Download Cell Cycle

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Since the cell cycle is known, now we must
ask what controls it
Noted that healthy cells in contact will not
divide
◦ Essentially, this is how our skin heals
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But what drives the cycle?
Sequential control?
Experiments have shown that proteins control
it
Experiment 1
Experiment 2
S
G1
M
G1
S
S
M
M
When a cell in the S phase was
fused with a cell in G1, the G1
cell immediately entered the S
phase—DNA was synthesized. S
cells contained something that
induced regulation in G1 cells.
When a cell in the M phase
was fused with a cell in G1,
the G1 cell immediately began
mitosis—a spindle formed and
chromatin condensed, even
though the chromosome had
not been duplicated. Something
in M phase induced interphase
cells to divide.
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Conclusion: the S phase proteins work on G1
nuclei, M phase works on everything
Biologists named these proteins “cyclins”
These are used in all three portions of
interphase
Each is referred to as a “checkpoint”
Collectively, they are called growth factors
The cell has mechanisms that ensure each
phase is complete before moving onto the
next
We have seen this already with the possibility
of a cell entering G0
G0
G1 checkpoint
G1
If a cell receives a goahead signal at the G1
checkpoint, the cell
continues on in the cell
cycle.
G1
If a cell does not receive a
go-ahead signal at the G1
checkpoint, the cell exits
the cell cycle and goes into
G0, a nondividing state.
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Overall, it appears as though there are many
factors, internal and external that control the
cell cycle
Ex. Kinetochores not attached to
microtubules
Ex. Density dependent inhibition
Ex. Anchorage dependence, where cells have
to be attached to a substratum (solid surface)
to divide
Cells anchor to dish surface and
divide (anchorage dependence).
When cells have formed a complete
single layer, they stop dividing
(density-dependent inhibition).
If some cells are scraped away, the
remaining cells divide to fill the gap and
then stop (density-dependent inhibition).
Normal mammalian cells
25 µm
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Cancer can be thought of as uncontrolled
growth of cells
◦ They can lack the mechanisms, do not respond
properly to them, or have an error in the pathways
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If they stop, it is at a random point
Cancer cells do not exhibit anchorage dependence
or density-dependent inhibition.
25 µm
Cancer cells
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A mass of cancer cells is known as a tumor
◦ If this tumor stays in the original site – benign
◦ If it spreads to surrounding tissue - malignant
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A individual tumor cell can break free from
the group and invade other organs
◦ It is said to have metastasized
◦ http://www.youtube.com/watch?v=rrMq8uA_6iA
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Unfortunately, these cells can continue to
grow if supplied with nutrients
◦ Normal cells divide 25-50 before dying
Cancer
Lymph
vessel
Tumor
Blood
vessel
Glandular
tissue
Cancer cell
A tumor grows from a
single cancer cell.
Cancer cells invade
neighboring tissue.
Cancer cells spread
through lymph and
blood vessels to
other parts of the
body.
Metastatic
tumor
A small percentage
of cancer cells may
survive and establish
a new tumor in another
part of the body.
The two most common treatments we have
are chemotherapy and radiation treatments
Chemotherapy
 By definition, treatment of any condition via
chemicals
 Our focus is on antineoplastic drugs – cancer
fighters
 Act by targeting rapidly dividing cells
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◦ However, this also includes healthy cells such as
bone marrow (blood cells), hair follicles, and sex
cells
Common side effects – hair loss and an
compromised immune system
 Essentially theory is the drugs will kill the
cancer faster than the patient
 If not discovered soon enough, treatment
would take too long
Radiation Therapy
 Beam of subatomic particles that damages
DNA
 Has to focus on a tumor
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With more knowledge on mechanisms of
cancer, new treatments are being proposed
Viruses are being designed to specifically
target cancer cells