Dichloroacetate / Warburg Cancer Research Results

DCA, Dichloroacetate: Click to Expand ⟱

Features:

Dichloroacetate (DCA) is a metabolic modulator that targets the altered metabolic state of cancer cells by inhibiting PDKs. This action impacts several key pathways:

• Reversal of the Warburg effect
• Restoration of mitochondrial function and promotion of apoptosis
• suppresses glycolysis and promotes oxidative phosphorylation, thereby increasing mitochondrial ROS-mediated apoptosis in tumor cells • Increase in ROS production leading to oxidative stress
• Inhibition of cell cycle progression
• Modulation of HIF-1α signaling: DCA might decrease HIF-1α stabilization, thereby reducing the expression of genes that support glycolysis, angiogenesis, and survival under low-oxygen conditions.

-DCA has been primarily used in treating congenital lactic acidosis—a rare genetic disorder characterized by the buildup of lactic acid in the body.
-DCA is an experimental anti-diabetic and lipid-lowering drug, as well as treating myocardial and cerebrovascular ischemia.

-Do not add DCA to hot or warm beverages(theorical). DCA is unstable at higher temperatures
-Caffeinated may increase effectiveness
-Vitamin B1 reduces neuropathy (500mg-2500mg/day)
-Possibly 20 grams of citric acid 20 minutes before taking DCA
-Procaine, Diclofenac or Sulindac may increase SMCT1
-Omeprazole 80mg/day to increase DCA effectiveness
-Scorpion venom to increase DCA effectiveness
-Metformin 1000mg to 1500mg/day
-Propranolol (Ref.)
-Fenbendazole shows strong synergy when combined to DCA, So it may make very much sense to combine the two.
"Note: DCA is not tumor cell specific,> and therefore the same shift in glucose metabolism that occurs in cancer cells will also take place in immune cells, leading to induction of Tregs (Ref.). In order to avoid this possibility, while using DCA I would also use Treg inhibitors such as Cimetidine (Ref.) or low dose Cyclophosphamide (Ref.)."
"DCA should not be used in association with allopurinol, NSAIDs, or flavonoids because they reduce cellular DCA uptake."
"triple association of DCA, metformin and celecoxib, which has never been experimentally tested in patients, deserves well planned phase II clinical trials"

Research Dose: 10mg/kg/day and increase slowly to about 25mg/kg/day:(1/2morn,1/2evening) take 5 days on, 2 off? OR 2wks on/ 1wk off: https://www.thedcasite.com/dca_dosage.html
Done by mixing it in water and drinking, suggested that DCA not be taken on an empty stomach.

****
DCA-induced apoptosis in cancer cells requires sodium-coupled monocarboxylates transporter SLC5A8 (SMCT1)
-Inhibitors of DNA methylation induce reactivation of SLC5A8
-Procaine is a DNA-demethylating agent with growth-inhibitory effects in human cancer cells.
-SMCT1 was found to be stimulated by some other NSAIDs (diclofenac, meclofenamate and sulindac), by activin A143 and by the probiotic Lactobacillus plantarum.

SMCT1 has been found to be inhibited by some NSAIDs (ibuprofen, ketoprofen, fenoprofen, naproxen135 and indomethacin94), phytochemicals (resveratrol and quercetin) **** Hence these should be avoided with DCA(theorical). (also theorically AVOID Bromide, iodide and sulfite )

****
GSTZ1 an/or chloride anion transport inhibitors also reduce resistance to DCA (if the tumor expresses GSTZ1 and contains a high chloride anions level, the GSTZ1 will be stable, maintaining the resistance to DCA).

