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Transcript
BB20023/BB20110
DNA & disease (cancer biology)
Dr. Momna Hejmadi
[email protected]
https://moodle.bath.ac.uk/moodle5/login/index.php
How to access learning materials:
Go to the URL above and click Yes to both security alert and display questions.
LOGIN with your BUCS username & password.
Click on the DNA and disease course listed to access all learning materials related
to this unit.
Any problems? Email me at [email protected] (FIRST please ensure that
you are registered to do the unit with Teresa Buckley [email protected])
How is this unit assessed?
 Part of the lecture content (DNA replication, damage and repair
mechanisms) is incorporated as part of an interactive teaching resource
that is available at the following URL
https://moodle.bath.ac.uk/moodle5/login/index.php . This tutorial is
designed to help you understand and learn some of the fundamental
mechanisms of DNA replication, damage and repair at your own pace
based ONLY on
and time. It is meant to be an overview of the whole process and you
online tutorial on
could then read up texts / reviews to get in depth information.
DNA replication,
 There will be 2 workshop sessions per degree cohort (E.g.
damage and repair
biochemistry, MCB etc) which is aimed at supporting the content of
mechanisms (contents
the tutorial. You are strongly encouraged to go over the tutorial
of the tutorial
PRIOR to attending the workshop, to enable you to fully participate
handout).
and benefit from these sessions.
A written report on a single laboratory practical on DNA repair will
comprise 20% of the unit marks.
In order to do this practical, you have to do 2 things
Practical report 1) Try the animation of experiment 1 of the practical, which has been
designed to understand the process
2) Complete the pre-practical quiz online (see this Moodle site for details)
1 hr examination on the lecture topics (lectures 9-21 ) ONLY. This will
Exam essay be held on the ‘unit assessment days’ in Jan 2007 (Example paper below)
Multiple
Choice
Questions
(MCQ)
20%
20%
60%
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 by MVH in 3WN 2.1
Dates
1 4/10
6/10
2 11/10
13/10
3 18/10
20/10
4 25/10
27/10
5 1/11
3/11
6 8/11
10/11
7 15/11
17/11
8 22/11
24/11
9 29/11
1/12
10 6/12
8/12
tbc
11 13/12
15/12
Time
11.15
12.15
11.15
12.15
11.15
12.15
11.15
12.15
11.15
12.15
11.15
12.15
11.15
12.15
11.15
12.15
11.15
12.15
11.15
12.15
tbc
11.15
12.15
TOPICS
Introduction: nature of cancer
DNA replication
Biochem
Workshop 1
DNA damage and repair
Biochem
Workshop 2
DNA replication
MCB/NS/other Workshop 1
DNA damage and repair
MCB/NS/other Workshop 2
DNA replication
Biology
Workshop1
DNA damage and repair
Biology
Workshop 2
Revision session on above
Oncogenic viruses
No lecture
Apoptosis video
MCQ test (VENUE 3WN 2.1 and 3WN 3.8)
No lecture (No Room Available!)
Oncogenes & tumour suppressor genes 1
Oncogenes & tumour suppressor genes 2
Oncogenes & tumour suppressor genes 3
Apoptosis
Angiogenesis and metastasis
Cancer therapy 1 - conventional
Cancer therapy 2 – Angiotherapy
Lab report assessment
Cancer therapy 3: Immunotherapy
Cancer therapy 4 – gene therapy
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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