Transcript LECTURE #9: Introduction to Cancer

Mitosis and
Cancer
PART 3
Honors
Genetics
Ms. Gaynor
Another Type of Cell
Division: Binary Fission
Prokaryotes
(bacteria)
Reproduce by a type of
cell division called
binary fission
In binary fission,
 The bacterial chromosome replicates
 The two daughter chromosomes move
replication
apart

Origin of
Cell wall
Plasma
Membrane
E. coli cell
1 Chromosome replication begins.
Soon thereafter, one copy of the
origin moves rapidly toward the
other end of the cell.
2 Replication continues. One copy of
the origin is now at each end of
the cell.
3 Replication finishes. The plasma
membrane grows inward, and
new cell wall is deposited.
Figure 12.11 4 Two daughter cells result.
Two copies
of origin
Origin
Bacterial
Chromosome
Origin
The cell cycle is HIGHLY
regulated
 The
frequency of cell division
 Varies with the type of cell
 These cell cycle differences
 Result from regulation at the
molecular level

http://highered.mcgrawhill.com/sites/0072495855/student_view0/chapter2/animatio
n__how_the_cell_cycle_works.html
Cell Cycle Checkpoints


The clock has specific checkpoints

a critical control point where stop and “go-ahead”
signals can regulate cycle

These signals report whether crucial cellular
processes up to that specific point have been
completed and completed correctly
There are 3 checkpoints
 G1 checkpoint
 G2 Checkpoint
 M checkpoint
 spindle assembly checkpoint
The Cell Cycle Control System

The sequential events of the cell cycle

Are directed by a distinct cell cycle
control system, which is similar to a clock
G1 checkpoint
Control
system
S
G1
M
Figure 12.14
M checkpoint
G2
G2 checkpoint
G1 Checkpoint
G0
G1 checkpoint
G1
If a cell receives a go-ahead
signal at the G1 checkpoint, the
cell continues on in cell cycle.
G1
If a cell does not receive a go-ahead
signal at the G1checkpoint, cell
exits the cell cycle and goes into
G0, a nondividing state.
G1 Checkpoint




Restriction point just
before entry into S phase
Checks cell size & original
DNA for damage
Makes key decisions 
should cell divide or delay
division and enter G0
(resting) phase
Most cells stop at this
stage and enter a resting
state called G0
G2 Checkpoint
Checks cell size
 Triggers start of M
phase
 DNA is frequently
damaged prior to
mitosis  if this
happens, the cell cycle
is arrested via
inactivation of cell
cycle “control”
proteins

M Checkpoint
Makes sure spindle
assembly is correct
 Makes sure all
chromosomes are
aligned at the
mitotic plate

The Cell Cycle Clock:
Cyclins and
Cyclin-Dependent Kinases
types of regulatory
proteins in cytoplasm are
involved in cell cycle control
 Cyclins
 Cyclin-dependent kinases
(Cdks)
 Two
INACTIVE FORM
CYCLIN DEPENDENT
KINASE (CDK)
CYCLIN
+
ACTIVE FORM
CDK/CYCLIN
COMPLEX
Active vs. Inactive??

What happens when cyclins and
cdks are in the ACTIVE form?


Cells can pass through the cell
cycle to the NEXT phase
What happens when cyclins and
cdks are in the INACTIVE form?

Cells can NOT pass through the cell
cycle to the NEXT phase
cyclin
degrades
& breaks
apart
cyclin
degrades
& breaks
apart
What degrades
(breaks down) cyclins?
 Proteolytic
 Break
enzymes (proteins)
down/degrade cyclins 
cause them to fluctuate in [ ]
 “PROTEO” means protein
 “LYTIC” means break or lyse
REMEMBER:
 Cyclin concentration fluctuates
(changes)
 Cdk concentration stays the SAME
Important Cyclins and CDKs
Cyclin D-CDK4
Cyclin E-CDK2
Cyclin A-CDK2
Cyclin B-CDC2
Control of Cell Cycle
Animations

http://highered.mcgrawhill.com/sites/0072495855/student_vie
w0/chapter2/animation__control_of_th
e_cell_cycle.html
Amination #8
http://www.cellsalive.com/apop.htm