-Dichloroacetate-dca-treatment-strategy GSTZ1 an/or chloride anion transport inhibitors. .
-Etacrynic acid is a Cl(-)-ATPase inhibitor
-Lansoprazole and Omeprazole inhibit chloride channels.
-Chlorotoxin found in scorpion venom (see my post on scorpion venom) can also inhibit chlorine channels

Sources:
https://northernhealthproducts.com/shop/
https://www.dcalab.com/
Excellent DCA review

Dichloroacetate — Dichloroacetate, usually administered as sodium dichloroacetate, is a small-molecule metabolic modulator that inhibits pyruvate dehydrogenase kinases and thereby activates the mitochondrial pyruvate dehydrogenase complex. It is formally classified as an investigational metabolic drug and pyruvate dehydrogenase kinase inhibitor. DCA is a synthetic chlorinated acetate historically investigated for congenital mitochondrial and lactic-acidosis disorders; it is not an approved anticancer therapy. Its principal translational limitation is the narrow separation between concentrations that alter tumor metabolism and chronic exposures associated with peripheral neuropathy.

Primary mechanisms (ranked):

Inhibition of PDK isoenzymes, especially PDK2, causing ↓ inhibitory PDH phosphorylation and ↑ pyruvate entry into mitochondrial oxidation.
Partial reversal of the Warburg phenotype through ↓ lactate-producing glycolytic flux and ↑ mitochondrial oxidative phosphorylation.
Remodeling of cancer-cell mitochondrial membrane potential and restoration of intrinsic apoptotic susceptibility.
↑ mitochondrial ROS and oxidative stress in susceptible cancer cells, particularly under hypoxic or treatment-stressed conditions.
Attenuation of the HIF-1α–PDK metabolic adaptation to hypoxia, with context-dependent effects on tumor oxygenation and treatment resistance.
Radiosensitization and chemosensitization through metabolic reprogramming, increased oxidative stress, altered autophagy and reduced hypoxia-associated resistance.
Context-dependent modulation of Kv1.5, intracellular K⁺, NFAT and Ca²⁺-linked apoptotic signaling.

Bioavailability / PK relevance: Oral DCA is systemically bioavailable, but its pharmacokinetics are nonlinear and time-dependent. DCA is metabolized primarily by GSTZ1, while DCA also irreversibly inhibits GSTZ1, producing reduced clearance and progressive drug accumulation during repeated exposure. GSTZ1 genotype, age and treatment duration can substantially alter plasma exposure. Chronic exposure is limited principally by reversible or incompletely reversible peripheral sensory and motor neuropathy; gastrointestinal, hepatic and hematologic adverse effects have also been reported.

In-vitro vs systemic exposure relevance: Many anticancer studies use approximately 1–20 mM DCA, frequently 5–20 mM. Sustained human plasma concentrations at the upper end of this range are generally not achievable without substantial toxicity. Clinical PK data indicate that tolerated concentrations may inhibit constitutive PDK2 but may be inadequate for less-sensitive or highly induced PDK isoforms. Consequently, strong cytotoxicity observed at high millimolar concentrations should not be assumed to translate directly to patients.

Clinical evidence status: Extensive preclinical evidence; several small phase I and phase II human studies; one randomized placebo-controlled phase II adjunct study with cisplatin chemoradiotherapy; no phase III validation and no regulatory approval for cancer. Early trials demonstrate measurable metabolic effects and generally manageable short-term administration, but objective anticancer efficacy remains inconsistent and unproven. A randomized head-and-neck cancer study did not establish a clear survival advantage, while reporting increased low-grade fever and thrombocytopenia. DCA remains an investigational adjunct rather than a standard anticancer treatment.

