Glossary
A
Agent-based model (ABM)
Simulation that includes multiple independent agents who follow a set of rules, and emergent system behavior can be studied as a product of interactions between agents.
Allele
One of several variants of the same gene, for example the ABCC11 gene has alleles 538G (wet earwax) and 538A (dry earwax).
Anabolism
Constructive metabolic processes where complex biomolecules are built from the simpler ones, consuming energy.
Aneuploidy
Abnormal number of chromosomes in a cell (extra or missing), which commonly disrupts function and is frequent in cancers.
Angiogenesis
Formation of new blood vessels that supply nutrients and oxygen to growing tissues and tumors.
Anoikis
Programmed cell suicide triggered when cells lose appropriate attachment to the extracellular matrix.
Antagonistic pleiotropy theory
Idea that evolution selects genes which increase early-life fitness but decrease late-life fitness, contributing to aging.
Apical–basal polarity
Built-in “top–bottom” orientation of epithelial cells that lets tissues know which side faces the outside and which faces the inside.
Apoptosis
Controlled cell death process initiated by the cell itself (intrinsic apoptosis) or by other cells (extrinsic apoptosis) after intracellular stress or oncogene activation, as opposed to necrosis (uncontrolled cell death)
ATAC-seq
Lab method that maps which parts of DNA are open and active by tracking where enzymes can easily cut, giving a snapshot of gene control regions.
Autocrine signaling
Type of cell signaling where signals are secreted and then immediately detected by the same cell.
Autophagy
Intracellular recycling process that degrades damaged components to maintain homeostasis or survive stress.
B
Base excision repair (BER)
DNA repair system that fixes small, common chemical damages to single DNA bases by cutting them out and patching the gap.
Basement membrane
A thin, supportive sheet of proteins beneath cell layers that acts like both a scaffold and a barrier.
BCL-2
Anti-apoptotic mitochondrial membrane protein that blocks cell death and can enable therapy resistance.
Beta-catenin
Wnt pathway mediator that regulates gene expression and can drive proliferation when stabilized.
C
Cancer immunoediting
Idea that the immune system interacts with cancer in three stages: elimination (removes abnormal cells), equilibrium (holds tumors stable), and escape (selects for cells that evade detection).
Canine transmissible venereal tumor (CTVT)
Naturally transmissible cancer lineage that spreads between dogs by cell transfer.
Caspase-3
Executioner protease in apoptosis that cleaves many substrates to dismantle the cell.
Catabolism
Destructive metabolic processes where complex biomolecules are broken down into the simpler ones, releasing energy.
Cell competition
Process where fitter cells eliminate less-fit neighbors, preserving tissue quality under mutation pressure.
Cell cycle
The repeating process by which a cell grows, copies its DNA, and divides into two new cells.
Cell-cycle checkpoints
Built-in safety stops during the cell cycle that test whether DNA is intact and conditions are right before proceeding.
Cell surveillance
Ongoing monitoring of tissues by immune cells (e.g., T cells, natural killer cells) that spot and remove abnormal or infected cells.
Chemokines
Small secreted proteins that guide immune cell migration and shape inflammatory responses.
Chemotaxis
Directed cell movement along chemical gradients of attractants or repellents.
Chromatin
DNA wrapped around proteins and folded into higher-order structures, which helps control whether genes are on or off.
Chromothripsis
One-off cancer-associated event where chromosomes are shattered and haphazardly reassembled, creates many DNA changes at once.
Clonal cooperation
Interactions between distinct cell clones that collectively enhance growth, survival, or invasion beyond what single clones achieve.
Clonal interference
Competitive interactions between cell lineages that expand at the same time.
Clonal selection
The natural-selection-like process by which cell lineages with growth or survival (fitness) advantages expand more than others.
Contact inhibition
Suppression of cell proliferation or migration upon cell crowding or direct cell contact in healthy tissues.
