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cell lecture 14
Stem Cells
Early-stage cells are stem cells, meaning they have the potential to turn into any type of cell in the body.
What Stem Cells Can Become
This shows that one stem cell can become many different types of specialized cells:
Muscle, Fat, Bone, Blood, Nerve, Immune, Epithelial (skin), Sex cells.
This process is called differentiation — where a generic stem cell becomes a specific type of cell depending on signals it receives.
What Multicellularity Needs
This slide explains what’s required for cells to live together as a multicellular organism:
Communication: Cells must talk to each other through signals.
Regulated division: Cells don’t just divide randomly; it’s tightly controlled.
Differentiation + Division: Some cells specialize, and some continue to divide to maintain tissues.
Core Features of Stem Cells
This breaks down the main features of stem cells:
Self-renewing: They can divide and make more of themselves.
Undifferentiated: They’re not specialized yet — they don’t have a specific job like a nerve or blood cell.
Why Stem Cells Can Become Different Cells
All cells in your body have the same DNA because they come from the same original cell.
So what makes them different? The cellular processes that control which genes are turned on or off.
Definitions of Each Potency
This gives text definitions for the types of stem cells from Slide 6:
Totipotent – very early stem cells (can become any cell, including placenta).
Pluripotent – can become any body cell.
Multipotent – can become some types (like blood or brain cells).
Oligopotent – very limited options.
Unipotent – one cell type only, but still self-renewing.
Why Later Cells Can’t Become Everything
This is a research summary asking:
Answer: Epigenetic changes (like DNA methylation) lock certain genes in the “off” position.
Over time, these changes limit the flexibility of cells.
The paper also discusses trying to reprogram cells to become more flexible again (like germ cells).
Division vs Differentiation (Concept)
Every organism starts as one cell, which divides and differentiates.
Differentiation means gaining a specific function, but usually losing the ability to divide further.
Division vs Differentiation (Mechanism)
Stem cells persist in tissues like the skin and intestines.
Each time a stem cell divides:
One daughter cell keeps dividing (stays a stem cell).
The other differentiates (becomes a specialized cell).
This balance allows tissues to renew and repair.
Cancer Overview
Key Points:
Cancer = most common genetic disease, but it’s important to distinguish:
Genetic = caused by mutations in DNA (can happen during life).
Hereditary = passed down from parents (inherited mutations).
Cancer is the #1 cause of death in Canada, even more than heart disease.
Breast cancer: affects 1 in 8 women.
Prostate cancer: affects 1 in 8 men.
Benign vs Malignant Tumors
Benign Tumor:
Not cancerous.
Cells divide abnormally but stay localized.
Can still cause problems (e.g., pressure on brain stem), but won’t spread to other parts.
Malignant Tumor:
Cancerous.
Invades surrounding tissues and spreads (metastasis) through blood or lymph.
This type of tumor is dangerous and often life-threatening.
What Causes Cancer
Main Ideas:
Cancer is caused by problems in cell division.
Normally, the body balances cell division and cell death.
Cancer happens when that balance is disrupted — too much division or not enough death.
Diagram details:
Genes like Rb, p53, and Ras control the cell cycle and survival:
Rb regulates entry into cell division.
p53 helps stop division if there’s DNA damage.
Ras promotes growth signals.
Mutations in these genes lead to uncontrolled cell growth.
This leads to the formation of a tumor (aka neoplasm) — a mass of abnormal cells.
Types of Cancers
This slide continues the theme from the last one and focuses on where cancers come from:
Carcinomas (~90% of all cancers):
Come from epithelial cells (surface layers — skin, lining of organs).
Most common type.
Sarcomas:
Come from supporting tissues like bone, cartilage, muscle, or fat.
Lymphomas & Leukemias:
Come from blood-forming tissues (hematopoietic cells).
Lymphomas = solid tumors in lymphatic system.
Leukemias = cancer cells in the blood.
Common Causes of Cancer
Cancer is a genetic disease — it’s caused by mutations in DNA.
These mutations can come from:
Mutagens: anything that causes DNA changes (e.g., radiation, chemicals).
Carcinogens: substances that cause cancer.
Replication errors: mistakes when cells copy DNA.
Viruses: some insert their DNA into our cells and disrupt genes.
Age is the biggest risk factor: the longer you live, the more time your cells have to acquire mutations.
Replication Errors
About 50–65% of cancers come from random DNA copying mistakes, not preventable environmental causes.
DNA polymerase makes an error about 1 in 100,000 bases, but most get fixed.
Still, some escape repair: ~1 in a billion remains.
We have ~35 trillion (3.5×10¹³) cells, and about 300 billion divide daily — mostly in blood and intestines.
So even with low error rates, a few mistakes each day can add up, leading to cancer over time.
Carcinogens and Precarcinogens
Carcinogens: chemicals that directly cause cancer by mutating genes.
Precarcinogens: not harmful at first, but become dangerous after being processed by the body.
Example: 2-naphthylamine in tobacco smoke → becomes a carcinogen after liver enzymes (CYP450) modify it.
