How does cancer occur? - Molecular basis of occurrence of cancer
Автор: Dr. Abhinav Kumar in UK
Загружено: 2016-04-17
Просмотров: 1077
You may know cancer occurs because of that one random cell that mutates and starts multiplying faster than rabbits but I'll delve into the molecular basis of how a cell becomes cancerous.
1. Cancer is a genetic disease. That doesn't only mean it's hereditary, but also that your genes may mutate due to reasons entirely your own and become cancerous.
2. DNA of a cell changes in 2 ways due to external factors. Either it gets damaged so much that the cell dies, or it's damaged just enough to deviate from it's well regulated function and become alpha rabbit.
3. It's a multi step process from normal cell to becoming a cancerous cell and it's that one cell's clones that cause cancer. During surgical removal of cancerous mass, doctors make sure that not a single bad cell is left behind cuz every cancerous cell… is an alpha rabbit.
Now, jumping on to the real deal. The molecular basis.
1. Self sufficiency in growth signals: Oncogenes. The genes with a potential to become cancerous are called proto oncogenes. Mutations cause the normal behaving proto-oncogenes to become badass oncogenes. These oncogenes influence any of the 5 stages of cell's response to growth signals that was previously supervised by proto oncogenes.
a. Cells multiply only when there's an external growth signal. But cancer cells learn to produce their own growth signals.
b. The growth signals are received by receptors on the cell membrane that pass on the message to cell's nucleus. But cancer cell's receptors pass on the message without a growth signal being present.
c. The message travels from receptor to stimulate the nucleus and after its job is done, it terminates. But in cancer cells, the message keeps on stimulating the nucleus till the cows come home. Like… (Pause… Look at what's approaching from outside the screen. Show animation of cows returning. Run outta the frame.)
d. The nucleus, in response to message activates DNA transcription factors which activate growth promoting genes. In cancer cells, these factors are activated on their own.
e. When triggered, the growth promoting genes start cell multiplication cycle. When their job is done, they're silenced by their inhibitors. In cancer cells, either the genes are triggered on their own, or their inhibitors… are inhibited. Malfunction.
2. Insensitivity to Growth Inhibitory Signals: Normally, there are tumor suppressor genes that control cell growth and suppress tumor formation. So a second way of carcinogenesis results from the failure of their function. Most important genes in this category is p53 gene. It attempts to repair damaged DNA, failing which it kills the cell. If this very gene is damaged, god doctors help us.
3. Evasion of apoptosis: Cells die naturally in our body in a programmed manner called apoptosis. Cancer cells either increase anti-apoptotic genes or decrase pro-apoptotic genes to prevent Grim reapers from getting close to them. (Billy and Mandy)
4. Limitless Replicative potential: We know secret to immortality is the telomeres on the end of chromosomes that gradually shorten with cell replication. Once they are too short, the cell won't replicate to create a new cell, but the old ones will keep dying. Cancer cells have this enzyme called Telomerase that don't let the telomere length shorten, so these Noble Rabbits keep multiplying.
5. Development of blood vessels to the growing cancer mass to fulfill their oxygen and nutrition demand is another skill of the cancer cells.
6. Ability to evade immune system: Our immune system is almost always taken for granted. They eat up any unhealthy cells and foreign substance in our body. Even though cancer cells are unhealthy and are pretty much foreign substances to our body, they've watched a lotta Prison break and know how to evade our immune system.
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