CRISPR/Cas9
Gene editing method that uses a guide RNA (gRNA) to target the Cas9 enzyme to a specific DNA sequence, Cas9 then makes a cut in the DNA.
CRISPR screens
Large assays that switch genes off or on across many cells via CRISPR to find which genes matter for a chosen trait.
Crowding pressure
Mechanical or spatial constraints that cells experience in a densely packed tissue.
Cyclins
Proteins that act as timed switches to drive a cell through the stages of the cell cycle.
Cytokines
Signaling proteins, often immune-derived, that modulate inflammation, growth, and cell survival.
D
Death pact
Governance strategy that enforces organization-level priorities by triggering collective agent death under specific failures or contexts.
De-Darwinization
Evolutionary pressure to reduce competition among cells in a multicellular organism.
Devil facial tumor disease (DFTD)
Transmissible cancer threatening Tasmanian devils that spreads by biting.
DNA damage response (DDR)
Cellular network that senses DNA lesions and coordinates repair, checkpoint activation, or cell death.
DNA methylation
A chemical tag added to DNA bases that usually dampens gene activity and helps set long-term patterns of gene activity.
Disposable soma theory
Idea that evolution de-prioritizes long-term maintenance in favor of routing limited resources to reproduction, contributing to aging.
Driver mutation
Genetic change to a cell within a tissue that confers it a fitness advantage over its peers and promotes cancer development.
E
E2F transcription factors
Proteins that drive expression of cell proliferation genes required for mitosis S-phase entry.
ECM
ExtraCellular Matrix, a part of tissue outside of the cells, consisting of a network of macromolecules and minerals that provides structural and biochemical support to surrounding cells.
ECM remodeling
Changes to the extracellular matrix that alter tissue stiffness, signaling, and cell behavior, often via matrix metalloproteinases.
EGFR signaling
Proliferation and survival pathway activated by EGF, often activated in cancer.
EMT (epithelial-mesenchymal transition)
Cell identity shift from epithelial (sedentary) state to a mesenchymal (mobile) state, granting increased motility and invasiveness - happens both in normal development and in cancer.
Endocrine signalling
Type of cell signalling where signals are transmitted via central circulatory system (bloodstream).
Epigenetics
Changes in gene activity that are heritable through cell divisions without altering the DNA sequence, typically via DNA methylation or chromatin changes.
Epigenetic landscape
2D visualization of potential cell states as a height map, forming valleys that correspond to progression of cell types.
Eutely
Developmental pattern in some species where adults have a fixed number of somatic cells and growth occurs only by cell enlargement.
Evolutionarily stable strategy
Behavior pattern that, once common in a group, cannot be easily displaced by an alternative strategy.
F
Field cancerization
Region of seemingly normal tissue that shares early mutations, raising the chance that multiple tumors can arise there.
Flower (Drosophila)
Cell-surface protein that marks relative fitness for cell competition in flies.
Focal adhesions
Specialized cell-cell contact points where cells grip the surrounding matrix and sense mechanical forces and signals.
G
Gene expression
Level of gene activity, tracking whether the specific gene is transcribed to RNA or stays silent.
Gene regulatory network (GRN)
Computational model of a gene network that calculates internal gene states that drive effector outputs based on sensory inputs in the cell model.
Genome instability
Collection of various mutations and chromosomal alterations that drive somatic evolution.
Germline
Immortal lineage of reproductive cells (such as egg and sperm cells) that passes its genetic material from one generation to another (as opposed to mortal soma that forms the rest of the body)
Gradient (chemical)
Spatial variation in morphogen concentration that cells can sense to bias movement or growth.
Growth factors
Extracellular proteins such as EGF and IGF that bind to cell receptors and stimulate cell proliferation and survival pathways.
H
Hallmarks of aging
Commonly used checklist of biological changes—such as DNA damage and impaired protein quality—that tend to worsen with age.
HeLa cells
Immortalized human cancer cell line widely used in research.
Hedgehog signaling
Cell pathway active during embryonic development, it regulates tissue patterning but can also be activated in cancers.
