Unit 13: Apoptosis and Cancer
The cell's own self-destruct program, and what happens to a lineage of cells when that program and the checkpoints that call it both fail.
6 topics · 23 questions
Each topic is a path, not a menu: work down it in order and every question builds on the one above. Click any of them to watch the answer draw itself.
Apoptosis and the Caspase Cascade
- How it worksHow does a cascade of caspase enzymes activate one another to dismantle a cell from the inside?
- How it worksWalk me through how a dying cell packages itself into membrane-bound fragments instead of bursting open.
- Worked exampleFind how many substrate molecules one active caspase-9 enzyme cleaves per minute if it turns over 2 substrates per second.
- Common mistakeWhy isn't apoptosis the same process as a cell dying from injury or infection?
- Going furtherWhat happens to a developing hand's webbing between the fingers if apoptosis fails there?
Your turn1 of 2
Find how many substrate molecules one active caspase-9 enzyme cleaves per minute if it turns over 4.33 substrates per second.Intrinsic and Extrinsic Apoptotic Pathways
- How it worksHow does the intrinsic pathway sense internal damage and release a signal from the mitochondria to start apoptosis?
- How it worksHow does the extrinsic pathway instead get triggered by an external death signal binding a surface receptor?
- Common mistakeWhy isn't the mitochondrion's role in apoptosis about the cell running out of ATP?
- Ties togetherHow do both the intrinsic and extrinsic pathways converge on activating the same executioner caspases?
Your turn1 of 2
During the intrinsic apoptotic pathway, mitochondria release specific signaling proteins into the cytosol that help trigger cell death. A student assumes this must mean the cell is dying because its mitochondria have simply run out of ATP to power the cell. Why isn't the mitochondrion's role in apoptosis about the cell running out of ATP?Cancer as a Disease of Cell Cycle Control
- How it worksHow does a cell that has lost its cell cycle checkpoints keep dividing past the point a normal cell would stop?
- Common mistakeWhy isn't cancer one single disease with one shared cause, even though every case involves cell cycle failure?
- Going furtherWhat happens to a tumor's growth rate as it accumulates more mutations that disable additional checkpoints?
Your turn1 of 2
Every cancer, regardless of the tissue it starts in, involves cells that have lost normal control over the cell cycle. A student concludes that cancer must therefore be one single disease with one shared underlying cause. Why isn't cancer one single disease with one shared cause, even though every case involves cell cycle failure?Oncogenes and Tumor Suppressor Genes
- How it worksHow does a mutation turn a normal proto-oncogene into an oncogene stuck in the 'on' position?
- How it worksHow does losing both copies of a tumor suppressor gene remove a brake that normally stops uncontrolled division?
- Common mistakeWhy doesn't a single mutated oncogene alone usually cause cancer by itself?
- Going furtherWhat happens to cancer risk when someone inherits one already-mutated copy of a tumor suppressor gene like BRCA1?
Your turn1 of 2
A cell acquires a single mutation that turns one proto-oncogene into an active oncogene, permanently switching on a growth-promoting protein. A student assumes this one mutation should be enough, by itself, to cause cancer. Why doesn't a single mutated oncogene alone usually cause cancer by itself?p53 and the Guardian of the Genome
- How it worksHow does p53 detect DNA damage and halt the cell cycle to allow time for repair?
- How it worksHow does p53 trigger apoptosis instead when the damage turns out to be beyond repair?
- Common mistakeWhy isn't p53 itself the cause of cancer, given that it's the gene mutated in about half of all tumors?
Your turn1 of 2
The p53 gene is found to be mutated in roughly half of all human tumors. A student concludes p53 itself must be the gene actually responsible for causing cancer, since it shows up mutated so often. Why isn't p53 itself the cause of cancer, given that it's the gene mutated in about half of all tumors?Metastasis and the Hallmarks of Cancer
- How it worksHow does a cancer cell detach from its original tissue, invade nearby blood vessels, and colonize a distant organ?
- How it worksWalk me through how a tumor recruits its own blood supply through angiogenesis to keep growing.
- Common mistakeWhy isn't cancer simply a single disease that behaves the same way regardless of which tissue it starts in?
- Ties togetherHow do the cancer hallmarks of evading apoptosis, escaping p53, and driving angiogenesis arise from distinct failures?
Your turn1 of 2
A lung cancer and a colon cancer both show uncontrolled cell division, but they differ substantially in which mutations drive them, how fast they progress, and how they respond to treatment. A student assumes cancer must be a single disease that behaves the same way no matter which tissue it starts in. Why isn't cancer simply a single disease that behaves the same way regardless of which tissue it starts in?