Why Do Cancer Fighting Drugs Kill Cancer Cells

Cells need to be small which means there must be space between them. If the cells get into contact they die. This is called Contact Inhibition; it’s how cancer-fighting drugs kill cancer cells. The purpose of the drugs is to put in the body cells that get in contact with the cancer cells and destroy them. The drugs also prevent DNA replication. The cells are most vulnerable when they are rapidly dividing. Cancer-fighting drugs fall into several different classes.

One of these classes is DNA binding agents. They form a covalent bond with the DNA or stick to it noncovalently very tightly. A covalent bond is a chemical bond. It involves sharing of electron pairs in the middle of atoms. These electron pairs are known as shared pairs or bonding

pairs. The stable balance of engaging and repelling forces between atoms when they share electrons is known as covalent bonding. The effect is to mess up DNA replication. When failed repair occurs it results in double-strand breaks, where both strands of DNA duplex are cut. The defect has to be repaired by cutting our or patching the break or fixing the modified bases or it will hit a roadblock. When the cell fails to replicate the DNA properly it will eventually kill itself.
Topoisomerase inhibitors are another type of cancer-fighting drugs. Topoisomerase inhibitors are agents designed to interfere with the movement of topoisomerase enzymes. Topoisomerase enzymes control the changes in the DNA structure. When DNA is replicated it has to be unwound. Topoisomerase is a type of protein which does that. The topoisomerase inhibitors bind to the Topoisomerase once it has attached to the DNA. It can also work by making the DNA that the replication fork is approaching even more snarled. It hits a road block when the DNA polymerase comes along, the replication stops and the cell dies.
To be able to divide, a cell has to rebuild its cytoskeleton to draw apart and pinch in the cell membrane. Tubulin destabilizers destabilize it so the cell can’t rebuild the microtubules. A tubulin stabilizer stabilizes the microtubules so that the cell can’t break them. Microtubules are filamentous intracellular structures that are responsible for several kinds of actions in eukaryotic cells. Both of the drugs prevent the cell from dividing properly and the cell eventually kills itself.
The last popular cancer-fighting drug is metabolic product mimics. They are small molecules that resemble molecular building blocks. Sometimes enzymes will latch onto them instead of the regular substrates. The purine and pyrimidine analogs look like the DNA building blocks but if the enzymes try to process them they will get stuck. The DNA replication stops and the cell dies. The same thing goes with folic acid analogs. The folic acid is needed to makes the purines; the purines construct DNA and RNA. The dihydrofiliate reductase picks up the folic acid mimic and irreversibly binds to it, which deactivates the enzyme. This doesn’t let the cell divide because the DNA replication can’t progress so the cell dies.
Cancer cells are just cells gone wrong. Cancer cells don’t respond to signals that control the cellular growth and death. The cells originate within tissues and when they grow and divide they diverge further from the normal. These cells become increasingly resistant to the controls that maintain normal tissue over time. As a result they divide more rapidly than progenitors and become less dependent on the signals from other cells around them. Cancer cells can evade programmed cell death even though their multiple abnormalities would make them prime targets for apoptosis. Apoptosis is the process of programmed cell death. In the late stages of cancer the cells break through normal tissue boundaries and spread to new sites in the body.