In This Lesson:
Unit 5
Mitosis and the
Cell Cycle
(Lesson 1 of 3)
Today is Tuesday,
November 24th, 2015
Pre-Class:
From where do cells originate?
Because they don’t come from this 
P.S. Get a paper towel and
have your guided reading on
your desks.
http://animalsneedkisses.files.wordpress.com/2009/03/teenage_....jpg
Today’s Agenda
• Chromosome basics.
• The Cell Cycle.
• Mitosis.
– Where division = multiplication.
• But first…
– Class baby pictures. Yes, you.
• Where is this in my book?
– Chapter 12.
By the end of this lesson…
• You should be able to describe a normallyfunctioning somatic cell cycle and analyze
what would happen if it no longer functioned
properly.
• You should be able to identify several
chromosomal diseases using karyotypes.
• You should be able to contrast mitosis and
binary fission.
A Rather Striking Introduction
• i am so proud of you – Don Hertzfeldt
Class Baby Pictures
• On the next slide, I have photos of some of
you as wee lil’ babies.
– Maybe not all, but at least some.
• Please thank your parents for keeping it a
secret.
– They did keep it a secret, right?
• Let’s see…who’s up first…?
You.
• It’s your first diploid cell. The zygote. You all
started this way.
– You’ve come a long way.
http://www.alphascientists.org/images/uploads/images/Zygote_1.jpg
Okay then…
• …let’s get to some Challenge Questions.
The Cell Theory
• Think back to the cell theory…
– All living things are made of cells.
– Cells are the basic units of structure and function.
– All cells come from preexisting cells.
• That last one is the big one for us right now.
You again.
• You started as a microscopic single cell – a
zygote, the cell that resulted from the fusion
of gametes – far smaller than the period at the
end of this sentence.
Aw, you
were so
cute then…
Since then…
• From that point forward, you’ve been dividing and
dividing your cells.
– Remember, that’s all you are. Just a bunch of overgrown
zygotes.
• Now you’re a trillion-celled living, breathing, thinking
emoting human being with a cell phone addiction.
Why Divide?
• Growth is just one reason. Cell also divide for
• Reproduction if they’re unicellular. If they’re part of a
multicellular organism, they may divide for
• Repair or renewal, such as when a cut heals or
• Differentiation, since they need to grow up and get
jobs.
• Not to mention, cells also have to divide because they
really can’t get bigger without ruining that whole
surface area-to-volume ratio.
So what do we need to know?
• To fully understand the cellular division
process, which itself is mostly review of what
you’ve already learned, we need to
understand the following:
– Chromosomes
• Hey, how do you pronounce that? Dialect Survey!
– Karyotyping
– The Cell Cycle
Chromosomes [Review]
• Recall that humans have 46 chromosomes arranged
in 23 pairs in each of their somatic cells, of which
22 pairs are considered autosomes.
– Somatic cells are body cells, as in “not reproductive
cells.”
• Any cell that’s not sperm/egg.
– Autosomes are “body chromosomes” – they don’t
directly have anything to do with sex characteristics.
• Any chromosome that’s not a sex chromosome.
• One pair of chromosomes is the sex chromosomes.
– Female = XX; male = XY.
Chromosomes [Review]
• Humans have 46 chromosomes in 23 pairs.
– This is a diploid arrangement, also given by the
designation 2n – we have 23 chromosomes with 2
copies of each.
– Each chromosome in a pair (homologous
chromosomes) is similar to the other, one carrying
info from mom and one carrying info from dad.
• It’s like having a pair of shoes. You need both and they are
different, but they’re still mostly the same.
Chromosomes [Review]
• Gametes are reproductive cells (such as
sperm/ova), and they have a 1n (haploid)
arrangement.
– Each gamete provides half the BFF
necklace/chromosomes needed for a full somatic
cell.
– When they fuse, the two gametes form a zygote.
Diploid and Haploid
Somatic Cells
Mom
1.
2.
3.
.
.
.
.
.
.
23.
Gametes
Dad
Diploid Arrangement
Homologous
Chromosomes
1.
2.
3.
.
.
.
.
.
.
23.
