Cancer and the Cell Cycle

Chapter 2
 The price we pay for being multicellular

Cancer is a complication of being many-celled

organism.
 What causes cancer?
Cancer arises from the mutation of a normal gene.
Mutated genes that cause cancer are called
oncogenes.
It is thought that several mutations need to occur to
give rise to cancer
Cells that are old or not functioning properly
normally self destruct and are replaced by new
cells.
However, cancerous cells do not self destruct and
continue to divide rapidly producing millions of new
cancerous cells.
 Cell division rates for normal and cancer
cells-between divisions

Normal cells Cancer cells

Lining cells of large Stomach 72 hrs
intestine 39 hours Lung 196-260 hrs
Lining cells of rectum 48 Acute myelobastic
hrs leukemia 120 hrs
Fertilized ovum 36-60 hrs
Carcinogens
Ionising radiation X Rays, UV light

Chemicals tar from cigarettes

Virus infection papilloma virus can be

responsible for cervical cancer.

Hereditary predisposition Some families are

more susceptible to getting certain cancers.
Remember you cant inherit cancer its just that
you maybe more susceptible to getting it.
 Benign or malignant?
Benign tumours do not spread from their site of
origin, but can crowd out (squash) surrounding cells
eg brain tumour, warts.

Malignant tumours can spread from the original site

and cause secondary tumours. This is called
metastasis. They interfere with neighbouring cells
and can block blood vessels, the gut, glands, lungs
etc.
Why are secondary tumours so bad?

Both types of tumour can tire the body out as they

both need a huge amount of nutrients to sustain the
rapid growth and division of the cells.
Cancer Cells
Animation: How Cells Reproduce

Cancer video
HHMI video
How Is Genetics Involved?

Two classes of genes: Oncogenes and tumor

suppressor genes

Proto-oncogenes: control cell division

Tumor suppressor genes turn off cell division

Mutated alleles, oncogenes, and tumor suppressor

genes cause cells to divide uncontrollably
 Mutations in Tumor Suppressor Genes

Tumor suppressor genes

Normal genes
(regulate cell growth)

Tumor suppressor genes Active oncogene

1st mutation
(susceptible carrier)

No brakes!
2nd mutation or
loss (leads to
cancer)

No brakes!

Active oncogene
 G2/M checkpoint
4
Cell
division
3
DNA
repair

Mitosis 1
G2
Cell
grows,
G1 doubles
in size
S

Chromosome
2 duplication
G1/S
checkpoint
Regulation of Cell Cycle

G1/S checkpoint

G2/M checkpoint

Tumor suppressor genes and proto-oncogenes

control these checkpoints
Tumor suppressor genes turn off or decrease rate
of cell division
Proto-oncogenes turn on or increase rate
Signal Transduction

In normal cells, signals from outside cell can

Activate tumor suppressor genes (turning off
cell division) or
Activate proto-oncogenes (turning on cell
division)

Signals can be proteins, hormones, nerve

signals, steroids, pollutants, and other molecules
Process of Signal Transduction

Signal binds to a receptor in plasma membrane

Binding sets off series of interactions inside cell

Signal molecule may remain outside cell

Binding of signal changes shape of receptor and

allows it to transmit signal to other proteins

May alter gene expression

Outside cell
Signal molecule

Signalreceptor
binding Receptor

Plasma
membrane

Cytoplasm
Cellular
response

Protein
molecules
Nucleus

Changes in gene
expression
Ras Signaling

This is a detailed view

of Ras interactions in
pathways leading to:
cell proliferation
cell survival
differentiation
cell cycle control
cell motility
tumorigenesis
Cancer Genes on other Chromosomes
Environmental Factors and Populations

Determine types of cancer populations may

develop

Many forms of cancer related to:

Physical surroundings
Personal behavior
Or both

At least 50% of all cancer can be attributed to

some type of environmental factor
Characteristics of Cancer

Tumors begin with a single cell that reproduces

by mitosis

Cells in tumors divide continuously

Metastasis: Process in which cells are invasive

and move to other sites in the body
Monoclonal or polyclonal