BGM3065 : Biochemistry of Cancer and Chronic Diseases
- Offered for Year: 2017/18
- Module Leader(s): Professor Craig Robson
- Lecturer: Professor Julie Irving, Dr Julian Rutherford, Professor Bert van den Berg, Professor Neil Perkins, Dr Niall Kenneth, Dr Ian Cowell, Professor Derek Mann, Professor Steven Clifford
- Owning School: Biomedical Sciences
- Teaching Location: Newcastle City Campus
|Semester 1 Credit Value:||20|
Through lectures and seminars this module aims to;
1. to provide an understanding of the biochemistry and clinical aspects of a number of chronic human diseases
2. to explain how knowledge of the biochemistry of a disorder can be used to develop rational drug design for its treatment
3. to provide an opportunity for students to further develop their written skills and critical analytical skills.
4. To inform students about the genetic and molecular basis of cancer
5. To examine the mechanisms of action of oncogenes and tumour suppressor genes
6. To promote understanding of the basic mechanisms of apoptosis
7. To introduce current technologies used in cancer detection, diagnostics and molecular pathology.
8. To discuss how experimental models and imaging techniques are being applied to advance our
understanding of cancer.
9. To provide an understand of the basis of and problems associated with cancer treatments.
Outline Of Syllabus
The biochemistry and clinical aspects of a number of chronic human diseases, to explain how knowledge of the biochemistry of a disorder can be used to develop rational drug design for treatment. Topics include:
The biochemistry of trace metal sensing and its relevance to disease
It is estimated that more than 30% of all proteins require metals for function and the correct metals must locate to the correct proteins. Metals such as iron and copper drive Fenton chemistry leading to the production of reactive oxygen species. Human disease can be caused by inadequate supply of an essential metal, either due to genetic (e.g. copper in Menkes and Wilson diseases; zinc in acrodermatitis enteropathica) or environmental factors. Disease can be caused by essential metal excess (e.g. iron-overload, Hereditary haemochromatosis) or exposure to non-essential toxic metals (eg itai itai disease and cadmium). It is increasingly apparent that mis-localisation of metals to the 'wrong' proteins or the 'wrong' cellular compartments, and/or abnormal metal-coordination, is feature common in neurological disorders (Alzheimers, CJD, Parkinsons, Freidreichs Attaxia, Motor neurone disease). Competition for metals such as iron and manganese is also central to pathogenicity. Lectures will briefly highlight some of the core mechanisms of metal- homeostasis (metallochaperones, metal-sensing transcriptional and translational regulators, metal-specific transporters and storage proteins) and provide some examples of the ways in which these processes fail in disease
NF-kB signalling in health and disease
The five members of the mammalian NF-kB family of transcription factors regulate the expression of a large number of genes encoding proteins involved in inflammation, regulation of cell death, cell adhesion and proliferation. The NF-kB signalling pathway is both our friend and our foe. It is essential for a normal healthy immune system and other important functions that allow us to respond to infection and physical stresses such as DNA damage. However, aberrant activation of this pathway can contribute to many types of human disease. In particular, NF-kB has an important role in many inflammatory diseases and cancer. Moreover, NF-kB is activated by many cancer therapies and can have an inhibitory effect on these treatments. The pathways regulating NF-kB are therefore thought to be good targets for the development of new anti-inflammatory and anti-cancer drugs
Cancer is one of the major causes of mortality. This module provides a background to the biochemistry and molecular biology of cancer. The course introduces cancer as a genetic disease and how the onset of cancer is a multi-step process. It discusses the role of oncogenes and tumour suppressor genes particularly with respect to retinoblastoma and p53. An overview is given of familial cancers and examples of inherited predisposition to cancer. The roles of failures in the DNA repair mechanisms in causing cancer are also described. The factors that lead to metastasis (the development of secondary tumours at sites remote from the primary) are also discussed. Mention is made of experimental genetic models of tumour development and the advantages of transgenic animal models over cell lines highlighted.An important part of this module is a discussion of the methods of anticancer treatment. Many anticancer drugs are themselves carcinogens. Some tumour cells can become drug resistant. The ways in which drugs can be targeted to the tumours are described. Examples and mechanisms of treatments based on growth factors and hormone mechanisms (eg breast cancer and prostate cancer) are mentioned,along with new approaches for tumour specificity:targeting surface receptors;targeting cytotoxic drugs to tumour cells;specific inhibition of key tumour enzymes (in leukaemia);gene array techniques for identifying new targets. Many novel and powerful techniques are described that identify specific cancers.
|Scheduled Learning And Teaching Activities||Lecture||27||1:00||27:00||N/A|
|Scheduled Learning And Teaching Activities||Small group teaching||4||1:00||4:00||Seminars|
|Scheduled Learning And Teaching Activities||Workshops||1||3:00||3:00||Oral Presenations|
|Guided Independent Study||Independent study||1||166:00||166:00||N/A|
Teaching Rationale And Relationship
Lectures will provide the students with essential information to achieve learning outcomes. Seminars will provide additional information and develop the students critical skills. The essay feedback seminar will help students to further their written skills and their ability to interpret scientific literature. The workshop will be student (assessed) presentations. Independent study will enable students to widen their knowledge through reading recommended references and journal articles.
The format of resits will be determined by the Board of Examiners
|Written Examination||120||2||A||80||2 essay questions from a choice of 4|
|Module Code||Module Title||Semester||Comment|
|BGM3024||The Molecular Basis of Cancer||2||N/A|
|Prof skill assessmnt||1||M||10||Oral Presentations (10 minutes including questions)|
Assessment Rationale And Relationship
The examination primarily assesses students' knowledge and understanding. The essay, written after a tutorial discussion, will develop the students' ability to assimilate and analyse complex scientific information and to develop their written skills. Oral presentations develop students’ ability to distil information into a short form and to enhance their skills in platform presentation.