Haploid Arrangement
Chromosomes [Review]
•
•
•
•
Dog: 78 Chromosomes (39 pairs)
Orangutan: 48 Chromosomes (24 pairs)
Mouse: 40 Chromosomes (20 pairs)
Strawberry: 56 Chromosomes (7 groups of 8 octoploid)
• Adders-tongue fern: 1200 or 1260 Chromosomes
• Oxytricha trifallax (protozoan): ~16,000
chromosomes
Chromosomes [Review]
• The X chromosome is rather large and has
between 800 and 900 genes.
– They’re not particularly female-related.
• Colorblindness and hemophilia are linked to X-chromosome
genes, for example.
• The Y chromosome only has about 40 genes.
– They’re called holandric genes, by the way.
• Therefore, if you inherit a combination of X or Y
genes different from XX or XY, interesting changes
occur.
Chromosomes [Review]
• XXX – Trisomy X
– Female, otherwise healthy. (1 in 1000 females)
• XXY – Klinefelter Syndrome
– Male, reduced sex characteristics, some female
characteristics.
• X0 - Turner Syndrome
– Female, appear normal but sterile.
• XYY
– Male, otherwise healthy. (1 in 1000 males).
Chromosomes [Review]
• Chromosomes are often studied in a
karyotype.
– A karyotype is either:
• A photo/diagram showing all the chromosomes of an
organism/individual, OR
• The actual chromosomes present in the cell of an
organism/individual.
• Let’s take a look at some…
Karyotypes
• Human Male
http://kennethtls.blogspot.com/2010/11/gender-crisis.html
Karyotypes
• Human Female – Turner Syndrome
http://kennethtls.blogspot.com/2010/11/gender-crisis.html
Karyotypes
• Human Male – Klinefelter Syndrome
http://kennethtls.blogspot.com/2010/11/gender-crisis.html
Other Chromosomal Diseases
• Any case of an abnormal chromosome number is
called aneuploidy.
• For example:
– Three copies of chromosome 21?
• Down Syndrome (Trisomy 21)
– Three copies of chromosome 13?
• Patau Syndrome
– Two copies of chromosome X?
• Female…no, really, this one’s interesting.
Females
• If males can survive with only one X
chromosomes, how come females don’t suffer
problems with two copies?
• Turns out, in females, a single X chromosome in
each cell is randomly inactivated shortly after
conception.
• The inactivated X chromosome is called a Barr
body.
– Remember this for a cool fact later. We’ll also talk
about how all these aneuploid issues arise.
From females to…bacteria?
• For most of the rest of this PowerPoint we’re
going to be discussing eukaryotic somatic cell
division (mitosis), but we do need to get
something out of the way first:
– Binary fission.
• Binary fission is prokaryotic cell division and it’s
pretty simple:
– Copy DNA.
• They only have a single, circular, folded-up DNA molecule.
– Divide.
Binary Fission
Back to Chromosomes [Review]
• Chromosomes are only
visible during mitosis.
• During other parts of the
cell cycle, they’re invisible
to a light microscope in a
form known as chromatin.
– Chromatin is simply DNA
wrapped around spherical
proteins known as histones.
– The histone/DNA complex is
known as a nucleosome.
https://www.broadinstitute.org/files/news/images/2010/chromatin_states_2a.png
And speaking of the cell cycle…
• The Cell Cycle consists of these stages:
• G1
– Gap 1 (growth phase).
• S
– Synthesis (DNA is copied).
• G2
– Gap 2 (growth phase).
– New organelles are made.
• M
– Mitosis (nucleus divides).
• Cytokinesis
– Cytoplasm divides.
The Cell Cycle [Review]
• There’s also a bonus
stage called G0.
– That’s pronounced “G
naught.”
• Cells in G0 do not divide
by mitosis, like brain cells
and some muscle cells.
– G0 is thus not part of the
cell cycle.
M
Mitosis
G2
Gap 2
S
Synthesis
G1
Gap 1
G0
Resting
The Cell Cycle [Review]
• G1, S, and G2 together make up
interphase, the collective name for the
“resting phase.”
– “Resting phase” is a bad name.
• The nucleus is present and easy to spot.
– DNA is in the form of chromatin.
The Cell Cycle [Review]
• During S phase, all six feet of DNA needs
to be copied.
– Error rate in copying? 1 in 100 million DNA
bases.
– With ~30 billion bases in the mammalian
genome, that’s around 30 errors each cycle.
• Not evolution – these are body cells.
Terminology [Review]
• We’re almost there.
• Before we get into M phase details, there’s
one last thing to talk about – chromosome
terminology.
