of this computer. So we were talking about mitosis in relation to the cell cycle. We haven't gotten to mitosis yet.
And we're going to try to finish this up today, hopefully. We are about a day behind, but we're going to see if we can catch up on Friday. So we said that we were talking, and I'm going to go back a minute. We said that these cyclins and CDKs are really important in moving the cell cycle around and that CDKs 4 and 6 are important in specific phases of the G1 to S transition.
And that prior... to us understanding these things, there is something called negative breast cancer. There's even something called triple negative breast cancer, where the cells don't have markers.
There's a marker called HER, which makes it easier to treat the breast cancer cells. It's a protein on the surface. If that protein is absent, it was very difficult to treat the cancer. Now, because we understand these cyclin-dependent kinases 4 and 6, and that they permit transition from G1 to S, we actually use these drugs, which you can't even talk about. You can't even say their names, right?
And you don't have to know their names. What we want you to understand is that CDK4 and 6 inhibitor drugs have been developed because we understand that part of the cell cycle. And that gave us options to treat women with negative breast cancer.
As a matter of fact, one of my former professors that I studied under, his wife has had negative breast cancer and did really well, as I know. Okay, so let's talk now finally about body cell division, which is mitosis. Body cells, again, are called somatic cell.
And, you know, this is probably the easiest part of what we're going to do. There's the nuclear division where you divide the chromosomes, that's mitosis. And cytokinesis is the cytoplasmic division.
It's all kind of part of division. Again, these are body cells, they are always going to be diploid. Body cells never become haploid because a body cell has to be able to work on its own.
A body cell is not going to undergo fertilization, basically. So all the chromosomes have to be there. And the body cell, each body cell has to be able to have all the chromosomes to do its work. And so cells are always diploid, whether they're mother cells or daughter cells.
in meiosis in mitosis sorry um so body cells in humans have 46 chromosomes at the end of mitosis they're going to be diploid and they're still going to have 46 chromosomes you're like what but we're going to show you how it works you start out with what a replicated chromosomes Here are the spindle fibers. This is the mother cell. And then you get the daughter cells. And so, you know, in mitosis, you'll get a piece of this one and a piece of that one. So this might be mom number one.
and dad number one, or this could be dad number three. In body cell division, they're not all lined up numerically under each other. You could have like a number one from mom, and you could have like a number 23 from dad, but they're all there.
It's just that they're not all sequenced and everything, but they're all there, 46 lined up in a row. So in here, in this one, you would get like the other one, like maybe a... Number one from dad and one from mom.
So. Why is this diploid? Because pieces of the pair are still in the same cell, okay?
All the chromosomes that you inherited, pieces of them at least, the chromatid, what you call the chromatid, we call it unreplicated now, they're still there. And so when you go to S phase of the cell cycle, then you're going to make the other side again. Everybody's like, OMG. So let's look at this.
So you don't ever get haploid in body cell division. A haploid cell will be a dead cell, a dead body cell. Interphase, G1s and G2 of the cell cycle are not a part of division. The cell does all the other work that we talked about. We are in chapter...
12 hi kayla i'm happier here actually let me make you um annika couldn't be here so i'm happier here let me find you there let's make you a co-host yes okay we are in chapter 12 and we are right past um you Okay, we are right past, I can't see the number. Hang on, let me look at the number. I'm going to have to do it this way.
Is it going to let me see? It doesn't let me see the number. But we're in Chapter 12, and we're finally, we just started to talk about mitosis. Does that help? Okay, no problem.
Thank you for being here. Yeah, Anika couldn't be here this morning. She has another thing she needs to do. So prophase is the beginning of division in mitosis. Slide 37. Thank you.
Okay. I can see it when I'm in like another, but when I'm in Zoom, it doesn't let me do that. Okay. No problem. You are most welcome.
So prophase is the beginning of division. And there are certain things that happen. The spindle fibers form. This is, you know, basically, these are the microtubules.
They're going to pull the chromosomes around. These spindle fibers come from microtubule organizing centers, which are the centrioles, right? So we're going to look at prophase in a minute. So I'm going to show you pictures of this.
