1. BB20023/BB20110 DNA & disease (cancer biology)
Dr. Momna Hejmadi
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2. How is this unit assessed?
Multiple Choice Questions (20%)
Nature of cancer,
DNA replication,
DNA damage and
DNA repair
Wed 31st OCT
3WN 2.1 (all except NS students)
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

3. 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

4. All lectures & practicals by MVH

5. Cancers are clonal descendents of one cell
Figure 18.18

6. Cancer arises by successive mutations in a clone of proliferating cells
Figure 18.21

7. 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

8. Introduction: The 6 Superpowers

9. Introduction: The 6 Superpowers
Cancer Cell
Normal Cell 1 GO
STOP
SLOW
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.

10. Introduction: The 6 Superpowers
Cancer Cell
Normal Cell 1 GO 2
STOP
SLOW
Even if the neighbouring cells produce a ‘Stop’ signal, cancer cells override these signals and continue dividing.

11. Introduction: The 6 Superpowers
Cancer Cell
Normal Cell 1 GO 3
Apoptosis 2
STOP
SLOW
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.

12. Introduction: The 6 Superpowers
Cancer Cell
Normal Cell 1 GO 2
STOP
Apoptosis 3
SLOW 4
Food Supply
Cancer cells make sure they can keep dividing by stimulating the growth of new blood vessels to keep their nutrient supply lines open.

13. Introduction: The 6 Superpowers
Cancer Cell
Normal Cell 1 GO 2
STOP
Apoptosis 3
SLOW 5
Immortality
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. 4
Food Supply

14. Introduction: The 6 Superpowers
Cancer Cell
Normal Cell 1 GO 2
STOP
Apoptosis 3
SLOW 6
Metastasis
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. 4
Food Supply 5
Immortality

16. General cancer phenotype includes many types of cellular abnormalities

17. 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
Feature Figure b(1)

18. Changes produce genomic and karyotypic instability and often show gross rearrangements
Normal cells
Cancerous cells
Feature Figure b (2)

19. 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
Feature Figure c

20. Changes that enable tumor to disrupt local tissue and invade distant tissues
Feature Figure d
Ability to metastasize
Angiogenesis – secrete substances that cause blood vessels to grow toward tumor
Evasion of immune surveillance

21. Some cancers run in families such as retinoblastoma
Figure 18.20

22. 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

23. Most cancers result from aging
Figure 18.19

24. Tumours as complex tissues
Figure 18.19

25. Reading – any one of …