Cancer Mutations - Video Tutorials & Practice Problems

Cancer Mutations

Hi in this video, we're gonna be talking about cancer mutations. So cancer develops multiple mutations and these mutations accumulate in one self and that allows for the creation of cancer which is just sort of common fact that is how cancers form. Now. There are two classes of mutations. There is passenger mutations and these are mutations that have accumulated but they have no direct contribution to the cancer. They're not something that is resulting in growth. They're not something that's resulting in proliferation and they're not anything that's stopping apoptosis. It's just there's a lot of DNA damage and some of that is going to be in regions that have nothing to do with the cancer at all. So those are the passenger mutations. Then we have the driver mutations and these are the ones that are driving the cancer. Right? So they're causing the cancer cell. They're giving the cancer cells some way to grow abnormally or proliferate abnormally or stop death abnormally. So the driver mutations are really the ones that are causing the cancer or the passenger mutations are just kind of along for the ride, which is why they're named that way. Now within the driver mutations, there's two more classes and these are the two most common ones. So the first is called an ankle jeans and an uncle gene is a mutated alil. So normally this is usually a normal alil and but now it's mutated and it acts dominantly. So that means that if it's mutated, you're going to see some type of phenotype and that phenotype is going to be cancerous. And so the normal version of that gene is called a proto oncogene. So that's the wild type version, the mutated version. And when those proto oncogenes are mutated they become aka genes. So that's important. I feel like that's often a question on an exam is the difference between proto oncogenes and aka jeans. And so really make sure you understand uncle gene with a mutated form. Proto oncogenes are the wild type form. So examples of ankle jeans that you may read about is this rash gps which is a really important one in a signal transaction pathway but also the viruses E six and E seven from human papilloma virus. These are all um proto ankle genes which become ankle genes were mutated or integrated into the genome. The second class is a tumor suppressor and it's exactly opposite of that. So these alleles have a normal function and their normal function is to stop cell division. So when they become mutated they no longer can stop cell division. So tumor suppressors, their normal function is to suppress tumors. And so when they're mutated they lose that function they can no longer suppress them. So examples of these are retinoblastoma which I talked about before. Um in a previous video I remember this is the transcription factor that when mutated is going to stop suppressing the tumor. And allow those tumors to proliferate. Another one is P. 53 which is a big one you'll hear about is also a transcription factor which its normal function is to suppress tumors. But when it's mutated it can no longer do that and it allows tumors to grow Now. The important part of these is a lot of tumor suppressors are transcription factors and transcribe factors regulate a lot of genes. It's not just affecting one. So when P 53 becomes mutated, that means that every gene it regulates is also being like not expressed correctly, it's either being over expressed under expressed and that creates this huge phenotype from just this one mutation in this P 53 gene or this red no blast Oma jean. And so um Interestingly retinoblastoma. So p 53 these mutations are generally accumulated in somatic cells so they're not inherited but retinoblastoma, this is actually can be inherited. And we see it's a major cause of a certain type of eye cancer um and Children. And so that it can definitely be inherited and when um it's they act usually as recessive alleles. And so you need both copies to be mutated before you see the um phenotype, especially in retinoblastoma. That's the case. P 53 Not so much. But so essentially what happens here is you have a proto oncogene and it's normal but some type of cancer causing agent comes in, It activates it, meaning that it creates some type of mutation in it. And this with the accumulation of other cancer cells will lead to our cancer mutations will lead to cancer. So really make sure you understand the difference between anglo genes and tumor suppressors, because you will 100% see questions on the difference between the two. So with that, let's not move on.

A mutation in a tumor suppressor gene causes what to happen?

• A. The mutated tumor suppressor acts to suppress the tumor
• B. The mutated tumor suppressor can no longer act to suppress the tumor, and allows tumor growth
• C. The mutated tumor suppressor has no direct contribution to the cancer

True or False:Proto-oncogenes are mutated versions of oncogenes

• A. True
• B. False

Which of the following proteins is an example of a tumor suppressor?

• A. Ras GTPase
• B. HPV E6 protein
• C. p53 transcription factor