The Lab / Core medicine / Lesson 21
Every new cell in your body comes from an old one splitting in two. Follow one cell round the loop it takes to copy itself, see how cancer breaks that loop, then watch five kinds of chemotherapy strike, each at its own point.
Educational, not for clinical use
Build the idea
Your body is built from cells, tiny living units. To grow, heal and replace worn-out parts, a cell divides: it splits into two new cells, each a full copy of the first. Skin, blood and gut lining are renewed this way every day.
Build the idea
Inside a dividing cell sits the nucleus, its control room. It holds DNA, the long coded instructions for building and running the cell, wound into bundles called chromosomes. Before a cell divides, it must copy every chromosome, so each new cell gets a full set.
Build the idea
The cell cycle is the loop a cell goes round to divide. It has four phases, or stages, always in the same order: grow, copy the DNA, check, then split. One trip round makes two cells, and each can start again.
Build the idea
The first phase is G1 (first gap): the new cell grows, makes what it needs and checks its surroundings. At the end of G1 sits a checkpoint, a gate where the cell decides whether to go on and divide.
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The gate is pushed open by CDKs (cyclin-dependent kinases). They are enzymes, tiny machines that each do one job, switched on by partner proteins called cyclins. Two of them, CDK4 and CDK6, push the cell out of G1.
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In S phase (synthesis, meaning making), the cell copies all of its DNA. The two strands unzip, and the cell adds matching DNA building blocks, one by one, along each strand, so every chromosome ends up doubled.
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DNA is twisted, like a rope. Unzipping it to copy winds the rest tighter. Topoisomerases are enzymes that cut the DNA, let it untwist and join it up again, so copying, and later splitting, can carry on.
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In G2 (second gap), the cell grows a little more and checks the copied DNA for damage. If it finds breaks it cannot fix, a healthy cell stops here, or destroys itself rather than pass on faulty instructions.
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M phase is the split, in two parts. First mitosis: the doubled chromosomes line up, and a spindle of thin protein ropes, microtubules, grabs them and shrinks to pull one copy to each end. Then cytokinesis: the cell pinches in two.
Build the idea
Most cells in your body are not dividing. They have stepped out of the loop into G0, a resting state, and simply do their jobs. Some can step back in when needed, for example to heal a wound.
Build the idea
Put together: cells grow, copy, check and split, or rest. Some healthy tissues divide all the time, like the bone marrow, the soft centre of bones that makes blood. Key measures: how many cells build up, and how many new blood cells are made.
What changes it
Cancer is cells dividing out of control. Damaged DNA jams the engines on and breaks the checkpoint, so fewer cells rest and a tumour, a growing lump of extra cells, builds up. Chemotherapy means drugs that kill dividing cells or stop them dividing.
What changes it
Antimetabolites are look-alike DNA building blocks, or drugs that stop the cell making real ones. Cells in S phase take them up and copying jams, so those cells die. Cells in other phases are spared, for now.
What changes it
Both jam the spindle. Vinca alkaloids stop its microtubule ropes from growing; taxanes freeze them so they cannot shrink and pull. Either way the chromosomes are not pulled apart: cells get stuck in mitosis and die.
What changes it
Alkylating agents stick chemical groups onto DNA, damaging it so it cannot be copied properly. Some, with two sticky ends, also tie the two strands together, as shown here. They work in any phase, even in resting cells, but dividing cells suffer most.
What changes it
Topoisomerase inhibitors trap the untwisting enzyme after it has cut the DNA, so the cut is never joined again. Breaks pile up while the cell copies and checks its DNA, in S phase and G2, and the cell dies.
What changes it
CDK4/6 inhibitors are targeted drugs, aimed at two engines, not all dividing cells. They block CDK4 and CDK6, so the G1 gate stays shut: cancer cells that rely on them wait in G1, and the tumour grows more slowly rather than being killed.
Start with Next, or use the arrow keys. Pictures are illustrative, not measurements. Blood cells and the immune system are in Lesson 20; how drug levels rise and fall is in Lesson 17.
Loading reference values…
Normal teaching baseline: the marrow makes new blood cells as usual.
The blue line on each bar, and the large number beside it, show where an illustrative teaching model sits: not a patient measurement and not a sourced value. The shaded bands are the reference ranges quoted under each row, and a thin tick marks the source’s mean where it gives one. The picture and every bar come from the same model. Choosing a condition applies it to the model, and the dashed line shows the model without it. An arrow labelled “Cited” appears only where the quoted source gives that row’s direction; where it does not, no arrow is shown and the marker is the teaching model alone.
These quoted statements explain why fast-dividing bone marrow is hit by drugs that kill dividing cells. They give no range and no direction for the rows above, so they are quoted here rather than offered as conditions with arrows.
The five chemotherapy classes are animated in the Lesson and in Explore freely. On this tab they are not listed as states, with arrows, and no drug is applied to the model, because the references quoted here give no direction for any chemotherapy class on these values, and every state here must quote its source. The marrow control above is the lesson model’s second key measure, how many new blood cells are made; it is not a drug and not a cited effect.
An illustrative teaching model of a growing tumour and the bone marrow side by side. Choose how fast the tumour divides, add chemotherapy (drugs combine) and watch where in the cycle cells die or get stuck, how big the tumour gets and how many new blood cells the marrow makes. Dashed marks are the untreated run, this lesson’s normal; solid marks are your settings.
Cells sit in five boxes: resting (G0), G1, S, G2 and M. Each phase is left at a steady rate set by how long it lasts, G1 longest and M shortest; a cell leaving M becomes two cells in G1. Some G1 cells step out to rest and some resting cells step back in. The run starts from the mix of phases an untreated population settles into, and the tumour and the bone marrow use the same loop with different resting habits. The tumour speed control speeds up or slows down every phase of the tumour only.
Each drug class either blocks the way out of a phase or kills cells while they sit in a phase. An antimetabolite slows S phase and kills cells in it. A vinca alkaloid or taxane holds cells in M and kills them there. An alkylating agent damages DNA in every phase and kills a few cells in each, resting ones least; the model does not separate one-ended agents, which only add chemical groups, from two-ended ones, which also tie the strands together. A topoisomerase inhibitor kills cells in S and G2. A CDK4/6 inhibitor blocks most of the way out of G1 and kills none, and acts less strongly on the marrow in this model. Drugs combine: their kills add up and their blocks stack. Tumour size is compared with the untreated tumour of the same speed at the end of the run; new blood cells are all the divisions the marrow made over the run, compared with untreated.
Left out: how drugs are absorbed and cleared (Lesson 17), DNA repair, resistance, the body’s own control of blood cell making, side effects other than the marrow, and every difference between cancers and between people. Nothing here predicts a real tumour, and nothing here is a treatment plan.