Dichloroacetate Mechanistic Profile

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	PDK inhibition and PDH activation	↓ PDK activity ↓ p-PDH ↑ active PDH	↓ PDK activity ↑ glucose oxidation	P–G	Redirects pyruvate toward acetyl-CoA and mitochondrial oxidation	Canonical mechanism. PDK2 is relatively sensitive; inhibition of other PDK isoforms may require higher exposure.
2	Warburg metabolism and glycolysis	↓ glycolytic dependence ↓ ECAR ↓ lactate production	Variable metabolic shift	R–G	Reduces fermentative glucose metabolism and extracellular acidification	Effect magnitude depends on PDK expression, mitochondrial competence, substrate availability and tumor lineage.
3	Mitochondrial respiration	↑ pyruvate oxidation ↑ OCR ↑ OXPHOS	↑ glucose oxidation ↑ mitochondrial workload	R–G	Restores mitochondrial use of glucose-derived carbon	Increased respiration is not intrinsically cytotoxic and can support survival in metabolically flexible tumors.
4	Mitochondrial membrane potential and apoptosis	↓ pathological hyperpolarization ↑ cytochrome c release ↑ caspase activation	Usually less pronounced	R–G	Lowers the threshold for intrinsic apoptosis	Strongest in models with cancer-associated mitochondrial hyperpolarization; not universal across tumor types.
5	Mitochondrial ROS increase	↑ mt-ROS ↑ oxidative damage (context-dependent)	↔ or ↑ ROS with prolonged exposure	R–G	Produces redox stress and apoptotic sensitization	ROS direction is model-dependent. Increased respiration can raise ROS, but improved electron flow may reduce ROS in some systems.
6	HIF-1α and hypoxic adaptation	↓ HIF-1α signaling ↓ PDK1-mediated adaptation (context-dependent)	Limited evidence	G	Weakens hypoxia-driven glycolysis, survival and treatment resistance	DCA can also increase cellular oxygen consumption; the net effect on tumor hypoxia depends on perfusion and oxygen delivery.
7	Radiosensitization	↑ radiation sensitivity ↑ ROS-mediated injury ↓ hypoxic resistance	Potential normal-tissue sensitization (context-dependent)	R–G	Enhances radiation response in selected models	Supported preclinically and evaluated clinically as an adjunct, but a definitive therapeutic benefit has not been established.
8	Chemosensitization	↑ sensitivity to cisplatin, 5-FU, paclitaxel and selected metabolic agents (model-dependent)	Potential additive toxicity	G	Reduces metabolic and hypoxic drug resistance	Combination effects vary markedly. Preclinical synergy does not establish clinical efficacy or safe dosing.
9	Autophagy	↑ or ↓ autophagic flux (context-dependent)	Insufficient evidence	G	May promote adaptation or enhance treatment-induced death	Autophagy is bidirectional: DCA-induced autophagy can be protective in some tumors and therapeutically exploitable in others.
10	Kv1.5 NFAT and Ca²⁺ signaling	↑ Kv1.5 ↓ intracellular K⁺ ↓ NFAT activation Ca²⁺ modulation	Variable	R–G	Facilitates apoptotic signaling and suppresses proliferation	Mechanistically important in selected early models but less consistently demonstrated than the PDK–PDH axis.
11	Transport and metabolic sensitivity	SLC5A8 may ↑ intracellular DCA response GSTZ1 and chloride modify sensitivity	GSTZ1 controls systemic clearance	G	Determines cellular exposure, metabolism and resistance	SLC5A8 dependence is model-specific. GSTZ1 genotype and self-inactivation are clinically important determinants of exposure and neuropathy.
12	Clinical Translation Constraint	High millimolar concentrations often required heterogeneous PDK expression metabolic plasticity	Peripheral neuropathy variable clearance possible hepatic and hematologic toxicity	G	Restricts sustained target coverage and therapeutic index	Human exposure may inhibit PDK2 yet remain below concentrations used for broad in-vitro cytotoxicity. DCA is investigational and not an approved cancer treatment.

P: 0–30 min R: 30 min–3 hr G: >3 hr

Older Table:

Rank	Pathway / Target Axis	Direction	Primary Effect	Notes / Cancer Relevance	Ref
1	Pyruvate dehydrogenase kinase (PDK) → PDH gatekeeper	↓ PDK activity → ↑ active PDH (dephosphorylated)	Warburg reversal (pyruvate into TCA)	DCA’s canonical mechanism: inhibits PDK, restoring PDH activity and oxidative metabolism in cancer	(ref)
2	Glycolysis output (lactate / ECAR)	↓ lactate production / ↓ ECAR	Reduced acidification; metabolic reprogramming	DCA decreases PDH phosphorylation and lowers glycolytic output (lactate/ECAR) in cancer models	(ref)
3	Mitochondrial membrane potential remodeling (ΔΨm)	↓ cancer-associated mitochondrial hyperpolarization (depolarization)	Restores apoptosis susceptibility	Glioblastoma work: DCA reverses cancer-specific mitochondrial remodeling (hyperpolarization → depolarization), enabling apoptosis	(ref)
4	ROS generation (especially under hypoxia)	↑ ROS	Oxidative stress trigger	DCA increases ROS in hypoxic cancer cells (reported strongly under hypoxia), linking metabolic shift to cytotoxic stress	(ref)
5	Voltage-gated K+ channel axis (Kv1.5) / NFAT signaling	↑ Kv1.5 expression/activity	Pro-apoptotic electrophysiology shift	Endometrial cancer study: DCA engages mitochondrial + NFAT–Kv1.5 mechanisms associated with apoptosis sensitization	(ref)
6	Intrinsic apoptosis (mitochondrial pathway)	↑ apoptosis	Programmed cell death	DCA induces apoptosis in glioblastoma and endometrial cancer models as mitochondrial remodeling is reversed	(ref)
7	PUMA-mediated apoptotic priming	↑ PUMA-dependent sensitization	Lower apoptotic threshold	Endometrial cancer paper explicitly reports a PUMA-mediated component in DCA apoptosis sensitization	(ref)
8	Hypoxia resistance axis (HIF-1α / PDK1)	↓ hypoxia-associated resistance (HIF-1α/PDK1 axis engaged)	Improved treatment responsiveness	DCA attenuates hypoxia-associated resistance in gastric cancer context with reported linkage to HIF-1α and PDK1	(ref)
9	Radiosensitization (hypoxic tumor cells)	↑ radiosensitivity (esp. under hypoxia)	Therapy potentiation	DCA increases ROS under hypoxia and enhances radiotherapy response in TNBC models	(ref)
10	In vivo / translational anti-tumor activity (glioblastoma)	↓ tumor growth / ↓ proliferation (model-dependent)	Demonstrated anti-tumor effect	Glioblastoma study includes translational evidence that DCA can reverse tumor metabolic remodeling with anti-tumor effects	(ref)

Warburg, Warburg Effect: Click to Expand ⟱

Source:

Type: effect

The Warburg effect (aerobic glycolysis) is a metabolic phenotype where many cancer cells use high glycolytic flux and lactate production even when oxygen is available. Tumors often contain hypoxic regions that further drive glycolysis, but Warburg metabolism can also occur under normoxic conditions (“pseudo-hypoxia”) via oncogenic signaling and metabolic rewiring.

Hypoxia-inducible factor 1 alpha (HIF-1α) is one important driver in hypoxic tumor regions. HIF-1α upregulates glycolytic genes (e.g., GLUT1, HK2, LDHA) and promotes reduced mitochondrial pyruvate oxidation in part through induction of PDK (which inhibits PDH), shifting carbon toward lactate.

Warburg effect (GLUT1, LDHA, HK2, and PKM2).
Classic HIF-Warburg axis: PDK1 and MCT4 (SLC16A3) (pyruvate gate + lactate export).

Here are some of the key pathways and potential targets:

Note: use database Filter to find inhibitors: Ex pick target HIF1α, and effect direction ↓

1.Glycolysis Inhibitors:(2-DG, 3-BP)
- HK2 Inhibitors: such as 2-deoxyglucose, can reduce glycolysis
-PFK1 Inhibitors: such as PFK-158, can reduce glycolysis
-PFKFB Inhibitors:
- PKM2 Inhibitors: (Shikonin)
-Can reduce glycolysis
- LDH Inhibitors: (Gossypol, FX11)
-Reducing the conversion of pyruvate to lactate.
-Inhibiting the production of ATP and NADH.
- GLUT1 Inhibitors: (phloretin, WZB117)
-A key transporter involved in glucose uptake.
-GLUT3 Inhibitors:
- PDK1 Inhibitors: (dichloroacetate)
- A key enzyme involved in the regulation of glycolysis. PDK inhibitors (e.g., DCA) activate PDH and shift pyruvate into TCA/OXPHOS, reducing lactate pressure.

2.Pentose phosphate pathway:
- G6PD Inhibitors: can reduce the pentose phosphate pathway

3.Hypoxia-inducible factor 1 alpha (HIF1α) pathway:
- HIF1α inhibitors: (PX-478,Shikonin)
-Reduce expression of glycolytic genes and inhibit cancer cell growth.