– It’s gonna get complicated in hurr…
Terminology [Review]
S Phase
Chromosomes are
copied
Sister Sister
Chromosome
Chromosome
Chromatid
Chromatid
Pre-S Phase
Post-S Phase
Terminology [Review]
• Chromatid
– Half of a duplicated (X-shaped) chromosome.
– Prior to duplication, it was called a chromosome.
• Sister Chromatids
– The two identical chromatid copies that make up an Xshaped chromosome.
• Centromere
– The site at which the two sister chromatids join.
• It’s really just a stretch of DNA, so it’s there before and after S
phase (DNA duplication).
– Basically the same as the kinetochore – where spindle
fibers (later) will attach.
Terminology [Review]
Sketch me!
Sketch me!
Sketch me!
Sketch me!
Sketch me!
Sketch me!
http://www.janewhitney.com/img/sister_chromatids.jpg
Phew. Time for Mitosis.
• Key organelles in mitosis:
– Nucleus (duh)
– Centrioles
• Aid in cell division, remember?
• Something new: Centrioles are found in a region of the
cell known as the centrosome.
• There is one centrosome for each of the two pairs of
centrioles.
Mitosis [Review]
• What it looks like:
http://royaleb.files.wordpress.com/2009/04/mitosis_phases1.jpg
Mitosis [Review]
• What it kinda looks like:
http://www.geekosystem.com/wp-content/uploads/2010/07/donut-mitosis.jpeg
Mitosis [Review]
• What it doesn’t look like:
http://icanhascheezburger.files.wordpress.com/2008/03/funny-pictures-mitosis-rabbits.jpg
Mitosis [Review]
• Mitosis (M phase) is the division of the nucleus.
• There are four main phases of mitosis:
– Prophase
• Some people put an additional step here: Prometaphase.
– Metaphase
– Anaphase
– Telophase
• Got a way to remember these?
http://student.ccbcmd.edu/courses/bio141/lecguide/unit6/genetics/DNA/DNArep/images/early_late_prophase1_pc.jpg
Prophase [Review]
• Chromatin condenses into chromosomes.
– Chromosomes have been copied by now and look like little
X’s.
• Nuclear membrane/nucleolus breaks down.
• Mitotic spindle fibers (the “ropes”) form.
– The spindle fibers are made of microtubules (actin/myosin).
http://img.sparknotes.com/figures/D/d756b5b73abe2974f3521a828791899f/prophase.gif
Prometaphase
• Prometaphase is an intermediate
step between Prophase and
Metaphase (obvious).
– Starts when the nucleus breaks down,
centrioles have moved apart, and
spindle fibers are forming and hooking
onto the chromosomes.
• This centromere/spindle structure is called
a kinetochore.
– Ends when the chromosomes are
being moved into the center of the
cell.
http://student.ccbcmd.edu/courses/bio141/lecguide/unit6/genetics/DNA/DNArep/images/metaphase1_ac.jpg
Metaphase [Review]
• Chromosomes line up in the middle of the cell at
the metaphase plate.
– Sometimes called the equator.
http://img.sparknotes.com/figures/D/d756b5b73abe2974f3521a828791899f/metaphase.gif
http://student.ccbcmd.edu/courses/bio141/lecguide/unit6/genetics/DNA/DNArep/images/early_anaphase1_pc.jpg
Anaphase [Review]
• Centromeres divide.
– Sister chromatids are pulled apart.
– Chromatids move toward the poles.
http://img.sparknotes.com/figures/D/d756b5b73abe2974f3521a828791899f/anaphase.gif
Anaphase: Chromosome Movement
• Some really famous research was
devoted to figuring out how
chromosomes are brought
toward the poles.
– We know it’s partially with the use
of motor proteins (see diagram).
– Are microtubules (spindle fibers)
dismantled near the centrosome or
near the kinetochore?
• It’s the centrosome end that’s
shortened.
• 
Aside: Spelling Counts
• Don’t be my former student…
http://student.ccbcmd.edu/courses/bio141/lecguide/unit6/genetics/DNA/DNArep/images/telophase_ac.jpg
Telophase [Review]
• Nuclear envelope re-forms.
• For just a little while, there are two nuclei.
– These are the daughter nuclei.
• Chromosomes expand into chromatin.
