Thursday, 2 June 2016

Independent reading log one(ZhengHang)

Name:Chian ZhengHang                                  
Index Number:8

Date: 2nd June 2016

What I did:
I went to BBC and reached for articles and found an article called “cancer is a nasty by-product of evolution” and decided to read it.I wanted to do a summary of the article and some new words.

What I learned: 

Words I do not understand:
apoptosis-In multicellular organisms, cells that are no longer needed or are a threat to the organism are destroyed by a tightly regulated cell suicide process known as programmed cell death or apoptosis.

proliferation-Proliferation is a rapid multiplication of parts or the increase in the number of something. 

substrate-In biochemistry, the substrate is a molecule upon which an enzyme acts. Enzymes catalyse chemical reactions involving the substrate(s). In the case of a single substrate, the substrate bonds with the enzyme active site, and an enzyme-substrate complex is formed.

     According to Cancer Research UK, 54% of men and 48% of women will get cancer at some point in their lives.Cancer is an unfortunate by-product of the way evolution works. Large and complicated animals like humans are vulnerable to cancer precisely because they are large and complicated.The cells inside a tumour change and evolve just like animals in the wild.Humans each started out when an egg and sperm cell met and fused. Within a few days, that egg and sperm had turned into a ball containing a few hundred cells. By the time we reach adulthood about 18 years later, those cells have divided so much times that scientists cannot agree, even to the nearest few trillion, exactly how many cells our bodies contain.Cell division in human’s bodies is very heavily controlled. For instance, when humans were first growing your hands, some cells went through "cell suicide” to carve out the spaces between human’s fingers.Cancer is also all about cell division, but with one important difference. A cancerous cell breaks all the rules of controlled division that human’s other cells follow.Cancer are like different organisms, so the better that cell gets at dividing faster than its neighbours and gaining nutrients, the more successful it will be as a cancer, and the more likely it will survive and grow.We have several "corrective" genes which send instructions to kill any corrupted cells.The threat comes from the tiny number of corrupt cells that do not get fixed.But some of the corrupted cells may not be discovered and thus will multiply and cause cancer.Cancer cells are not all alike. Whenever a cancerous cell divides, it has the potential to pick up new mutations that affect its behaviour. In other words, they evolve.The fact that tumours are constantly changing their genetic makeup is one of the reasons why cancers are so hard to "kill".The evolution that goes on inside a cancer tumour as like a tree with many branches. At the base of the tree are the original mutations that triggered the tumour in the first place: mutations that should be shared by all of the cancer cells in the tumour.A therapy that targets one of those base mutations should destroy every cell in the tumour.This therapy may not work well because there will be one or more cells in the tumour branches that has a resistance mutation that allows it to outwit the therapy.
Swanton and his colleagues have studied the problem to see if they can develop a therapy with a better outcome.What they come up with is an approach where they sequence tumours and produce the truncal antigens on a patient-by-patient basis.He begins by teasing out the resistant cancerous cells, which he calls "clones". Patients are given a particular drug therapy and then monitored to see when a particular cancerous "clone" rises to dominance in the tumour because it has developed drug resistance.Then they stop treating the cancer with the drug. This removes the evolutionary pressure that allowed the clone to become so successful. Without that pressure, other types of cancer cell in the tumour also have a chance to flourish. They "fight back" against the dominant clone. In effect, the cancer effectively begins to war with itself. 
When some of those other clones have gained ground, it is time to administer the drugs again, as these new clones should not yet have developed resistance.They use clones against clones, they then wait for the winners, then take out the pressure; the drug. The winners at this point are unfit and start to disappear, and then others take over. So they use the tumour against itself.If people decide that they all want to live to more than 70, then they have to accept that sooner or later they will get cancer because it is inevitable because our cells have not evolved to maintain their DNA for as long as people now live.

No comments:

Post a Comment