So in prophase, the nuclear, and here's like a little chart for you to see, the nuclear membrane breaks down. Because when you're going to pull chromosomes over eventually, you can't have the nucleus in the way. The nucleolus, the dark spot in the nucleus, disappears. And the spindle fibers start to form.
The DNA starts to condense down. When you're going to move DNA, it's like trying to move spaghetti. You don't want it to flop all over the place and break. You don't want to lose genes.
Okay, we're not going to do prometaphase. We're not doing this one. So here you can see what it looks like. In metaphase, the spindle is fully developed and now we make sure the spindle fibers are almost...
at the chromosomes and they are now going to hook up. So basically in metaphase we make sure that all the spindle fibers of the microtubules are hooked up onto the chromosome's centromere, which is the protein pad that holds the chromosome together. They're lined up.
They can either be vertical, or they could line up horizontally. Each sister chromatid is attached to a spindle fiber. So there's the centromere and it actually has a thing out here, a little extra nubby. This is called the kinetochore and the spindle fibers actually touch those and it says I'm hooked up. Yes, they're illustrations of, this is cells that are fluoresced.
So you can see now at metaphase, these are all the chromosomes. And this is how extensive the spindle fiber apparatus really is. It's huge.
In anaphase, we are going to pull the sister chromatids apart. There is actually a protein. that coats the centromere that holds the spindle fibers together.
So this protein is called cohesin. So this protein is dissolved which allows the sister chromatids to come apart. Okay and so here you can see we have pulled these These are, I'm doing this in green, probably not the best thing to do it in.
I'm going to do it in pink. These are the chromosomes which are now being pulled to the poles because in an animal cell, the cytoplasm later on is going to divide right down the middle. You can't have the chromosomes in the middle because you'll lose them.
So you have to get them to the thighs out of the way. So any other phase. We are pulling the sister chromatids to the poles.
DNA still condensed down. In telophase, the chromosomes are at the opposite end. Nuclear membrane starts to reform.
Spindle fibers start to break down and go back where they came from. And the DNA relaxes, okay? Starts to relax again. And then in cytokinesis, this is the cytoplasmic division. Animal cells are different than plant cells in the way they do this.
So you've probably all seen mitosis before. And so here I've written all this down. There is a system in yeast known as MAD. It's called mitotic active.
defective, mitotic, active, defective. And they found this system in yeast. And this system is like a signaling system that tells the chromosome it's hooked up with the spindle fiber.
Now, we have a different system in humans. It's a different name that we're not going to... tell you and you don't have to just you just need to know MAD exists.
You don't need to know all what the letters mean. But in humans, we have a different system that's similar. But these systems don't always work. And we're going to see that.
Okay, so this is mitosis. This is happening in body cells. It happens for growth and repair purposes.
The cells are always deployed. Always, even though you pull sister chromatids apart, you still, so here you have one, two, three, four, you have, you will have a piece of each of these chromosomes in the daughter cells. That means they're diploid. They're unreplicated after this. Here they're replicated, two sister chromatids.
Here they're unreplicated, one chromatid. but they're still diploid. And here we see a close-up of the kinetochore. This is a big part of the centromere, that bump out that we showed you, where the spindle fiber is going to come over. Don't worry about all this stuff.
And it's going to touch and say, I'm hooked up. So the division of the cytoplasm is different in plants versus animals. Let's do this down here. In animals, there's actually a ring of microfilaments that goes around like a lasso, and it literally pulls until it cuts the cytoplasm in him.
So in animal cells, the cytoplasm starts to divide from the outside in. Out to in. Okay, so from the outside in.
in animals. In plants, it's different. Because there's a cell wall, this is a tougher process. So in plants, we go from inside to out with the cytoplasm.
In to out, just the opposite of animals, because there's already a cell wall formed. Okay, so animals outside to in for the cytoplasm. That's how it divides. Plants inside out. Questions yet?
Would there ever be a question that shows like a plant cell or like an animal cell and then they ask like which one? So they'd show like a cleavage or... So we will not give you diagrams at all because diagrams can be iffy. Well, we may ask a question.
Cytokinesis in an animal goes from inside to outside, outside to inside, side to side, you know, something like that. Does that help? Yes, thank you.
Okay. So summary of mitosis. Let's get rid of that stuff. The purpose of mitosis is to make genetically identical daughter cells. These cells are used in growth or repair.