Histones
Nuclear protein “beads” that DNA wraps around to form chromatin, helping package the genome and regulate gene activity.
Homologous recombination (HR)
Precise DNA repair process that uses an intact copy as a template to fix breaks in a damaged copy.
Hyperfunction theory
Idea that aging mainly results from growth and development programs running too strongly or too long later in life.
Hypoxia
Low oxygen conditions common in densely packed tumor interior, triggers HIF-driven adaptive responses.
I
IGF signaling
Insulin-like growth factor pathway that promotes growth and survival, often activated in cancers.
Immune checkpoints
T-cell receptors that restrain T-cells from attacking the body’s own cells, but also from attacking some cancer cells.
Immune surveillance
The process by which immune cells detect and remove emerging cancer cells.
Indeterminate growth
A life-history pattern where organisms continue growing after maturity through continued cell proliferation.
Inflammaging
Persistent inflammation-like tissue state that increases with age and contributes to tissue dysfunction.
Integrins
Receptor proteins that connect cells to the extracellular matrix and relay mechanical and chemical signals.
iPSC
Induced Pluripotent Stem Cells, an adult somatic cell line that has been artificially induced to undergo reprogramming into a stem-like state.
Iteroparity
Life-history strategy where organisms reproduce multiple times over the lifespan, as opposed to semelparity (single reproduction event).
J
JAK–STAT pathway
Protein signaling cascade from cell-surface receptors to the nucleus that turns on genes regulating proliferation, inflammation and apoptosis.
Juxtacrine signaling
Type of cell signaling where signals are transmitted via direct contact between two cells
K
Karyotype
Complete set of a cell’s chromosomes, described by their number and appearance.
Kin selection
Idea that helping relatives can spread shared genes, so altruism and cooperation can evolve among related cells or organisms.
Kinase signaling
Intracellular protein modification cascades (such as MAPK or PI3K-AKT) that transmit signals from cell membrane receptors to transcription factors.
L
Lateral inhibition
Tissue patterning mechanism where a cell adopting one fate actively prevents its neighbors from doing the same.
LEGI (local excitation, global inhibition)
Computation method that enables cell models to sense chemical gradients and adapt to them.
Lewontin’s conditions
Three minimal requirements for evolution by natural selection: phenotypic variation, differential fitness, and heritability of fitness-related traits.
Lineage commitment
Step in embryogenesis where a developing cell narrows its options and chooses a particular future identity.
Lineage hierarchy
Ordered tree of stem cells, intermediate progenitors, and mature cells that builds and maintains a tissue.
Lineage tracing
Experimental methods that label cells and follow their descendants to map how tissues develop and regenerate.
Loss of heterozygosity (LOH)
A way to start a tumor: in cells where one copy of the tumor suppressor gene is mutated but the second copy of the tumor suppressor gene is healthy, deletion of the only healthy copy makes the cell tumorigenic.
M
MAPK pathway
Mitogen Activated Protein Kinase signaling cascade, a chain of proteins (Ras-Raf-MEK-ERK), often mutated in cancer cells, that transmits proliferation and differentiation signals from growth factor receptors into the nucleus.
Matrix metalloproteinases (MMPs)
Enzymes that degrade extracellular matrix to enable remodeling and invasion.
MET (Mesenchymal-to-epithelial transition)
Cell identity shift from a mesenchymal (mobile) state to an epithelial (sedentary) state during normal development or cancer.
Metastasis
Late stage of cancer, when tumor cells enter circulation and spread to distant organs via invasion and colonization.
Microsatellite instability
Pattern of frequent small DNA repeats gaining or losing units because the proofreading system is broken.
Mismatch repair
DNA repair pathway that corrects wrongly paired bases that slip through during DNA copying.
Mitotic catastrophe
Type of cell death or permanent arrest triggered by severe errors during cell division.
Morphogen
Diffusible signal whose concentration gradient provides positional information to cells, which is important for developmental patterning.