DNA Damage
Carcinogens can damage DNA in multiple ways:
Crosslinking DNA strands
Damaging or removing bases
Causing strand breaks
Some specifically target important genes:
Example: PAHs (polycyclic aromatic hydrocarbons) in cigarette smoke often damage the p53 gene, a major tumor suppressor.
Ionizing and UV Radiation
Ionizing radiation (like X-rays and radioactive isotopes) strips electrons → causes DNA strand breaks.
More radiation = more risk of mutation and cancer.
UV radiation (from the sun) damages DNA mostly in the skin.
UV Radiation Effects
UV causes pyrimidine dimers: thymine or cytosine bases bond to each other inappropriately.
If not repaired, this creates mutations like CC → TT.
These "UV signatures" are a hallmark of skin cancer, seen in mutation patterns.
Viruses and Cancer
Oncogenic viruses cause cancer by inserting their DNA into host cells:
Disrupt normal genes and activate oncogenes.
Examples:
EBV (Epstein-Barr Virus) → Burkitt's lymphoma.
HPV (Human Papillomavirus) → warts and certain genital/skin cancers.
Cancer Development is a Multistep Process
Cancer doesn’t happen all at once — it’s a gradual evolution of cells.
Cells that grow faster or can escape normal control mechanisms (like cell death or checkpoints) are more likely to survive and expand.
Tumors often start off slow-growing, but become aggressive and invasive as mutations build up.
Main Stages of Cancer Development
1. Initiation
A normal cell gains mutations (e.g., from chemicals, radiation).
These changes don’t cause cancer yet, but make the cell more vulnerable.
These "initiated" cells are called precancerous.
2. Promotion
These precancerous cells are exposed to promoting agents (like hormones, chronic inflammation, or more mutagens).
This causes:
More mutations or epigenetic changes (e.g., changes to DNA packaging).
Proliferation (division) and selection of more aggressive cells.
Over time, this leads to a clonal population of abnormal cells.
3. Tumor Progression
Cells now have:
Faster growth
Greater ability to invade tissues
Resistance to control signals
Tumor becomes more heterogeneous (mixed cells), and invasive/metastatic forms dominate.
Hallmarks of Cancer
This slide explains the biological "hallmarks" of cancer — traits that all cancers tend to develop:
Self-sufficiency in growth signals – They grow without external cues (e.g., mutated Ras gene).
Insensitivity to antigrowth signals – Ignore stop signals (e.g., Rb gene loss).
Evasion of apoptosis – Don't die when damaged (e.g., p53 mutations, BCL2 overactivity).
Limitless replication – Keep dividing forever (e.g., telomerase activation).
Sustained angiogenesis – Stimulate blood vessel growth to feed the tumor.
Tissue invasion and metastasis – Spread to other tissues.
All of this happens due to genetic instability, which is caused by:
Mutations from radiation, chemicals, viruses, etc.
Inactivation of tumor suppressor genes or activation of oncogenes.
Cancer Biology Summary
This ties classic hallmarks to specific cellular misbehaviors:
Cancer cells:
Ignore apoptosis (e.g., p53 mutation)
Bypass senescence (e.g., activate telomerase)
Escape immune removal
Resist cell cycle checkpoints
Abnormal behavior includes:
Making their own growth factors
Growing without contact or anchorage
Ignoring density (will keep piling up)
Genetic Instability
Cancer cells accumulate mutations rapidly, due to:
Defective DNA repair
Chromosome instability (aneuploidy)
Mitosis defects (bad spindle/chromosome segregation)
These changes drive cancer progression and diversity in tumors.
Anchorage-Independent Growth
Normal cells need to stick to something (matrix/tissue) to grow.
Cancer cells grow without being attached to a surface.
In lab settings, they even grow in liquid (suspension culture).
They bypass apoptosis normally triggered by detachment.
Density-Independent Growth
Normal cells stop dividing when crowded (contact inhibition).
Cancer cells:
Ignore crowding.
Keep dividing and pile up in layers (as seen in culture dishes).
This leads to tumor formation in tissues.
Cancer Cell Immortality
Normal cells eventually stop dividing due to telomere shortening.
Cancer cells activate telomerase, which:
Rebuilds telomeres
Prevents senescence (aging)
Enables unlimited division (e.g., HeLa cells have been growing since 1951!)
Cell Cycle Dysregulation
Cancer cells ignore normal cell cycle controls.
They:
Skip checkpoints (e.g., G1 restriction point)
Ignore signals that would pause or stop division (growth factors, DNA damage)
Often block apoptosis even if DNA is badly damaged.
Angiogenesis
Tumors stimulate blood vessel growth to get:
Oxygen
Nutrients
A way to spread (metastasize) through blood
Key players:
VEGF & FGF: growth factors that stimulate vessel formation.
MMPs: enzymes that degrade tissue barriers so new vessels can grow.
Hypoxia (low O₂) in tumors stimulates even more angiogenesis.
HPV DNA was found in HeLa cells — immortal cells widely used in research.