The cells are always going to be diploid. Again, they have to have all the chromosomes, all 46, or a piece thereof until they get the S phase and make the other half because they have to be able to do everything by themselves. The daughter cells can do everything the mother cell can do.
They have to have everything. And they are body or somatic cells. Twins we're going to talk about when we get into Chapter 15. Or maybe we'll talk about them in Chapter 13. This is body cells, so this doesn't have anything to do with twins.
in meiosis, when you make eggs, that has to do with twins. And we'll talk about that maybe a little bit then. So now we're going to integrate the stages of the cell cycle with how many chromosomes do you have? And are they replicated and unreplicated? But we have a rule.
You don't ever want to break this rule. For us, we're... artificially always going to start at prophase of the cell cycle to answer these type of problems. We're going to go around from prophase. Why?
Because at prophase, the chromosomes are diploid and replicated. You have to start with replicated chromosomes that have two sister chromatids, okay, to get correct answers. Here we go. A cell is 2n equals 16. Okay, in these kind of problems, the very first thing, and you realize it on this, is multiple, multiple parts, and it goes on for a long time.
And so there are all these problems about meiosis and mitosis thrown around. What does this mean? This is the most important first step. Does this mean there are 16 total? Yes.
Does this mean there are 16 pairs? No. This is a no. This does not mean 16 pairs. This means 16 total or 8 pairs.
8 times 2 is 16. You can never get higher. then the number across from the equal sign. So 2n equals that number. 46 isn't human. That means we have 46 total, not 92. 92, we wouldn't be human, okay?
We'd be something else. So this number across from the equal sign, that is the maximum chromosome number. You cannot ever get higher than that. that turns you into a different species.
That number is your species number. Okay, questions? Yeah, so 2n equals 16 if the cell is in G1 after mitosis.
So you draw a little cell cycle where you see the cell cycle in your head. Here's mitosis, here's prophase, metaphase, anaphase, telophase, and cytokinesis. Here's G1, there's S, there's G2, and oh, there's G0s coming out of here, right? There's a G0 coming out of here, a G0 coming out of here, and a G0 coming out. Now you got your cell cycle.
We start out with 16. We start at prophase where we had 16 replicated chromosomes. We go through cell division. At G1, what do we have? We still have 16 per cell because these cells are always diploid. Now, they look like this at this point, okay?
They're unreplicated at this point, but they're 16 per cell. Again, you never get haploid in body cell division. Are the chromosomes replicated? They're unreplicated. We just did mitosis to pull the sister chromatin.
Is the cell diploid or haploid? Always diploid in mitosis. You get one representative part of each chromosome. So here I put the answers down.
Now at G1. Because you haven't been through S phase yet, again, they're unreplicated. If you go through S phase or after S phase or G2, then they become replicated again. Yes. So replicated means this with two sister chromatids held together by a centromere.
Unreplicated means what you used to call a chromatid. We call them unreplicated chromosomes. Does that help?
Okay. Okay, good. Okay, because you can see what's happening. So here, somebody just said, how do you know?
So in prophase, they're replicated, okay, because we just saw this, right? In metaphase, they're still replicated. In anaphase, we start to pull them apart.
By telophase and cytokinesis, they are pulled apart. In G1, we haven't been to S phase yet. They're still pulled apart.
In S phase, we make the other side of these things. So in G2, they're replicated again. It's all related to the functions inside the cell cycle that we talked about. So we're talking about G1, S, and G2 individually. Okay.
So let's try some more. So there's lots of practice up in web courses about this, but I know... You guys are probably still trying to work on your test. And then we actually have exam number four next Wednesday, a week from today.
This is hurricane compression. It's not fun. Let's try this.
A cell is 2N equals 32. It's at G2 after mitosis. Okay. Cell is 2N equals 32. So you can see, this is a really good thing to have on your note card that you can carry with you into the test. You have a little cell cycle. You have what all the chromosomes look like, whether they're replicated or unreplicated, diploid or haploid.
Right now, everything is diploid. When we get to meiosis, we'll have some diploid times and some haploid times. So these are really good things to draw on your note card.
