bb20023/bb20110 dna & disease (cancer biology) dr. momna hejmadi [email protected] how to access...
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BB20023/BB20110 DNA & disease (cancer
biology)
Dr. Momna [email protected]
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])
https://moodle.bath.ac.uk/moodle5/login/index.php
EXAM essay (60%)EXAM essay (60%) Topics areOncogenic virusesApoptosisOncogenes & Tumour suppressor genesAngiogenesis & metastasisCancer therapy (4 lectures)
How is this unit assessed?Multiple Choice Multiple Choice
Questions (20%)Questions (20%) Nature of cancer, DNA replication, DNA damage and DNA repair
3WN 2.1 (all except NS students)3WN 2.1 (all except NS students) 8W 2.30 (Natural Sci students) 8W 2.30 (Natural Sci students)
Wed 31st OCT 11.15 - 12.05Wed 31st OCT 11.15 - 12.05
Lab Report (20%)Lab Report (20%)
Peer assessed
DNA repair practical
• 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
General Reading List
All lectures & practicals by MVHDates Room Time TOPICS 1/10 8W1.1 9.15 Introduction: nature of cancer 3/10 3WN2.1 11.15 DNA replication Biology Workshop 1 8/10/ 8W1.1 9.15 DNA damage and repair Biology Workshop 2 10/10 3WN2.1 11.15 DNA replication MCB/ NS/ other Workshop 1 15/10 8W1.1 9.15 DNA damage and repair MCB/ NS/ other Workshop 2 17/10 3WN2.1 11.15 DNA replication Biochem Workshop1 22/10 8W1.1 9.15 DNA damage and repair Biochem Workshop 2 24/10 3WN2.1 11.15 Revision session on above 29/10 8W1.1 9.15 Oncogenic viruses
31/10 3WN2.1 11.15 MCQ test VENUE
3WN2.1 (all except NS students) 8W 2.30 (Natural Sci students)
5/11 8W1.1 9.15 Apoptosis video 7/ 11 3WN2.1 11.15 Apoptosis 12/11 8W1.1 9.15 Oncogenes & tumour suppressor genes 1 14/11 3WN2.1 11.15 Oncogenes & tumour suppressor genes 2 19/11 8W1.1 9.15 Oncogenes & tumour suppressor genes 3 21/11 3WN2.1 11.15 Angiogenesis and metastasis 26/11 8W1.1 9.15 Cancer therapy 1 - conventional 28/11 3WN2.1 11.15 Cancer therapy 2 – Angiotherapy 3/12 8W1.1 9.15 Cancer therapy 3: Immunotherapy 5/12 3WN2.1 11.15 Cancer therapy 4 – gene therapy 10/12 8W1.1 9.15 Spare / revision session 13/12 8W1.1 11.15 Lab report : Peer assessment session
Cancers are clonal descendents of one Cancers are clonal descendents of one cellcell
Cancer arises by successive mutations Cancer arises by successive mutations in a clone of proliferating cellsin a clone of proliferating cells
Cancer phenotype results from Cancer phenotype results from accumulation of mutations in the clonal accumulation of mutations in the clonal
progeny of cellsprogeny 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
GOGO
STOPSTOP
Normal CellCancer Cell
SLOWSLOW
1
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
GOGO
STOPSTOP
Normal CellCancer Cell
SLOWSLOW
2
1
2. Even if the neighbouring cells produce a ‘Stop’ signal, cancer cells override these signals and continue dividing.
Introduction: The 6 Superpowers
GOGO
STOPSTOP
Normal CellCancer Cell
SLOWSLOW
2
1
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.
3
Apoptosis
Introduction: The 6 Superpowers
GOGO
STOPSTOP
Normal CellCancer Cell
SLOWSLOW
3
2
1
Apoptosis
4 Food Supply4. 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
GOGO
STOPSTOP
Normal CellCancer Cell
SLOWSLOW
4
3
2
1
Food Supply
Apoptosis
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
GOGO
STOPSTOP
Normal CellCancer Cell
SLOWSLOW
4
5
3
2
1
Food Supply
Immortality
Apoptosis
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.
Introduction: The 6 Superpowers
General cancer phenotype includes many types General cancer phenotype includes many types of cellular abnormalitiesof cellular abnormalities
Changes that produce genomic Changes that produce genomic and karyotypic instabilityand 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 Changes produce genomic and karyotypic instability and often karyotypic instability and often
show gross rearrangementsshow gross rearrangements
Normal cells Cancerous cells
Changes that produce a potential Changes that produce a potential for immortalityfor 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 Changes that enable tumor to disrupt local tissue and invade distant tissueslocal 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 Some cancers run in families such as retinoblastomaas retinoblastoma
Most cancers result from exposures to mutagensMost 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 agingMost cancers result from aging
Tumours as complex tissuesTumours as complex tissues
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Reading – any one of …Reading – any one of …