessel formation supplies oxygen and routes for dissemination. It is driven by VEGF, angiopoietins, FGF and inflammatory cytokines under hypoxia.
Invasion / metastasis
EMT
Epithelial–mesenchymal plasticity, driven by TWIST/SNAIL/ZEB and TGF-β/Wnt/Notch inputs, reduces adhesion and increases motility and stem-like features.
Invasion / metastasis
Invasion
Invasion requires adhesion turnover, cytoskeletal protrusion and protease-mediated matrix remodelling (MMPs, uPA).
Invasion / metastasis
Metastasis
Metastasis is a cascade of local invasion, intravasation, survival in circulation, organ tropism, extravasation and colonization, shaped by pre-metastatic niches.
Stemness
Cancer stemness
Stem-like programmes (Wnt, Notch, Hedgehog, ALDH, CD44) can support self-renewal, quiescence and therapy tolerance in a minority population.
Resistance
Drug efflux
ABC transporters such as ABCB1/P-gp, ABCC1 and ABCG2 export structurally diverse drugs and contribute to multidrug-resistance phenotypes.
Metabolism
One-carbon / methionine metabolism
Folate-methionine cycles supply nucleotides and methylation. Some tumours show methionine dependence and PHGDH or SHMT rewiring.
Metabolism
NAD+/NADH
NAD+ pools support redox balance, PARP activity and sirtuins. NAMPT-dependent salvage is a vulnerability in some models.
Signalling
Hippo / YAP
Hippo signalling restrains YAP/TAZ transcriptional co-activators. NF2 loss, common in mesothelioma, derepresses YAP-driven growth programmes.
This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.