Of course, you have to be concise and be able to, you know, see what you're drawing. It's going to have to be a little bit bigger. Okay, so this cell is a G2 after mitosis.
First of all, how many chromosomes will you have? How many? You tell me how many. 32. Yes.
Because you're always diploid in body cell division, you have 32 chromosomes. Okay. Now, you have been through mitosis, prophase, metaphase, anaphase, telophase, and cytokinesis. So first you pulled them apart. Then you went to G1 where that didn't change.
Then you went to S phase. where you made the other half. In S phase, you take these and you make the other half because body cells are going to divide a lot of times, like your hair is always dividing. If you only have this in a cell and you want to make two daughter cells later on from the next mitosis, one's going to have DNA and the other is going to be dead. That doesn't work.
This is what S phase is for. You copy. the other side and make the other side of the chromosome so you're ready for the next division where you can give part of it so they are replicated at this point because once you are in s phase or after s phase you are replicated so you have 32 replicated and this cell at g2 is is checking after it copies dna it checks to make sure it you know to fix the mistakes it might might have made and copying, and then it's going to make some more protein.
It's going to go into division again next. So questions, confusion, again, there's lots of practice up, and I know many of you are still trying to like recap your studying for this exam that is running right now, exam three. Questions.
Okay, let's try another one. Cell is 2N equals 64. How many chromosomes does it have? 64. We're in G1.
Have we been to S phase yet? Nope. So they have pulled apart in cell division and they are unreplicated. Okay, so let me draw you a little cell cycle here.
Oh, that needs to be better. make you a little yes anaphase so here's the cell cycle here's prophase metaphase anaphase this is when they're going to become unreplicated that anaphase telophase and cytokinesis still unreplicated g1 unreplicated s replicated g2 replicated, prophase replicated, metaphase replicated. So it's right here. And in anaphase, in the beginning, they are replicated, but then they pull apart. It's right here where they're unreplicated.
Anaphase, telophase, cytokinesis, G1, and mitosis. Does that help? But he's like, OMG. Yes. OK, good.
So let's again go over what this means. This is the biggest mistake that students make on this kind of exam. 2N equals 32 means there are 32 pairs.
No, there are 32 total chromosomes. Yes. or there are 16 pairs. Oh yeah, we have more time. So in a normal mammal body cell, Division only occurs 20 to 50 times before cells die.
They're not immortal. They don't live forever. Yes. Okay, so we said somebody has a question with this. There are 32 total chromosomes, just like humans, we have 46 total, we don't have 46 pairs.
There are 32 total, a pair is two. So 32 divided by two, 16 pairs, or 32. In body cell division, the pairs never find each other. They're lined up single file.
So in normal body cells, our cells, they divide 20 to 50 times before they die. This chromosome, see these tips in pink? These are called telomeres. These are highly repeated DNA areas, but they're very important. They're like the cell clock that counts.
how many divisions and how much time the cell has to live. Okay. And that it's much more complicated, but this is one of the factors. So every time at a certain age and stage, these start to shorten. As you get older, they start to shorten.
You have an absence of a critical enzyme. And so So right now, my husband's about 80% down on his telomerase. And there's no other, we're going to see this in chapter 16, DNA synthesis.
There's no other enzyme in mammals that can keep these lengthened. And then the cell will die. And it will have to be replaced if you can. What are some of the factors that affect cell division?
Growth factors. For a cell to divide, to do mitosis, there need to be these growth factors there. Cells have anchorage dependence.
Most plant and animal cells will not divide unless they're in contact with the right tissue they're supposed to be in. So as an example, you ate a granola bar, it's crunchy this morning. It's crunchy, it's sharp. You swallow it.
Cells from your throat and your esophagus get knocked off by the sharp, crunchy stuff. So with the granola, your esophagus cell and your throat cells are now in your stomach. Those cells know they're in the wrong place and they turn off. They're not going to start to make your throat and your esophagus colonize your stomach.
That's normal stuff. Okay, we're going to talk about that. We're going to talk about that in a minute. Trying to lengthen the telomeres. turns cells cancerous.
We haven't been able to do it so far. Then there's density dependent. Density dependence means, oh yeah, density dependence, but that's a really good thought. Everybody's thinking about, can we do that actually? Density dependence means that cells will stop division if they're touching one another, like your skin cells.