• Cytokinesis begins.
http://img.sparknotes.com/figures/D/d756b5b73abe2974f3521a828791899f/telophase.gif
http://www.bio.miami.edu/~cmallery/150/mitosis/sf8x9a.jpg
Cytokinesis in Animal Cells [Review]
• The cell divides into two daughter cells.
• A belt of actin microfilaments pinches the membrane
together between nuclei – forms a cleavage furrow.
• Cell walls are a little different (next slide).
http://img.sparknotes.com/figures/D/d756b5b73abe2974f3521a828791899f/cytokinesis.gif
http://wpcontent.answers.com/wikipedia/commons/thumb/5/5b/Phragmoplast.png/300px-Phragmoplast.png
Cytokinesis in Plant Cells [Review]
• Cell plate forms from vesicles, which themselves form a
pair of cell membranes (sent from Golgi).
– Cell wall is inside the vesicle membrane.
• Cell wall forms on top of the cell plate, dividing the cell
into two daughter cells.
http://student.ccbcmd.edu/courses/bio141/lecguide/unit6/genetics/DNA/DNArep/images/telophase2_pc.jpg
Cytokinesis in a Plant Cell
Mitosis in a Plant Cell
Mitosis in Onion Roots
Mitosis in Animal Cells
Mitosis in Whitefish
Mitosis Summary
• This really cool company called Hybrid Medical
Animations put together an awesome CGI look
at mitosis in a cell.
• http://www.hybridmedicalanimation.com/wo
rk/animation/the-stages-of-mitosis/
Mitosis Scope Activity
• Okay, here’s a change-of-pace.
• At each of your lab tables is a microscope along with a
slide showing mitosis in onion root tips.
• Take a look around the slide and, with your group, see
if you can spot cells in different stages of mitosis.
–
–
–
–
As I walk by, point some out to me.
Make sure you all rotate in to view the scope.
Hint: where on the root would mitosis be happening most?
Lastly, don’t goof off. Just because there aren’t any
questions doesn’t mean you can’t learn from this.
• Triple negative?
Summary of Mitosis
Start with one diploid cell
that has 46 chromosomes.
46
Mitosis
46
End with two cells called?
They each have how many
Twochromosomes?
diploid daughter
cells each with 46
chromosomes
46
Mitosis
• What it actually really looks like (see the spindles?):
http://www.geekosystem.com/wp-content/uploads/2010/07/donut-mitosis.jpeg
Mitosis Fun Facts
• 300,000,000 cells die and are replaced every
minute – roughly equal to the population of
the United States.
• 50,000,000 cells are born in the time it takes
me to read this.
• Nerve cells do not divide but are replaced
from glial cells through neurogenesis.
Aside: How Old Are You?
• While it’s true that cells divide relatively
quickly, they also don’t last forever.
• Right now, the oldest cells in your body are 79 years old.
– That’ll stay the same throughout your life – always
7-9 years old, max, for your cells…
• …which means that nothing living about you
is actually as old as…you.
– Whoooooooa.
Mitosis Rap
• Yep, not kidding…we’re going to listen to a
mitosis rap.
– I didn’t do it…could you have guessed?
Mitosis Rap Lyrics
“I” is for Interphase is step 1
the step before mitosis has
begun.
“P” is for Prophase is step 2
the chromosome double dog
that’s what they do.
“T” is for Telophase is step 5,
right
two daughter cells are made in
both of our life…a’ight.
Mitosis tells all my cells to
divide.
“M” is for Metaphase is step 3
Each cells put chromosomes to
the chromosomes line up as you opposite sides.
can see.
It makes daughter cells that
are two of a kind, two of a
“A” is for Anaphase is step 4
kind.
as chromosomes move away
from the core.
Other Mitosis Stuff
• Mitosis App
– https://itunes.apple.com/us/app/mitosis/id34818
4626?mt=8
• Mitosis – Phase Contrast Microscope video
Cell Division Practice
• Time for a Quia quiz: Labeling Mitosis.
– This one’s important!
• Leave your computer on but closed when
you’re done.
Cell Cycle Game
• Grab yo’ laptops and find The Cell Cycle Game:
• http://nobelprize.org/educational/medicine/2001/in
dex.html
– Also linked from my Biology Links page – UNIT 4.
• Complete the Quia activity called Cell Cycle
Game.
• Keep an eye on the dial in the upper left
corner and the “energy” in the upper right!
