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2011/2 Provisional Module Catalogue - UNDER CONSTRUCTION & SUBJECT TO CHANGE
 Module Code: GTXM004 Module Title: DNA LESIONS, REPAIR AND MUTATION INDUCTION
Module Provider: Biosciences Short Name: GTXM004
Level: M Module Co-ordinator: PRICE SC Prof (Biosciences)
Number of credits: 15 Number of ECTS credits: 7.5
 
Module Availability
18-22 October ‘10
Assessment Pattern
Unseen 2.5 h written examination on the Friday of the module (50%)
Home-based assignment to be submitted within ten weeks (50%)
Module Overview
Prerequisites/Co-requisites
-
Module Aims
Learning Outcomes

Learning Outcomes:

 

 

The aims of this module are that the students will be able to understand:

 

·         Interaction of chemicals and radiations with genetic material

 

·         Exogenous and endogenous activities

 

·         Methods for detection of lesions

 

·         DNA repair activity, methods for the detection of activity

 

·         Structure/activity relationships

 

·         Conversion of a DNA lesion into gene and chromosome changes

 

·         Detection methods such as SSCP RSM FISH, CGH. Shuttle vectors

 

·         Mutation databases, mutation types and spectra

 

·         Relationships with cancer databases

 

·         Gene expression models

 

 

On the successful completion of the module the students should be able to assess cardiogenicity study reports in the context of overall toxicological evaluation. This will require:

 

·         A critical  understanding of the processes involved in mutation, DNA repair and carcinogenesis

 

·         An understanding of the basis of mutagenicity screening procedures and their limitations

 

·         Extrapolation of experimental data to man.

 

·         The ability to integrate knowledge of mutagenesis, into the process of risk assessment

 

·         Critical Evaluation of the data.

 

Module Content

Module content:

 

 

·         DNA modifications by ionising and non-ionising radiations

 

·         Chemically induced lesions, small adducts as illustrated by the alkylating agents.

 

·         Endogenous lesions, e.g. oxidative damage, the spontaneous lesion background.

 

·         Bulky adducts, e.g. polycyclic aromatic hydrocarbons such as benzo(a)pyrene, aflatoxins, synthetic molecules.

 

·         DNA reactive anti-cancer drugs, e.g. cis-platin, tamoxifen, non-DNA reactive anti-cancer drugs, e.g vinca alkaloids, taxol.

 

·         Lesion and adduct detection methods, 32P postlabelling, comet assay, immunological methods radiolabelled compounds, mass spectrometry.

 

·         Replication fidelity, mismatch repair, sensitivity to colorectal cancer. Base excision repair.

 

·         Nucleotide excision repair, post-replication and double strand break repair

 

·         Repair defective mutations. Human repair syndromes and their implications.

 

·         Detection methods for gene and chromosome changes such as SSCP, RSM, FISH, CGH.

 

·         The conversion of DNA lesions into gene and chromosome changes.

 

 

 


Methods of Teaching/Learning
Selected Texts/Journals

Pre-course Reading :

 

·         Friedberg E.C., Walker , G.C., Siede, W., et al (2006) DNA Repair and Mutagenesis, 2nd edn, pub: ASM Press (ISBN 1-55581-319-4) [core reading for all modules of the MTP]

 

·         A number of relevant papers will be selected from the Mutation Research journal.

 

 

Last Updated
February 2010