It's nice. It's smooth. They're not all over top of each other.
When cells lose their grip in their cell cycle and they're only lost a little bit of their grip, that's what warts are. A virus gets in there and messes with your cell cycle and the cells start growing over top of each other. Now that's not cancerous or anything.
It's just cells have lost their way in the cell cycle. They've lost their density dependent. So Cancer cells, they have a higher rate of growth. They're not properly regulated by growth factors. They lack density dependence.
So, you know, solid tumors, they grow into all these weird shapes. The cells grow over top of each other. They have larger nuclei and a smaller amount of cytoplasm.
So, you know, a person that works in a lab that has a tissue sample can tell a cancer cell by looking at it. It loses specialized features and reverts. They have the ability to metastasize, which is why I personally hate them so much, which means they don't shut down.
Like we talked about your stomach and your esophagus cells don't go into your, your esophagus and your throat cells don't go into your stomach and keep dividing. They literally shut down and die because they know they're in the wrong place. Cancer cells don't do that.
They get in your lymph system, which is this like kind of fluid circulation system that brings fluid back into your main circulation. They get into your bloodstream and they go other places and they can establish new colonies. The little buggers also have special things called metalloproteins that you don't have to memorize that cause blood vessels to grow over to them. They hate them very, very much. They are nasty.
Cancer cells are what we call immortal. They do not die after 20 to 50 divisions. They've lost that.
They break all the rules, which is why they're so hard to deal with. So somebody said explain density dependence. Density dependence is when cells like so.
If this is your skin and here's two cells, your skin knows that there's not a cut there. So your cells are not going to divide. They're actually going to go into G0 and sit there.
Okay. If. you get a cut so now we have one cell the other's the cells like hey there's nobody there behind me what's going on everything is gone then that cell will divide to replace that that's density dependence if they're touching each other they know their boundaries are there and they're not going to divide cancer cells divide like on top of each other to the side it becomes a big mess like this does that help Okay, yeah. So cancer is a thousand different diseases of a thousand different cell signaling pathways. And ultimately, they go back and affect the cell cycle.
We don't understand a lot of the pathways. Most cancer is based on these signals going wrong. For instance, and I talk about this a lot, there are 30 different subtypes of ovarian cancer cells. I was really lucky.
I had that 10 years ago and it was fairly early. It was stage 1c, which means it was stage 1, but the cells were loose everywhere. Chemo, my cell type was receptive to chemo. I had a really dear friend that then developed cancer a year after me. She had the kind of cells that are totally resistant.
Initially, they respond, and then they start, some of them live, and they start to go through alternate pathways that are not well understood and spit it back out. She didn't survive. So we want you to understand P53.
P53 is the master tumor suppressor gene in each of your cells. You have two copies, one you get from your mother and one from your father. These things are very important in suppressing tumor formation. There are many other tumor suppressors and many other things, but these are major.
They activate in response to DNA damage or some kind of weird process going on. And so this is how it works. If you have some type of a weird abnormality, in your DNA, this is actually an accessory chemical, you'll activate p53, which is a gene which makes protein 53. You'll stop the cell cycle, you'll allow time to repair DNA, and you'll restart the cell cycle if you're successful.
If there's too much damage or the damage is just out of range, you will go through programmed cell death. That cell can be used to stop the cell cycle. should activate a death pathway to kill itself to save the rest of you. That will eliminate the cell. Cancer cells cannot do this anymore.
They will never kill themselves. Over 50% of solid tumors that are cancerous, p53 is inactivated. And this is...
Everybody thinks, oh, cancer happens so fast. It's a very long process. It can take years and years to develop, okay?
There are lots of different things that happen, okay? So we're going to show you. Can you explain P53 again? Like, what exactly it is? P53 is the master tumor suppressor gene in all your cells, and you have two copies, one from each parent.
In order for it to become non-functional, Both copies have to mutate. So I was very talented. Both of mine mutated twice already.
And so it makes, P53 makes, that gene makes a protein. that allows you to stop the cell cycle and repair DNA damage and restart it. So there's like an egg timer that goes on the cell when this is happening.