Back to the Cell Cycle
• You’ve now reviewed all of the cell cycle, from
interphase through mitosis and cytokinesis.
– That’s the “what,” as in, “what is the cell cycle?”
• We now need to talk about the regulation of
the cell cycle.
– This is the “how,” as in, “how does the cell
manage this whole process and keep it from
getting out of control?
Cell Cycle Regulation
• Imagine, for a moment, what it would be like
if all cells in a bear had the same cycle?
– One moment it’d just be sitting there, the next
moment it would be TWICE AS HUGE.
• Normal growth and maintenance of a
multicellular creature thus requires careful
coordination of cell division.
Cell Division Frequency
• First of all, how long does it take the average cell to
divide?
– Embryonic cells = <20 minutes
– Skin cells = 12-24 hours
– Liver cells = 1-2 years (tend not to divide)
• Liver cells stay in G0 but can return to the cell cycle if signaled.
– Nerve and muscle cells = never (after maturity)
Cell Cycle Control
• As you saw in the game,
throughout the cell cycle are
several checkpoints.
1. During G1 to ensure that S phase
can begin.
• This is the most important signal.
• If the cell doesn’t get a “go,” it enters
G0.
2. After G2 to check that S phase
went smoothly and division can
occur safely.
3. During M phase (spindle
checkpoint – more later) to be
certain that spindles have
attached to chromosomes
correctly.
Checkpoints
http://skreened.com/scienceforscientists/dna-checks-itself-before-it-wrecks-itself
Cell Cycle Signals
• Okay, I’ve been mentioning “signals” a lot without
being specific. Here’s the cast of characters.
• Internal Signals
– Cyclins – regulatory proteins whose levels cycle (get it?).
– Cdks – cyclin-dependent kinases that phosphorylate
(activate) cellular proteins.
– MPF – a maturation (think “mitosis”) promoting factor.
• External Signals
– Density-dependent inhibition – cells are inhibited from
growing if there are a ton of cells around them.
– Anchorage dependence – cells need to grow on a substrate.
Cyclins and Cdk
• A cyclin is a protein molecule.
– That’s it. It can’t do anything on its own.
• There are cyclins for just about every stage in the
cell cycle. For example:
– G1-phase cyclin
– G1/S-phase cyclin
– S-phase cyclin
– M-phase cyclin
• Key: Their concentration varies throughout the cell
cycle.
Cyclins and Cdk
• A Cdk is a cyclin-dependent kinase.
– It’s a kinase, so it phosphorylates
stuff to activate it.
– As you might guess, it needs cyclin to
work.
• Key: Cdk concentration is stable
throughout the cell cycle.
• Cdks bind to cyclins as they are
produced.
• Key: Once Cdk activity passes a
certain threshold, the entire cell is
driven into the next phase of the
cell cycle.
Cyclins and CDK Activity
http://www.nature.com/scitable/topicpage/cdk-14046166
Cyclins and Cdk
• Hey…wait a second. Does something about
cyclins and Cdk sound vaguely familiar?
• Like…maybe…this?
From Cyclin to
Cdk to…
• There are a few different
cyclin/Cdk types out
there, but the first to be
discovered is the one
that leads to mitosis.
• Cyclin levels rise in late
G2, bonding to Cdk and
becoming known as
MPF (maturationpromoting factor).
– High MPF activity signals
the cell to enter mitosis.
Let’s Recap Briefly
• Cdk levels are constant; cyclin levels vary.
• When the cell is ready to go to the next step in the
cell cycle, specific cyclin concentrations go up.
– Which means cyclin/Cdk complexes become active.
– If the cell is in G2, the cyclin/Cdk complex is called MPF.
• When enough cyclin/Cdk activity occurs, the cell
moves into the next step of the cycle.
• Important: What happens to the cyclins that have
built up?
– Enzymes degrade them.
MPFs and APC
• While MPF is one of a few cyclin-Cdk complexes,
there is also an APC – anaphase-promoting complex.
– Not a cyclin/Cdk – this is a different kind of protein.
– Anaphase promoting complex surges in concentration
during metaphase…promoting anaphase as the next step.
– Remember the spindle checkpoint? APC helps regulate
that.
• By now you’re probably getting the idea that there
are lots of signals in play. In general:
– The main control mechanism is phosphorylation as carried
out by kinases.
– Internal signals are promoting/promotion factors.