Programmed Cell Death
(Apoptosis)



In apoptosis
http://www.biooncology.com/bioonc/research/apoptosis/ind
ex.m
Cell signaling is involved in
programmed cell death needed to
maintain healthy tissues/ cell
function
Figure 21.17
2 µm
Stop and Go Signs: Internal and
External Signals at the Checkpoints
 Both
internal (inside the cell)
and external (outside the cell)
signals
 Control the cell cycle
checkpoints
Internal and External Signals
Internal
signals
 DNA synthesis
 Growth/Nutrition
 CDK/Cyclins
External signals
 Growth factors & Hormones
 Density Dependent Inhibition
 Anchorage Dependence
Influences on Cell Division
Growth factors & hormones
 Stimulate other cells to divide
 In density-dependent inhibition
 Crowded cells stop dividing
 Most animal cells exhibit

anchorage dependence
 In
which they must be attached to
a structure to divide
Ex:
extracellular matrix of a tissue
(a)
Cells anchor to dish surface and
divide (anchorage dependence).
When cells have formed a complete single layer, they stop
dividing
(density-dependent inhibition).
Normal mammalian
cells.
**The
availability of nutrients,
growth
factors, and a
substratum for
attachment limits cell
density to a single layer.
If some cells are scraped away, the remaining cells divide to fill
the gap and then stop (density-dependent inhibition).
Figure 12.18 A
25 µm
Cancer cells
 Exhibit
neither density-dependent
inhibition nor anchorage dependence
 Immortal cells (if enough nutrients)
Cancer cells usually
continue to divide well
beyond a single layer,
forming a clump of
overlapping cells.
Figure 12.18 B
Loss of Cell Cycle
Controls in Cancer Cells
 Cancer
cells
 Do not respond normally to
the body’s control
mechanisms
 Form tumors
TUMOR=
mass or group of
abnormal dividing cells
Why?
 Don’t
need growth factors 
maybe they make their own
growth factors
 Mutations in GENES!!!
 Ex:
cyclin or Cdk genes
Loss of Cell Cycle
Controls in Cancer Cells

Cancer cells
 Normal cell  cancer cells using
process of transformation
 Form tumors
Benign  “fine”
 Clump
of cells remain at orginal spot
Malignant
 “mean” “cancer”
 Loose/destroy
attachments to
other cells  they can
spread!!!
Malignant tumors
 These
tumors invade surrounding
tissues and can metastasize
 Exporting cancer cells to other
parts of the body where they may
form secondary tumors
 USE BLOOD STREAM and
LYMPH VESSELS TO SPREAD!!!

http://www.hhmi.org/biointeractive/media/angiogene
sis-lg.mov
Tumor
Lymph
vessel
Blood
vessel
Glandular
tissue
Cancer cell
Metastatic
Tumor
1 A tumor grows from a
single cancer cell.
Figure 12.19
2
Cancer cells invade
neighboring tissue.
3 Cancer cells spread
through lymph and
blood vessels to
other parts of the body.
4 A small percentage of
cancer cells may survive
and establish a new tumor
in another part of the body.
Cancer Treatment
 destroys DNA in
cancer cells (these cells have
lost ability to repair damage)
 Chemotherapeutic drugs
interfere with specific steps in
cell cycle
 Also effects normal cells 
 Radiation
Cancer Causing Agents
Genetics (inherited)
2. Spontaneous mutation
3. Envinromental Mutagens
(a.k.a- carcinogen)
 Sun
 Viruses
 Chemicals
1.
Cancer AnimationsREVIEW
Cancer Movie
 http://www.cancerquest.org/index.c
fm?page=3102&lang=english

http://science.education.nih.gov/su
pplements/nih1/cancer/activities/ac
tivity2_animations.htm
Flashcard Vocabulary

http://highered.mcgrawhill.com/sites/0078757150/student_
view0/vocabulary_eflashcards.html