4.AMP-activated protein kinase (AMPK) pathway:
-AMPK activators: (metformin,AICAR,berberine)
-Can increase AMPK activity and inhibit cancer cell growth.

5.mTOR pathway:
- mTOR inhibitors:(rapamycin,everolimus)
-Can reduce mTOR activity and inhibit cancer cell growth.

Warburg Targeting Matrix (Cancer Metabolism)

Node	What It Does (Warburg role)	Representative Inhibitors / Modulators	Mechanism Snapshot	Typical Tumor Effects	Best-Fit Tumor Context	Common Constraints / Gotchas	TSF	Combination Logic
GLUT (glucose uptake) GLUT1 (SLC2A1) focus	Controls glucose entry; sets the upper bound on glycolytic flux.	Research/repurposing: WZB117 (GLUT1), BAY-876 (GLUT1), STF-31 (GLUT1 tool), Fasentin (GLUT), Phloretin (broad, weak) Dietary/indirect: some polyphenols reported to lower GLUT1 expression (context)	Blocks glucose transport or reduces GLUT1 expression → less substrate for glycolysis & PPP.	ATP stress (in highly glycolytic tumors), lactate ↓, growth slowdown; can sensitize to stressors.	High-GLUT1 tumors; hypoxic / glycolysis-addicted phenotypes.	Systemic glucose handling and glucose-dependent tissues; tumor compensation via alternate fuels.	P, R	Pairs with ROS/ETC stressors or LDH/MCT blockade; beware compensatory glutaminolysis/fatty acid oxidation.
Hexokinase (HK2) first committed glycolysis step	Traps glucose as G-6-P; HK2 often upregulated and mitochondria-associated in tumors.	Clinical/adjunct interest: 2-Deoxyglucose (2-DG; glycolysis + glycosylation stress) Research: Lonidamine-class glycolysis axis drugs (not “pure HK2”), 3-bromopyruvate (hazardous research agent; not for casual use)	Competitive substrate mimic (2-DG) → 2-DG-6P accumulation; HK flux ↓; ER glycosylation stress ↑.	ATP ↓, AMPK ↑, ER stress/UPR ↑, autophagy ↑, apoptosis (context); radiosensitization reported.	Highly glycolytic tumors; tumors with strong HK2 dependence; hypoxic cores.	Normal glucose-dependent tissues; ER-stress toxicities; dosing/tolerability limits in practice.	P, R, G	Pairs with radiation, pro-oxidant stress, or MCT/LDH blockade; watch systemic glucose effects.
LDH (LDHA/LDHB) pyruvate ⇄ lactate	Regenerates NAD+ to sustain glycolysis; LDHA supports lactate production and acidification.	Tier A direct inhibitors: FX11, (R)-GNE-140, NCI-006, Oxamate, Galloflavin, Gossypol Tier B indirect: polyphenols (often lactate/LDH expression ↓ rather than catalytic inhibition)	Blocks LDH catalysis → NAD+ recycling ↓ → glycolysis throttles; pyruvate handling shifts; redox pressure ↑.	Lactate ↓, glycolytic flux ↓, oxidative stress ↑ (often secondary), growth inhibition; immune microenvironment may improve if lactate decreases.	LDHA-high tumors; lactate-driven immunosuppression; glycolysis-addicted phenotypes.	Metabolic plasticity: tumors switch fuels; some LDH inhibitors have PK liabilities; “LDH release” ≠ LDH inhibition.	R, G	Pairs with MCT inhibition (trap lactate), NAD+ axis inhibitors, immune therapy (lactate suppression logic), and OXPHOS stressors (context).
MCT (lactate transport) MCT1 (SLC16A1), MCT4 (SLC16A3)	Exports lactate + H+ (acidifies TME); enables lactate shuttling between tumor subclones.	Clinical-stage: AZD3965 (MCT1 inhibitor; clinical trials) Research: AR-C155858 (MCT1/2), Syrosingopine (MCT1/4; repurposed), Lonidamine (MCT + MPC axis)	Blocks lactate export/import → intracellular acid stress ↑ (in glycolytic cells) and lactate shuttling ↓.	Acid stress, growth inhibition; may improve immune function by reducing lactate/acidic suppression (context).	MCT1-high tumors; oxidative “lactate-using” tumor fractions; tumors with lactate shuttling.	MCT4-driven export can bypass MCT1-only inhibitors; hypoxia upregulates MCT4; need target matching.	P, R	Pairs strongly with LDH inhibitors (cut production + block export), and with immune therapy rationale (lactate/acid microenvironment).
PDK (PDK1-4) PDH gatekeeper	PDK inhibits PDH → keeps pyruvate out of mitochondria; supports Warburg by favoring lactate.	Prototype: Dichloroacetate (DCA; pan-PDK inhibitor “classic”) Research: AZD7545 (PDK2 inhibitor; tool), newer PDK inhibitor series (research)	Inhibits PDK → PDH active ↑ → pyruvate into TCA/OXPHOS ↑; lactate pressure ↓.	Warburg reversal pressure (context), lactate ↓, mitochondrial flux ↑; can increase ROS in some settings (secondary).	PDK-high tumors; tumors with suppressed PDH flux; “glycolysis locked” metabolic phenotype.	Requires functional mitochondrial capacity; hypoxia can limit OXPHOS shift; effect is often modulatory rather than directly cytotoxic.	R, G	Pairs with therapies that exploit mitochondrial dependence or redox stress; can complement LDH/MCT strategies by reducing lactate drive.