– External signals are growth factors.
External Signals (Growth Factors)
• External signals, like we’ve learned
before, are released by cells and
have effects on others. What kind
of effects?
• Density-dependent inhibition is
when crowded cells don’t divide
anymore. Why?
– Growth factors released by cells are
bound by so many other cells that no
one can get enough growth factor to
divide.
External Signals (Growth Factors)
• It’s like this:
– Suppose we are feeding two people
with a pizza. Fine. Each person will
probably get enough to be full.
• AKA each cell gets enough growth factor
to divide.
– Now suppose we’re feeding two
thousand people with a pizza. People
simply aren’t going to get enough to
be full.
• AKA each cell doesn’t get enough growth
factor to divide.
Anchorage Dependence
• Cells, spoiled lil’ buggers that they are, have
touch receptors that need to be on a proper
substrate to grow.
– Substrate as in “growing surface,” not enzyme-y
stuff.
• This is called anchorage dependence.
• Cue the video: NOVA – Artificial Organ Growth
Case in Point: Growth Factor
• Let’s take an in-depth look at a growth factor and
related processes.
• This is a fantastic review of a lot of stuff we’ve
learned so far.
– Anything important that we’ve reviewed will be
underlined.
– Anything new and important will be bold and
underlined.
• The growth factor?
– Platelet-Derived Growth Factor (PDGF)
Case in Point: Growth Factor
• The story starts with erythropoietin (EPO),
which is a glycoprotein hormone made by the
kidney.
• When renal (kidney) oxygen levels drop too
low, kidneys release EPO which stimulates
bone marrow to make more red blood cells.
– Thus the blood can now carry more oxygen, thus
enabling greater ATP production through aerobic
respiration.
• This is a negative feedback loop.
Case in Point: Growth Factor
•
•
•
•
In that way, EPO is a GF of red blood cells.
Ever hear about EPO in the news?
Coughlancearmstrongcough…
Coughblooddopingcough…
http://upload.wikimedia.org/wikipedia/commons/thumb/4/47/Lance_Armstrong_%28Tour_Down_Under_2009%29.jpg/430px-Lance_
Armstrong_%28Tour_Down_Under_2009%29.jpg and Lance_Armstrong_MidiLibre_2002.jpg/800px-Lance_Armstrong_MidiLibre_2002.jpg
Case in Point: Growth Factor
• EPO has been used as a performance-enhancing drug
(PED) (in this case known as “blood doping”) because
it increases the oxygen-carrying capacity of the blood
by making it extra rich with blood cells.
• The downside?
– All those extra blood cells makes your blood considerably
thicker/more viscous.
– Dehydration also makes your blood thicker/more viscous.
– Thick/viscous blood = increased risk of stroke/heart
attack/death.
• Just say no to EPO.
Case in Point: Growth Factor
• But there’s another growth factor involved in
your blood.
– “Another GF? Scandalous!”
• Forget EPO for a second.
• Suppose you get a paper cut.
http://farm3.static.flickr.com/2062/1892872952_b4e38a6edc.jpg
Case in Point: Growth Factor
• Platelets in the blood near your cut bind
to the neighboring skin cells.
• They release PDGF (platelet-derived
growth factor, remember?).
• PDGF stimulates neighboring skin cells
to divide, healing your wound.
– Also, platelets stimulate more platelets to
arrive and release more PDGF, making this
an example of a positive feedback loop.
http://th05.deviantart.net/fs71/PRE/i/2012/102/d/3/paper_cut__by_xcrazyonyoux-d4vw2dj.jpg
So the logical question…
• We have all these checkpoints.
• What happens if something goes wrong?
• In a word?
– Cancer.
• Many cancers are caused by cells that escape
from the normal cell cycle.
– The brakes on cell division have been removed.
• Normal cells divide up to 60 times or so (more on
this in a little bit).
– Cancer cells? A lot more.
• TED: George Zaidan – How Cancer Cells Behave
Differently from Healthy Ones
Case in Point: HeLa Cells
• Many cancer cells used in research are
called HeLa cells.
– Named for Henrietta Lacks, a poor AfricanAmerican woman from the South.
• In 1951, Lacks sought treatment for
cervical cancer. Her doctor(s) took a
tissue sample from a tumor and cultured
it.
– “Cultured” meaning “grew in a lab.”
