Presentation on theme: "BB20023/BB20110 DNA & disease (cancer biology)"— Presentation transcript:
1 BB20023/BB20110 DNA & disease (cancer biology) Dr. Momna HejmadiHow 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? me at (FIRST please ensure that you are registered to do the unit with Teresa Buckley
2 How is this unit assessed? Multiple Choice Questions (20%)Nature of cancer,DNA replication,DNA damage andDNA repairWed 31st OCT3WN 2.1 (all except NS students)8W 2.30 (Natural Sci students)EXAM essay (60%)Topics areOncogenic virusesApoptosisOncogenes & Tumour suppressor genesAngiogenesis & metastasisCancer therapy (4 lectures)Lab Report (20%)Peer assessedDNA repair practical
3 General Reading ListThe Biology of Cancer by Robert Weinberg (Garland Publishers )Other useful books to consultCancer Biology (2000; 2nd ed) by RJB King (Prentice Hall Publishers)DNA repair and mutagenesis (2002) by Friedberg EC, Walker g and Siede WPlus reviews / articles
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 bodyForms tumor
9 Introduction: The 6 Superpowers Cancer CellNormal Cell1GOSTOPSLOWMost 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 CellNormal Cell1GO2STOPSLOWEven if the neighbouring cells produce a ‘Stop’ signal, cancer cells override these signals and continue dividing.
11 Introduction: The 6 Superpowers Cancer CellNormal Cell1GO3Apoptosis2STOPSLOWNormal 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 CellNormal Cell1GO2STOPApoptosis3SLOW4Food SupplyCancer 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 CellNormal Cell1GO2STOPApoptosis3SLOW5ImmortalityOne 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.4Food Supply
14 Introduction: The 6 Superpowers Cancer CellNormal Cell1GO2STOPApoptosis3SLOW6MetastasisMost 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.4Food Supply5Immortality
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 faithfullyIncrease rate of chromosomal aberrations – fidelity of chromosome reproduction greatly diminishedFeature Figure b(1)
18 Changes produce genomic and karyotypic instability and often show gross rearrangements Normal cellsCancerous cellsFeature Figure b (2)
19 Changes that produce a potential for immortality Loss of limitations on the number of cell divisionsAbility to grow in culture – normal cells do not grow well in cultureRestoration of telomerase activityFeature Figure c
20 Changes that enable tumor to disrupt local tissue and invade distant tissues Feature Figure dAbility to metastasizeAngiogenesis – secrete substances that cause blood vessels to grow toward tumorEvasion 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 notPopulations that migrate – profile of cancer becomes more like people indigenous to new location