If the damage is too bad, the cell will then activate its kill pathways to kill itself, to save the rest of you. Cancer cells have lost this. They can't do this anymore, most of them. Okay. And there are different kinds of cancer cells.
If p53 mutates, is it like antibodies getting stronger in that you won't get cancer again easily? We haven't ever seen that happen. The only way it's ever mutated is to lose function. We've never seen a gain of function. We wish we could.
But so far, we've never seen a gain of function, a gain function. So here is, we're going to look at... colon cancer, which is very prevalent in the United States. Here's the lining of your colon. Okay.
First mutation that this is one pathway. There are multiple colon cancer pathways. This is one pathway. Not that you have to memorize this.
We're trying to show you how long this takes and how many things have to go wrong for it to happen. APC is anaphase promoting complex. First, The genes that control you go into anaphase to get you out of division change. And so you start to make too much of your lining layer.
That's not cancer yet. Then KRAS, this is a signaler that's on the surface of the cells. And it says, turn on, turn off, turn on, turn off.
It can turn things off. All of a sudden now you're... your pathways all turned on all the time. Then you lose the density dependence gene and now this is an adenova.
This is not cancer yet. This is why they want people to do colonoscopies as horrible as they are because at this stage they can just snip this thing off and keep going and you don't have cancer yet. And then you there's more mutations and you lose p53.
and then it's cancer and there's all these other this this can take years to happen years um now you know why do some people start this process and then kind of be able to stop it on their own and other people keep going probably individual genetic background and we don't understand all that yet okay so what is the difference between benign versus malignant they're both tumors Okay, benign means it's not going to really cause you a big problem. It's not going to spread. It's not going to turn into cancer.
The cells can't travel and establish new colonies. Some benign tumors can become malignant over time if p53 mutates. That's why they like to take them out.
Okay, so. Telomerase is the enzyme we talked about, the name of the enzyme that keeps those telomere tips of chromosomes like that. Cells with shorter telomeres can't make this enzyme. And so we have the problem that as we age, the amount of telomerase decreases. We uncover more and more bad things and so this is a part of aging.
So there are some really not good companies out there that are doing unscrupulous things. You have like a happy birthday age, and you have a biological cell age, and they may be two different things. So for instance, they've said that, you know, they can predict a lot of things.
Well, you can see a difference sometimes in these ages. A very famous TV host once did this. Their age was, let's say, like 41. And then they had their telomere age done, which is very, that's very specific. Again, it's not always 100% correlated.
And so their telomere age came back older than their biological age, which doesn't bode well, but it's not always 100% correlated. There are things you can do to keep your telomeres lengthened longer, even if you just take a walk three times a week. or, you know, a little walk. They found in twin studies that twin couch potatoes, their telomeres were shorter than the ones that got exercise.
You don't have to be an Olympic athlete or anything, just like move a little bit. That's what they found. Telomerase is active every time you go to S phase and copy your DNA every single time. When you're young, you have a lot of it. As you get older, it dramatically decreases in your cells.
And as somebody asked, can't we keep your telomerase artificially elevated? Nope. That makes the cells turn cancerous.
They've tried it in mice. So there's a lot to aging. There's a lot more than this.
Aging is incredibly complex. They're finding certain genes are involved. It's incredibly complex. We don't understand it all yet. Some common treatments for cancer, radiation.
I did that. It was not the most fun thing in the world. It disrupts cell repair mechanisms. Chemotherapy, the kind that I did, disrupted my microtubules.
And so, you know, the basic thing is during mitosis. The cancer cells have a higher metabolic rate, so they should take up the chemo at a higher rate than your body cells. However, any dividing body cell will take up the chemo.
This is why some types of chemo cause you to lose your hair because your hair is dividing. It'll grow back. Your eyelashes and your eyebrows. My eyelashes are really not too great.
They grew back a little, little. That's why you can get an upset stomach because your stomach lining is constantly replacing those cells because there's mechanical churning going on in there and you lose some. So that's why we would like to target these treatments so specifically that there are no side effects. They do have some really, really good drugs for nausea now.
I have three levels that I could take. I only ever got to the second level that I needed to take. And that was when I was way far into chemo and almost done. So was there any kinds of pain medication you could take? Like probably not Tylenol, right?