Multipotent cell
A stem-like cell that can make several related cell types, but not every type in the body.
Mutation load
Cumulative number of mutations carried by a population of organisms or cells.
Mutational signatures
Characteristic patterns of DNA mutations that point to the causes of DNA damage (for example, UV light or tobacco smoke).
Mutator phenotype
Cancer cell state with abnormally high mutation rate, often because DNA repair is defective.
N
Necrosis
Uncontrolled cell death often associated with membrane rupture and inflammation, as opposed to apoptosis (programmed cell death).
NetLogo
Simple agent-based modeling environment used for education and prototyping.
NF-κB pathway
A stress- and inflammation-responsive signaling cascade that turns on genes for survival and immune functions.
Non-homologous end joining (NHEJ) repair
Quick-and-dirty DNA repair method that glues broken DNA ends together without a template, sometimes incorrectly.
Notch signaling
Cell-to-cell contact signaling pathway that controls cell fate decisions and is dysregulated in many cancers.
Nucleotide excision repair (NER)
DNA repair system that removes bulky lesions (such as UV-induced damage) by cutting out a short stretch of DNA.
O
Oncogene
Gene that promotes cell proliferation or survival during development, and, if inappropriately activated or overexpressed, can also drive cancer.
Oncovirus
Virus that increases the risk of cancer upon infection, such as Human Papillomavirus (HPV)
Organoids
Lab-grown tissue structures that mimic features of real organs for large-scale experimental assays.
Oxidative phosphorylation (OXPHOS)
Cell’s main way to make ATP (energy currency) in mitochondria by using oxygen to power an electron-driven turbine.
Oxidative stress
Imbalance between the production of toxic reactive oxygen species and the production of defensive antioxidant molecules, leading to high rates of damaged biomolecules such as DNA mutation.
P
p16-RB pathway
Tumor-suppressive protein pathway that enforces cell-cycle arrest by inhibiting CDK4/6 and maintaining RB activity.
p53 pathway
Central damage-response protein network that triggers repair, arrest, senescence, or apoptosis depending on context.
Paracrine signaling
Type of cell signaling where signals are transmitted short distances to nearby cells.
Passenger mutation
A genetic change that does not confer a selective advantage to the cell but co-occurs with beneficial driver mutations.
Peto’s paradox
Observation that large animals have similar cancer rates to small animals, despite having orders of magnitude more cells, implying stronger cancer defenses scaling with organism size.
PI3K-AKT-mTOR pathway
Central growth and survival pathway activated by growth factors and oncogenic mutations.
Planar cell polarity (PCP)
Coordinated head-to-tail or left-to-right alignment of cells across a flat 2D tissue sheet.
Pluripotent cell
Stem cell that can make almost any cell type in the body but not an entire organism on its own.
Principal-agent problem
Coordination problem between an entity with a goal (principal) who delegates power to an entity with selfish incentives (agent).
Proliferation
Regulated increase in cell number through mitosis, constrained by checkpoints, growth signal availability, and crowding.
Public goods
Shared resources that cells produce (such as growth factors or matrix) and other cells can benefit from without paying the cost of production.
Q
Quiescence
A reversible, non-dividing cell state where cells reduce metabolism and can re-enter the cell cycle at a later point.
Quorum sensing
coordination mechanism in bacteria, based on collective action upon secretion of autoinducer molecules, vulnerable to cheaters.
R
Reaction-diffusion models
Computational models that combine local reactions and diffusion to produce spatial patterns, often used for morphogen dynamics.
Replicative senescence
Permanent cell division arrest triggered by telomere shortening after repeated divisions.
S
SASP
Senescence-Associated Secretory Phenotype, the signal signature produced by senescent cells, can initiate tissue remodeling or immune cleanup.
SCANDAL hypothesis
Speciated by CANcer Development AnimaL, a controversial hypothesis where a lineage of cancer cells can undergo speciation and become a new species.
