Transcript Cell Division

Control of the Cell Cycle
Cyclins and Checkpoints
Control of the Cell Cycle
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Cell cycle checkpoints are used by the cell to monitor and
regulate the progress of the cell cycle.
Checkpoints prevent cell cycle progression at specific
points, allowing verification of necessary phase
processes and repair of DNA damage. The cell cannot
proceed to the next phase until checkpoint requirements
have been met.
Several checkpoints are designed to ensure that
damaged or incomplete DNA is not passed on to daughter
cells.
Two main checkpoints exist: the *G1/S checkpoint and
the *G2/M checkpoint.
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G1/S transition is a rate-limiting step in the cell cycle and is also
known as restriction point.
http://outreach.mcb.harvard.edu/animations/checkpoints.swf
Anchorage dependence
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Most animal cells will not
divide unless they are in
contact with a solid surface.
 Ex.
If cells in a lab are
suspended in a liquid they will
rarely divide. However if the
cells are poured onto a solid
surface where they can
attach, they begin dividing
immediately.
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This may keeps cells that
become separated from their
normal surroundings from
dividing inappropriately.
Density-dependent inhibition a.k.a.
contact inhibition
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Cell in a laboratory will
only grow in a single
layer and stop dividing
when they touch one
another.
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If some are removed from
the middle, the cells will
begin dividing again
(analogous to a cut in
your skin!)
If stimulated to divide by
adding growth factors,
the cells will still only
form a single layer but
they will be smaller and
more numerous.
Normal cells will fill in a gap and
then stop dividing…
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Cancer cells
do not
recognize
contact
inhibition and
continue to
divide.
Cancer
Uncontrolled Cell Division
The Cell Cycle and Cancer
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Abnormal growth of cells is called a neoplasm
 Benign neoplasms are not cancerous
 Encapsulated (enclosed)
 Do not invade neighboring tissue or spread
 Malignant neoplasms are cancerous
 Not encapsulated
 Readily invade neighboring tissues, and lymph nodes
which can carry the cancer cells to new locations.
 May also detach and lodge in distant places – metastasis
 Results from mutation of genes regulating the cell cycle
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Carcinogenesis – development of cancer
 Tends
to be gradual
 May be years before cell is obviously cancerous
Characteristics of Cancer Cells
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Lack differentiation
Have abnormal nuclei
Form tumors
 Mitosis controlled by contact
with neighboring cells – contact
inhibition
 Cancer cells have lost contact
inhibition
Undergo metastasis
 Original tumor easily fragments
 New tumors appear in other
organs
Undergo angiogenesis
 Formation of new blood vessels
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http://www.researchvegf.com/researchvegf/multimedia/in
dex.m?video=vegffull&mov=VEGF_Angiogenesis_Full.mp4&wmv=VEGF_A
ngiogenesis_Full.wmv
Tumor angiogenesis — the ability to form
new blood vessels – represents a critical
step in tumor development through which
the tumor establishes an independent
blood supply, consequently facilitating
tumor growth.
Cancer Cells Versus Normal Cells
Four groups of cancers
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Carcinomas: cancers that
originate in the external
or internal coverings of the
body, such as the skin or the
lining of the intestines.
Sarcomas: cancers that arise
in tissues that support the
body, such as bone and
muscle.
Leukemias and Lymphomas:
cancers of blood-forming
tissues, such as bone marrow,
spleen, and lymph nodes.
Origins of Cancer: Oncogenes
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Mutations in DNA repair
mechanisms
Oncogenes
 Proto-oncogenes
promote the
cell cycle in various ways
 Tumor
suppressor genes inhibit
the cell cycle in various ways
 Both
normally regulated in
coordination with organism’s
growth plan
 If
either mutates, may lose
control and become oncogene
Telomeres
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Telomeres are six nucleotide
sequences at the end of each
chromosome in the nuclei of
your cells. They are not genes,
rather they protect the
genetic information in the
chromosome.
When a cell divides, the DNA
in the chromosome is
reproduced except for the
very tip of the chromosome.
The telomeres sacrifice a
small amount of the repeated
sequences with each division
and thus the telomere and the
chromosome become slightly
shorter with each division.
Origins of Cancer:Telomerase
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Chromosomes normally have special material at each end
called telomeres (end parts)
These get shorter each cell division
When they get very short
 The cell will no longer divide
Telomerase is an enzyme that adds telomeres
Mutations in telomerase gene:
 Keeps adding new telomeres
 Allow cancer cells to continually
divide
Telomerase
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High levels of telomerase activity
are detected in embryonic stem
cells and cancer cells; little or no
telomerase activity is present in
most mature, differentiated cell
types.
Functions of telomeres and
telomerase appear to be
important in cell division, normal
development, and aging.
Scientists and doctors have been
attempting to target cancer
through telomerase. Telomerase
is one of the only constants
between almost all types of
cancers. Instead of hundreds of
therapies for hundreds of types
of cancers—we could be looking at
one type of therapy for all types
of cancers.
Cancer Treatments
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Disrupt cell division
 Chemotherapy
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Often antimitotic drugs
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Some interfere with the spindle fibers
Vinblastin: from the periwinkle flower, prevents the spindle
from froming
Taxol: from the Pacific yew, freezes the spindle after it
forms
 Radiation
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Focused, high energy radiation
Since cancer cells are dividing more rapidly than body cells
at any given time, so radiation can disrupt cell division
without seriously injuring the normal cells of the body.
Future treatments?
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Nanotechnology!
Blocking
telemerase?
This is a huge
field of research
with new
technologies and
treatments