One of the most reactive ROS—very damaging but very short-lived.
Glossary of Terms
Plain-English explanations of scientific terms you’ll see across OncoForge.
•
•OH (Hydroxyl Radical)
5
5-LOX (5-Lipoxygenase)
An enzyme that makes inflammatory signals (leukotrienes) which may support tumor growth.
A
AKT (Protein Kinase B)
A survival signal inside cells. When overactive (common in cancer), it pushes growth and resists cell death. Many agents try to turn it down.
ALDH (Aldehyde Dehydrogenase)
Detox enzymes; high ALDH activity can mark stem-like tumor cells in some cancers.
AMPK
The cell’s fuel gauge. When switched on, it generally slows growth pathways like mTOR.
Angiogenesis
The building of new blood vessels. Tumors hijack this process to feed themselves. Anti-angiogenic therapies try to cut off that blood supply.
Anti-Proliferative
Slows or stops cells from multiplying.
Antioxidant
Reduces oxidative stress. Timing around treatments can matter.
Apoptosis
A built-in, tidy self-destruct program for damaged cells. Many anticancer therapies try to switch this back on in tumor cells so they die cleanly.
Autophagy
Cellular recycling. It can help cells survive stress or, in some settings, lead to cell death.
B
Bcl-2
A “stay alive” protein. High levels can help cancer cells resist cell death.
Bioavailability
How much of a dose actually reaches the bloodstream and the target.
C
Cachexia
Cancer-related wasting—loss of weight and muscle with metabolic changes.
Caspase
A family of enzymes that carry out apoptosis once it’s been triggered.
Checkpoint Inhibitor
Immunotherapy drugs that take the brakes off T-cells (PD-1/PD-L1 or CTLA-4).
Chelator
A metal-binding compound (e.g., for iron or copper) that can alter redox and drug actions.
Chemo Sensitivity
How strongly a tumor responds to a chemo drug. “Sensitizers” try to boost this response.
Chemosensitizer
Makes tumor cells more responsive to chemotherapy.
Complex I (NADH Dehydrogenase)
The first big enzyme in the mitochondrial energy chain—targeted by some metabolic drugs.
COX-2
An inflammation enzyme that makes prostaglandins; frequently elevated in tumors.
CSC (Cancer Stem Cells)
A small, stubborn sub-group that can resist therapy and restart tumors.
CTL (Cytotoxic T Lymphocyte)
A T-cell that directly kills virus-infected or tumor cells.
CTLA-4
Another T-cell brake that checkpoint drugs can target.
CYP1A1
A drug-metabolizing enzyme induced by some plant compounds and pollutants.
CYP3A4
A liver enzyme that processes many drugs. Interactions can raise or lower drug levels.
Cytostatic
Slows or stops cell growth rather than killing cells outright.
Cytotoxic
Directly kills cells.
D
DC (Dendritic Cells)
Key coaches of the immune system. They present tumor pieces to T-cells to kick off attacks.
DNA Intercalation
When flat molecules slide between DNA bases and jam copying or reading.
DNMT (DNA Methyltransferase)
Adds methyl tags to DNA. DNMT inhibitors can lift certain gene silencing.
E
EGFR
A growth receptor on cell surfaces. When it’s too active, it can drive tumor growth.
EMT (Epithelial–Mesenchymal Transition)
A shift that makes tumor cells more mobile and invasive.
Endorphin
Natural “feel-good” chemicals that help with pain and well-being.
ER Stress (Endoplasmic Reticulum Stress)
When the cell’s protein-folding factory is overloaded, triggering stress responses that can end in cell death.
ETC Bypass (Electron Transport Chain Bypass)
Rerouting electrons around parts of the mitochondrial chain to keep energy or redox flowing.
F
Ferroptosis
A form of cell death driven by iron and lipid oxidation—different from apoptosis.
Fibrin
A mesh-like clotting protein. Tumors can use fibrin to shield themselves.
Fucoidan
A sulfated fiber from brown seaweed with immune-modulating and investigational anti-tumor effects.