With my kind of chemo, I could not take pain medicine. And it is, for my kind of chemo, it was doable. But for me, it was, I was uncomfortable when I.
about on my third day when I was the third day after chemo for me and it's different for different people and every person is different but I had been in a really bad car accident all those places where I had injured my bones it hurt so bad I couldn't sit I couldn't lay but it only lasted for a couple days like that bad and I could deal with it and I kept thinking this is what's saving me so hang in there you know um and it did it worked so far thank you god for me um and not everybody lives through ovarian cancer um so i was really lucky um there are some things they can do if it gets really bad there are ivy things they can give you like um they give you steroids sometimes they do the the day they're doing the chemo like it's chemo is really long mine my my one week it took like i got it once a week one week you They did an eight-hour run, and the next week they did a six-hour run because they run in Benadryl first, they run in all these steroids first, they do all this hydration, and then they run it in really, really slow. And so I had so many steroids in me that the day after chemo, I felt great. And then I could feel it wearing off, and I thought, here we go. But it was totally doable, totally doable. I don't want you to be scared about it.
And then immunotherapy is newer. But I have to say, immunotherapy, I know two people that did it, and it did not work at all on them. And the problem is, when you do immunotherapy, because they're going to supercharge your white blood cells, they take some of your white blood cells, teach them the cancer protein they're supposed to attack and give them and like they then they clone them up and put them back into you.
Because of that, you can't do immunotherapy and chemo at the same time. You have to choose one or the other. I had two friends that chose immunotherapy first. It didn't work. And by that time, they couldn't catch it with chemo anymore.
Some people, immunotherapy works incredibly well. It's very patchy right now. It's still not worked out well. Cells die two ways.
They die from either the normal way, like your dog bites you, they get poisoned, there's not enough oxygen, or they die from this internal decision called apoptosis. This is programmed cell death, that the cell commits suicide to save the rest of you. There are many, many genes, including p53 involved, and it doesn't only happen, you know.
Like if your cells trying to become a cancer cell, when you get sunburned, this happens. So, you know, if you've been sunburned bad enough that you blistered, you know, all of a sudden the blisters dry up and you peel. That's apoptosis. Those cells had such bad DNA damage that P53 did go off and the egg timer went on and your cell was like, can I fix this? Let me try.
And it was like, nope, this is global. ultraviolet damage to my DNA. I cannot possibly do this. And basically at that point, your cells died and externally peeled off to save the rest of you.
Internally, it's a similar process, but they don't peel off. A white cell comes and eats them. They shrink.
They disable all their like help enzymes. They trash compact their nucleus. Bubbles come up like in the cytoplasm, like you're frying an egg, the cell shrinks down, and then a white cell comes and eats it. That's when it's working, when everything works well.
Wow, I'm really sorry to hear some of you having these things have happened. Yeah, and for all those of you that do know people with cancer. There's so much research being done.
When I was a graduate student, I did cancer research, and I don't do research now anymore. I haven't been in and out of chemo. It's too hard. But I need to let you know that there are labs that run basically 24 hours a day trying to do research to help people.
And we do have a lot of advances, but we're just not far enough yet. And the only time our lab, the only time it didn't run when I was a graduate student was from two until five in the morning because we were in cell decontamination, like where you put on all these special lights in there to make sure there's no viruses and there's no nothing that are going to get in the cell cultures. And we were running almost 24 hours a day, every weekend, every holiday, because people are committed to trying to find ways to stop this.
There are many more options than there used to be. Even since I was in chemo, I was amazed from 10 years ago, and then three years ago, it was a different kind of cancer. And I was amazed at the advances and how much it just changed in seven years. But it just needs to change faster. So we talked about the sunburn cells.
So are freckles a similar case in terms of like skin damage? Nope. Freckles are normal genetic manifestations where instead of the pigment being distributed all throughout your skin, it's concentrated in the freckles.
And there are genes for that. There are multiple genes for that. Professor? Yes, go ahead.
This class ends at 1020, right? Yes, it does. Okay.
It's 1020. Yep. Okay. Thank you. So we are going to stop there. And then we will next time do meiosis.
We're going to try to get through meiosis in one day. We'll see how that's so that we can do a review on Monday, but we'll see how that goes. Professor? Excuse me. Go ahead.