Transcript The 6 Superpowers

BB20023/BB20110
DNA & disease (cancer biology)
Dr. Momna Hejmadi
[email protected]
https://moodle.bath.ac.uk/moodle5/login/index.php
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How is this unit assessed?
Multiple Choice Questions (20%)
Nature of cancer,
Wed 31st OCT 11.15 - 12.05
DNA replication,
DNA damage and
3WN 2.1 (all except NS students)
DNA repair
8W 2.30 (Natural Sci students)
EXAM essay (60%)
Topics are
Oncogenic viruses
Apoptosis
Oncogenes & Tumour suppressor genes
Angiogenesis & metastasis
Cancer therapy (4 lectures)
Lab Report (20%)
Peer assessed
DNA repair practical
General Reading List
• The Biology of Cancer by Robert
Weinberg (Garland Publishers )
Other useful books to consult
• Cancer Biology (2000; 2nd ed) by RJB
King (Prentice Hall Publishers)
• DNA repair and mutagenesis (2002) by
Friedberg EC, Walker g and Siede W
• Plus reviews / articles
All lectures & practicals by MVH
Dates
1/10
3/10
8/10/
10/10
15/10
17/10
22/10
24/10
29/10
Room
8W1.1
3WN2.1
8W1.1
3WN2.1
8W1.1
3WN2.1
8W1.1
3WN2.1
8W1.1
Time
9.15
11.15
9.15
11.15
9.15
11.15
9.15
11.15
9.15
31/10
3WN2.1
11.15
5/11
7/11
12/11
14/11
19/11
21/11
26/11
28/11
3/12
5/12
10/12
13/12
8W1.1
3WN2.1
8W1.1
3WN2.1
8W1.1
3WN2.1
8W1.1
3WN2.1
8W1.1
3WN2.1
8W1.1
8W1.1
9.15
11.15
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TOPICS
Introduction: nature of cancer
DNA replication
Biology
DNA damage and repair
Biology
DNA replication
MCB/NS/other
DNA damage and repair
MCB/NS/other
DNA replication
Biochem
DNA damage and repair
Biochem
Revision session on above
Oncogenic viruses
MCQ test VENUE
3WN2.1 (all except NS students)
8W 2.30 (Natural Sci students)
Apoptosis video
Apoptosis
Oncogenes & tumour suppressor genes 1
Oncogenes & tumour suppressor genes 2
Oncogenes & tumour suppressor genes 3
Angiogenesis and metastasis
Cancer therapy 1 - conventional
Cancer therapy 2 – Angiotherapy
Cancer therapy 3: Immunotherapy
Cancer therapy 4 – gene therapy
Spare / revision session
Lab report : Peer assessment session
Workshop 1
Workshop 2
Workshop 1
Workshop 2
Workshop1
Workshop 2
Cancers are clonal descendents of one
cell
Cancer arises by successive mutations
in a clone of proliferating cells
Cancer phenotype results from accumulation
of mutations in the clonal progeny of cells
• Clone of cells overgrows due to
accumulation of mutations controlling
proliferation.
• Disseminates through bloodstream to
other parts of body
• Forms tumor
Introduction:
The 6 Superpowers
Introduction:
The 6 Superpowers
Cancer Cell
Normal Cell
1
GO
STOP
SLOW
1. Most cells wait for a ‘Go signal before
dividing. Cancer cells don’t bother waiting…
they produce their own ‘Go’ chemical
messages and continue dividing.
Introduction:
The 6 Superpowers
Cancer Cell
Normal Cell
1
GO
2
STOP
SLOW
2. Even if the neighbouring cells produce a
‘Stop’ signal, cancer cells override these
signals and continue dividing.
Introduction:
The 6 Superpowers
Cancer Cell
Normal Cell
1
GO
2
STOP
Apoptosis
3
SLOW
3. Normal cells sometimes react to stress by
triggering a ‘Self Destruct’ button and killing
itself, but cancer cells sneak past these self
destruct signals and continue to divide, thus
accumulating more mutations.
Introduction:
The 6 Superpowers
Cancer Cell
Normal Cell
1
GO
2
STOP
Apoptosis
3
SLOW
4
Food Supply
4. Cancer cells make sure they can keep
dividing by stimulating the growth of new
blood vessels to keep their nutrient supply
lines open.
Introduction:
The 6 Superpowers
Cancer Cell
Normal Cell
1
GO
2
STOP
Apoptosis
3
SLOW
4
Food Supply
5
Immortality
5. One of the key superpowers is immortality.
Unlike normal cells which have a finite life
span, cancer cells manipulate their own DNA
(via repetitive DNA sequences called
telomeres) to keep dividing for a lot longer.
Introduction:
The 6 Superpowers
Cancer Cell
Normal Cell
1
GO
2
STOP
Apoptosis
3
SLOW
4
Food Supply
5
Immortality
6
Metastasis
6. Most tumours that show these traits are
trouble, but the lethal nature of cancer is due
to its ability to spread to other location or
metastasize. 90% of cancer deaths are due
to metastasis.
General cancer phenotype includes many types of
cellular abnormalities
Changes that produce genomic and
karyotypic instability
• Defects in DNA
replication machinery
– lost capability to
reproduce genome
faithfully
• Increase rate of
chromosomal
aberrations – fidelity of
chromosome
reproduction greatly
diminished
Changes produce genomic and
karyotypic instability and often show
gross rearrangements
Normal cells
Cancerous cells
Changes that produce a potential
for immortality
• Loss of limitations on the number of cell divisions
• Ability to grow in culture – normal cells do not grow
well in culture
• Restoration of telomerase activity
Changes that enable tumor to disrupt
local tissue and invade distant tissues
• Ability to metastasize
• Angiogenesis – secrete substances that cause blood
vessels to grow toward tumor
• Evasion of immune surveillance
Some cancers run in families such
as retinoblastoma
Most cancers result from exposures to mutagens
• If one sibling or twin gets cancer, other usually does not
• Populations that migrate – profile of cancer becomes
more like people indigenous to new location
Most cancers result from aging
Tumours as complex tissues
Reading – any one of …
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