Time-Scale Flag (TSF): P / R / G

P: 0–30 min (direct transport/enzyme flux effects begin)
R: 30 min–3 hr (acute ATP/NAD+/acid stress and signaling changes)
G: >3 hr (gene adaptation, phenotype outcomes, immune/TME effects)

Scientific Papers found: Click to Expand⟱

1884-

DCA,

Sal,

Dichloroacetate and Salinomycin Exert a Synergistic Cytotoxic Effect in Colorectal Cancer Cell Lines

in-vitro,

CRC,

DLD1

in-vitro,

CRC,

HCT116

eff↑, pH↓, PDKs↓, Warburg↓,

6683-

DCA,

Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts

Review,

Var,

PDK1↓, lactateProd↓, Apoptosis↑, TumCP↓, selectivity↑, other↝, Dose↝, BioAv↑, Half-Life↓, Glycolysis↓, OXPHOS↑, Casp↑, i-pH↓, COX2↑, Hif1a↓, angioG↓, HMG-CoA↓, GSTZ1↓, OCR↑, lipoGen↓, fatigue↓, survivin↓, miR-375↑, eff↓, CSCs↓, TumAuto↑, mTOR↓, TumCI↓, TumVol↓, TumW↓, ATP↓, Warburg↓, eff↑, e-pH↑, eff↑, eff↑, other↝, RadioS↑, toxicity↓, Dose↝, eff↑, eff↑, eff↑, toxicity↝, eff↓,

1873-

DCA,

Dual-targeting of aberrant glucose metabolism in glioblastoma

in-vitro,

GBM,

U87MG

in-vitro,

GBM,

U251

PDKs↓, eff↑, selectivity↑, MMP↓, ROS↑, Apoptosis↑, Warburg↓, eff↑, Dose∅, toxicity∅,

1875-

DCA,

Dichloroacetate inhibits neuroblastoma growth by specifically acting against malignant undifferentiated cells

in-vitro,

neuroblastoma,

in-vivo,

NA,

five mice were treated with 2.5 mg/kg/
dose of DCA, 14 mice were treated with 25 mg/kg/dose

mice

selectivity↑, AntiCan↑, TumVol↓, PDKs↓, mt-OXPHOS↑, MMP↓, Glycolysis↓, toxicity↓, Warburg↓, ROS↑, eff↑,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: Warburg, Warburg Effect

4 Dichloroacetate
1 salinomycin

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:288  Target#:947  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

Dichloroacetate / Warburg Cancer Research Results

Dichloroacetate Mechanistic Profile

Warburg Targeting Matrix (Cancer Metabolism)

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

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