Selection shadow
Decline in selection pressure after reproduction event, that allows late-acting deleterious traits to persist.
Senescent cells
Cells in a state of irreversible proliferation arrest, unable to properly function but also cancer-resistant.
Semelparity
Life-history strategy where organisms reproduce once and then die, as opposed to iteroparity (multiple reproduction events).
Senolytic therapy
Category of putative anti-aging treatments that selectively eliminate senescent cells accumulated over the lifespan of the organism.
Single-cell RNA-seq
RNA sequencing method that reads which genes are active in each individual cell, revealing the mix of cell types and states in a sample.
SNP
Single nucleotide polymorphism, an allele with a single-letter substitution in the gene, such as 538G>A substitution in ABCC11 gene manifesting as “dry earwax” trait in humans.
Soma
Non-reproductive tissues of the body, cells that won’t form a new organism and will die with the body (as opposed to immortal germline)
Somatic mosaicism
Presence of genetically different cells within the same person due to mutations that arise after fertilization.
Stem cell niche
Specialized tissue microenvironment, such as the base of intestinal crypts, that maintains stemness and allows stem cells to undergo proliferation and differentiation.
T
Telomeres
Repetitive chromosome ends that shorten with each cell division, telomeres act as a replication counter and a protective mutagen sink.
Telomerase
Enzyme that extends telomeres and supports replicative immortality in stem cells and many cancer cells.
TGF-beta signaling
Protein pathway that normally promotes tissue fibrosis and inhibits immune response, in cancer depending on the context it can either suppress early tumor growth or promote invasion and metastasis later.
Totipotent cell
Cell type that can form all cell types, including extra-embryonic tissues, creating a whole organism from itself.
Tragedy of the commons
Coordination problem where individuals overuse a shared public good, harming the group because each individual gains by taking more.
Transcription factors (TF)
Central components in the cell decision-making network, proteins that integrate incoming signals, bind DNA, and regulate gene expression.
Transit amplifying cells
Short-lived progenitor cells that rapidly divide to produce many non-dividing cells, intermediates between stem cells and fully differentiated cells in rapidly cycling tissues like skin and intestines.
Transmissible cancer
Cancer that spreads between individuals via clonal transmission of living cancer cells (as opposed to infection by an oncovirus).
Tumor microenvironment (TME)
Ecosystem of cancer cells, stromal cells, immune cells, and ECM that maintains and shapes tumor progression.
Tumor mutational burden (TMB)
The total number of DNA mutations found in a tumor, often used as a rough marker of how visible it may be to the immune system.
Tumor suppressor
Gene whose loss drives tumor formation, typically acts by constraining the cell cycle.
Tumor-suppressor theory of aging
Idea that mechanisms preventing cancer, like senescence, contribute to aging by limiting regeneration over the lifespan of the organism.
V
Vasculature
Arrangement of blood vessels in an organ or tissue
VEGF signaling
Protein signaling cascade driving the vascular growth program that promotes blood vessel formation during development, regeneration, and cancer.
W
Warburg effect
Tendency of many cancer cells to favor sugar-burning pathways that are less efficient but support fast growth, even when oxygen is available.
Weismann barrier
In some species, the irreversible separation between germline cells and somatic cell lineages in the developing embryo, limiting inheritance of acquired somatic mutations.
Whole-genome doubling
Event in which a cell accidentally duplicates its entire set of chromosomes, which benefits cancer cells by supporting higher mutational load.
Wnt signaling
Developmental signaling pathway that stabilizes beta-catenin to drive proliferation and patterning.
Y
YAP / TAZ – Hippo pathway
Mechanosensitive signaling pathway that regulates organ size, cell proliferation and apoptosis via either YAP/TAZ (promoting proliferation) or Hippo (inhibiting proliferation)
Yamanaka factors
Transcription factors Oct-4, Sox2, Klf4 and Myc (aka OSKM) that, when simultaneously active in a cell line, reprogram it to an embryonic-like stem cell state (iPS cells)