G
Galectin-3
A sugar-binding protein tied to fibrosis, immune tone, and spread (metastasis).
Glucose
Main sugar fuel for cells. Many tumors consume lots of it.
Glycolysis
The pathway that breaks down glucose for quick energy and building blocks—often dialed up in tumors.
GPx (Glutathione Peroxidase)
Antioxidant enzymes that detox peroxides using glutathione.
GSH (Glutathione)
A major antioxidant that helps detoxify cells and maintain redox balance.
GSTP1
A detox enzyme (glutathione S-transferase pi) linked to drug resistance.
H
HA (Hyaluronic Acid)
A water-holding sugar in the tissue space around cells. Lots of HA can make tumors stiffer and harder to reach with drugs.
HAS2/3 (Hyaluronan Synthase 2/3)
Enzymes that make hyaluronic acid. When very active, they can thicken the tumor matrix and hinder blood flow.
HDAC (Histone Deacetylase)
An epigenetic “tightener.” HDAC inhibitors can re-open silenced genes and slow growth.
Hedgehog Pathway
A developmental signal route (SMO/GLI) that some tumors co-opt for growth.
HER2 (ERBB2)
A growth receptor that’s amplified in some cancers (like breast and gastric). Targeted drugs can block it.
HIF-1α (Hypoxia-Inducible Factor 1-alpha)
A low-oxygen “sensor” that helps tumors adapt when oxygen is scarce. It can drive new blood-vessel growth and make treatment harder.
HRD (Homologous Recombination Deficiency)
A DNA-repair weakness that can sensitize tumors to PARP inhibitors and certain chemo.
HSP27 (Heat Shock Protein 27)
A stress-response helper protein that can protect tumor cells from death signals.
Hypoxia
Low oxygen—common inside tumors. It changes metabolism and can blunt treatment.
L
Lectin
A protein that sticks to sugars; some affect immunity or how cells stick and move.
M
Macrophage Activator
A compound that wakes up macrophages (innate immune cells) so they better recognize and attack threats.
MAPK/ERK
A growth pathway downstream of RAS/RAF. It’s frequently overactive in cancer.
Mcl-1
A BCL2-family survival protein linked to resistance. Turning it down can re-open cell death.
Membrane (Cell Membrane)
The cell’s fatty outer layer. Its makeup affects signaling and how drugs get in.
Metastasis
When cancer spreads to distant places through blood or lymph.
Mevalonate Pathway
The cholesterol/isoprenoid-making route. It supports “prenylation” of proteins like RAS and RHO that cancers use.
Microtubules
Protein fibers that pull chromosomes apart during cell division. Some chemo drugs target them.
Mito Toxin
A compound that disrupts mitochondria (the cell’s power plants) to stress or kill cancer cells.
MMP (Matrix Metalloproteinases)
Scissor-like enzymes that cut the tissue matrix; tumors use them to invade.
mTOR (Mechanistic Target of Rapamycin)
A major growth-control switch. In many cancers it gets stuck in “grow” mode. mTOR blockers aim to slow cell growth and division.
N
Nephro-Protect (Nephroprotective)
Kidney-protective—helps limit drug-related kidney injury.
Neuropathy
Nerve damage that causes numbness, tingling, or pain—sometimes a side effect of chemotherapy.
NF-κB
A hub for inflammation signals that can help tumor cells survive and resist therapy.
NGF (Nerve Growth Factor)
A growth factor that supports nerve survival.
NK Cells (Natural Killer Cells)
Front-line immune cells that can spot and kill abnormal cells—including some cancer cells—without needing prior training.
NO Donor (Nitric Oxide Donor)
Releases nitric oxide, which can affect blood flow, immune tone, and redox.
Nrf2
A control knob for antioxidant defenses. Helpful for normal cells, but if pushed too high in tumors, it may help them cope with stress.
O
OXPHOS (Oxidative Phosphorylation)
Mitochondrial energy production. Some tumors lean more on OXPHOS than glycolysis.
P
P-gp (P-glycoprotein)
A drug pump that can spit chemotherapy back out of cancer cells and cause resistance.
p53
A guardian protein that pauses growth or triggers cell death after DNA damage. Often broken in cancer.
