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The Cell Cycle and Cancer 

The Cell Cycle and Cancer 2011

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8/6/2019 The Cell Cycle and Cancer 2011

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The Cell Cycle and Cancer 

8/6/2019 The Cell Cycle and Cancer 2011

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Cell signaling: chemical

communication between cells.

Click on above to go to

animation

second chemical response inside the

cell. This may be the first step of an

entire chemical cascade of chemical

signals that trigger actions in the cell.

 Achemical

signal to a

receptor 

on theoutside of 

a cell may

trigger a

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Cancer � Normal cell division:

 ± Controlled by cell cycle checkpoints

� CHECKPOINTS ± critical control points that determine if a

cell will move to the next portion of the cell cycle.

� Cancerous cell division: ± Ignores the cell cycle checkpoints

� Caused by DNA mutations

� Cells grow and divide out of control

� Cancerous cells do not perform designated purpose.� Crowd out normal cells that do perform designated purpose.

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The Stages of the Cell Cycle

1. Click on picture for cell cycle animation ±will go to www.cancerquest.org)

2. Use alt-tab keys to go between website

and power point presentation.3. Click on blank space to proceed to next slide.)

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There are several factors that regulate the

cell cycle and assure a cell divides correctly.

1.Before a cell divides,

the DNA is checked

to make sure it has

replicated correctly. (If 

DNA does not copyitself correctly, a gene

mutation occurs.

DNA replication animation:click

on DNA picture

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Cell Cycle Checkpoints

� G1/S ± Monitors cell size and for DNA damage

� G2/M

 ± Replication complete, DNA damage?

� M

 ± Spindle fibers connected, etc.?

� G0 ± Does body require more of my type of cell?

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� Control of cellular division

 ± Genes code for proteins that either stimulate cell

growth or suppress it.

� Cyclins: proteins that control phases of the cell cycle.

 ± Examples:

» S-cycline stimulates DNA replication

» M-cycline helps trigger mitosis

� Growth factors supervise progress through the cycle.

 ± Sometimes trigger genes to make cyclins.

 ± Sometimes block cyclins

� Proto-oncogenes: genes involved in growth stimulation

 ± Mutation here can produce an ³onco-gene´ which triggersuncontrolled growth. GAS PEDAL

� Tumor suppressor genes: inhibit growth and division

 ± Mutation here = loss of inhibition BRAKE

» Cells divide out of control without normal functioning

suppressor gene

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� Example of a

tumor suppressor 

gene:

 ±p53 gene

codes for 

apoptosis:

(Programmedcell death)

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2. Chemical Signals tell a cell when to start

and stop dividing.

(Target cells animation: click on go

sign)

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Control of cell division continued:

Density Dependent Inhibition: Normal cells cease

dividing once critical cell density is reached. Cancer 

cells do not possess this trait.

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Neighboring cells communicate with dividing

cells to regulate growth.

(Normal contact inhibition animation: click on petri dish)

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� Anchorage dependence:

proteins located in plasmamembrane indicate

attachment to neighboring

cells/tissue

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DNA mutations disrupt the cell cycle.

Carcinogens:

1. radiation

2. smoking3. Pollutants

4. chemicals

5. viruses

6. Heredity

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What causes the mutations thatlead to cancer?

� Viruses: HPV --> cervical cancer  ± Bacteria: H. pylori --> gastric cancer (bacteria usually not a

known carcinogen)

� Chemicals --> lung cancer � UV radiation --> skin cancer 

� What do these agents have in common?

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u s ep rocess: ancer resu s rom

³multiple hits´

� Cancer requires mutation of multiple genes� Age relationship:

 ± Cancer rate increases dramatically with age.

� Delay between carcinogen exposure andonset

 ± 5-8 year delay between carcinogen exposure

(Hiroshima and Nagasaki) and onset of 

leukemia ± 15 year delay between tuberculosis X-ray

treatment and onset of breast cancer 

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 Age and Cancer 

� Note log scale for 

incidence rate

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Cancer is a disease of the cell cycle. Some

of the body¶s cells divide uncontrollably and

tumors form.

Tumors in Liver 

Tumor in Colon

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While normal cells will stop dividing if there is a mutation in

the DNA, cancer cells will continue to divide with mutation.

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Due to DNA mutations, cancer cells ignore the

chemical signals that start and stop the cell cycle.

They don¶t communicate with neighboring cells

and continue to grow and form tumors.

2 animations of cancer cells dividing: click on picture

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SUMMARYNormal Cell Division

1. DNA is replicated

properly.

2. Chemical checkpoints

signal start and stopof the cell cycle.

3. Cells communicate

with each other so

they don¶t becomeovercrowded.

Cancer Cells

1. Mutations occur in the DNA

2. Ignores normal checkpoints

= excessive division

3. Unusual # of chromosomes

4. Loss of attachment and

other control mechanisms

5. Immortality

6. Extensive angiogenesis

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Normal and Cancer 

Karyotypes

� (a) is a normal cell, (b) is a cancer cell

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Benign or malignant?

� Benign tumors do notspread from their siteof origin, but cancrowd out

surrounding cells.

� Malignant tumors

can spread from theoriginal site andcause secondarytumors. This is called

metastasis.

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� Metastasis: cells travelthrough blood vessels or 

lymph to other areas of thebody and grow there. Thisis what makes tumors solethal.

� interfere with normalfunctioning of other tissues

vital to survival.

.

Pathways of cancer:

cell signaling

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Treating Cancers

Cancer treatments include drugs that can stop

cancer cells from dividing.

Chemotherapy:

Radiation:Surgery:

Other medications designed to assist the body in

preventing cancerous cell division.

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Cancer therapies targets

� Classic cancer therapies target rapidlydividing cells ± Radiation

 ± Chemotherapy

� Side effects ± Hair loss

 ± Weakened immune system

 ± Digestive tract issues

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Cancer therapies target

� immune system may not target tumor cells because they appear to be ³self´

� Some therapies activate one's immunesystem against a cancer 

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Cancer therapies target

� Modern, therapies attack specificproteins that are abnormally expressed

in a tumor 

 ± Block over-expressed growth factor 

receptors --> Herceptin

 ± Target cancer cells so less side effects.