• Lacks died later in the year, with her
family not knowing that her cells had
been cultured.
– Today, her cells are still living and dividing
endlessly and are used in research all over
the world.
– Read that book! 
Cancer Terminology
• Tumor
– A mass of cancer cells.
• Remember, cancer cells divide A LOT.
– Benign tumors are sitting in their original spot.
– Metastatic or malignant tumors are spreading
throughout the body.
• Carcinogen
– Something that causes cancer.
• Like smoking, chewing tobacco, or other things CB
students do in bathrooms.
Cancerous Promoting Factors
• Proto-oncogenes are genes that cause cancer if
switched “on” and mutated.
– Ras is a group of genes like this and are involved in
30% of human cancers.
• Tumor-suppressor genes cause cancer if
switched “off.”
– p53 is a tumor-suppressor gene and is involved in 50%
of human cancers.
• So it follows that mutagens are things that cause
mutations and may also be carcinogens.
Cancer Inducers?
• Another factor in play is the degradation of
telomeres.
• Telomeres are “caps” on the ends of the
chromosomes that are made of junk DNA.
– With each cell division, however, telomeres get
smaller.
http://www.psychologytoday.com/files/u693/telomere.jpg
Aside: The Hayflick Limit
• In the 1960s, Leonard Hayflick
discovered that there was a limit
to how many times cells could
divide before their telomeres
were eroded completely away.
– That number is somewhere
between 52 and 60 times, and
it’s now called the Hayflick Limit.
• After that point, the cells may
either be told to die (apoptosis
– programmed cell death) or
simply won’t divide anymore.
http://www.nature.com/polopoly_fs/7.11184.1372152253!/image/Hayflick28.jpg_gen/derivatives/landscape_630/Hayflick28.jpg
Cancer Risk Factors
• Mutagens/Carcinogens
– UV radiation
• Tanning beds!
–
–
–
–
–
Chemicals
Radiation
Heat
Pollution
Cigarette smoke
• Other Factors
– Age
– Genetics
How does cancer work?
• Cancerous genes or cells are often found to be
activating lots of cyclins, thus pushing the cell
through the cell cycle too rapidly.
• Tumor suppressor genes prevent errant DNA from
being copied in mitosis.
– p53, for example, stops cell division if bad DNA is found,
but if p53 isn’t working…you get the idea.
• Subsequent growth and spread of tumors can begin
to block blood vessels, clog body systems, prevent
other cells from functioning…the list goes on…
Case in Point: p53
NORMAL p53
p53 allows cells
with repaired
DNA to divide.
p53
protein
DNA repair enzyme
p53
protein
Step 1
Step 2
Step 3
DNA damage is caused
by heat, radiation, or
chemicals.
Cell division stops, and
p53 triggers enzymes to
repair damaged region.
p53 triggers the destruction
of cells damaged beyond repair.
ABNORMAL p53
abnormal
p53 protein
Step 1
Step 2
DNA damage is
caused by heat,
radiation, or
chemicals.
The p53 protein fails to stop
cell division and repair DNA.
Cell divides without repair to
damaged DNA.
cancer
cell
Step 3
Damaged cells continue to divide.
If other damage accumulates, the
cell can turn cancerous.
Cancer Mutations
• There are six key mutations that must happen for cancer to
occur:
1. Unlimited growth
– Proto-oncogenes turned on.
2. Ignore checkpoints
– Tumor suppressor genes turned off.
3. Escape apoptosis
– Suicide genes turned off.
4. Immortality
– Chromosome maintenance genes (rebuild telomeres) turned on.
5. Blood vessel growth
– Blood vessel growth genes turned on.
6. Anchorage/density-independence
– Touch sensor genes turned off.
Cancer Treatments
• High-Energy Radiation
– Kill rapidly-dividing cells.
• Chemotherapy
– Stop DNA replication, mitosis/cytokinesis, and
blood vessel growth.
• Gleevec
– A relatively new anti-cancer drug that targets
enzymes found only in cancer cells.
• Guess what? It also doesn’t cause autism.
Exit Ticket
• Before this lesson ends, you must get a small
disposable piece of paper and on it write the
following:
–
–
–
–
Your name.
How prokaryotes divide.
The official definition of mitosis.
What two molecules combine to regulate the cell
cycle.
• You can’t leave until you do this. I’m serial.
• Put ‘em in the turn-in box on your way out.