PARP
A DNA repair enzyme. Blocking PARP can exploit certain tumor DNA-repair weaknesses.
PD-1
A brake on T-cells. When PD-1 meets PD-L1, immune attack slows. Checkpoint drugs lift this brake.
PD-L1
A “don’t attack me” signal some tumors show to shut down T-cells. Checkpoint drugs can block it.
PDK (Pyruvate Dehydrogenase Kinase)
Shifts metabolism toward glycolysis by turning down the enzyme that feeds mitochondria.
PDK1 (3-Phosphoinositide-Dependent Protein Kinase-1)
A kinase upstream of AKT in the PI3K pathway (different from the PDKs that act on pyruvate).
Perfusion
Blood flow through tissues. Better perfusion can improve oxygen and drug delivery.
Pharmacodynamics (PD)
What the drug does to the body—how it works at its targets and what effects it causes.
Pharmacokinetics (PK)
What the body does to a drug—absorption, distribution, metabolism, excretion.
PI3K
Relay switch upstream of AKT. Together, the PI3K–AKT–mTOR pathway is a major driver of tumor growth.
PPAR
A family of nuclear receptors (α/δ/γ) that tune lipid and glucose metabolism and inflammation.
Pro-oxidant
Pushes oxidative stress higher (often selectively in tumors at high doses).
Proteasome
The cell’s protein recycler. Blocking it can overwhelm tumor cells and trigger death.
Q
QoL (Quality of Life)
How a person feels and functions day to day during or after treatment.
R
Radiosensitizer
Makes tumor cells easier to damage with radiation.
Redox (Reduction–Oxidation Balance)
The cell’s see-saw between oxidants (like ROS) and antioxidants (like glutathione). Cancer cells often tilt this balance in their favor, and some therapies exploit that tilt.
Redox Cycler
A compound that flips between reduced and oxidized forms, often generating ROS along the way.
Rho (Rho GTPases)
Small switches that control cell shape and movement; can drive invasion and spread.
ROS (Reactive Oxygen Species)
Short-lived, very reactive oxygen molecules that can damage DNA, proteins, and cell membranes. Tumors often run “hotter” with more ROS. Some treatments deliberately push ROS higher to stress or kill cancer cells.
S
Senolytic
A compound that selectively removes old, damaged (senescent) cells.
Sirtuin
A family of stress-response enzymes linked to metabolism and aging.
STAT3
A signal-to-gene switch tied to inflammation, survival, and spread (metastasis).
T
T-Cell
Adaptive immune cells (CD4 helpers, CD8 killers) that coordinate and carry out anti-tumor responses.
Telomere
Protective caps at the ends of chromosomes. Tumors often maintain them to keep dividing.
Th1 Cytokines
Immune messages (like IFN-γ, IL-2) that support T-cell–driven anti-tumor responses.
Thrombolytic
A drug that dissolves clots (for example, plasminogen activators).
Topoisomerase II (Topo II)
A DNA “untangler.” Blocking it (with drugs like anthracyclines) stops proper DNA handling in dividing cells.
TRAIL
A natural signal (TNF family) that can trigger death receptors on tumor cells.
Treg Mod (Regulatory T-cell Modulation)
Reducing or reshaping suppressive T-cells so the immune system can better attack cancer.
TrxR (Thioredoxin Reductase)
A redox enzyme that keeps thioredoxin in its active state.
V
VDR (Vitamin D Receptor)
A gene switch turned on by vitamin D that can influence cell growth and differentiation.
VEGF
A key “grow more blood vessels” signal. Many anti-angiogenic drugs target VEGF.
W
Warburg Effect
Many tumors favor sugar-burning (glycolysis) even when oxygen is available, supporting rapid growth.
Wnt Pathway
A growth and differentiation pathway often miswired in cancer.
Β
β-Glucan
Immune-modulating fibers from yeast, oats, or mushrooms that can activate innate immune cells.
β-Oxidation
How mitochondria break down fats for energy.