BMS3012 : Cancer Biology and Therapy
- Offered for Year: 2019/20
- Module Leader(s): Professor Steven Clifford
- Lecturer: Dr Luke Gaughan, Dr Simon Bomken, Dr Daniel Williamson, Dr Ian Cowell, Professor James Allan, Professor Julie Irving, Dr Christopher Bacon, Professor Craig Robson
- Owning School: Biomedical, Nutritional and Sports Scien
- Teaching Location: Newcastle City Campus
|Semester 1 Credit Value:||20|
i) To inform students about the genetic and molecular basis of cancer.
ii) To examine the mechanisms of action of oncogenes and tumour suppressor genes.
iii) To understand the role of cell cycle disruption in cancer development.
iv) To understand the processes of metastasis and angiogenesis.
v) To understand the roles of cell signalling pathways in cancer.
vi) To understand the roles that chromosomal instability, DNA damage and repair play in carcinogenesis.
vii) To understand the basic mechanisms of apoptosis and their relevance to cancer.
viii) To provide an introduction to current technologies used in cancer detection, diagnostics and molecular pathology.
ix) To discuss how experimental models and imaging techniques are being applied to advance our understanding of cancer.
x) To understand the basis of and problems associated with cancer treatments.
xi) To provide students with an understanding of cancer stem cells.
Cancer is one of the major causes of mortality. This module provides a background to the molecular basis of cancer and its therapy. The various causes, cellular and genetic processes central to the development of cancer will be discussed, alongside how this understanding is being exploited for disease detection, diagnosis and therapy.
Outline Of Syllabus
- An introduction to the molecular basis of cancer
- Tumour suppressor genes (TSGs) I: Identification
- Tumour suppressor genes II: Mechanisms of action
- Metastases and Angiogenesis
- Cell signalling in cancer
- Viruses and Cancer
- Carcinogenesis and apoptosis
- DNA repair and cancer predisposition syndroms
- Genetic instability and cancer
- Cancer treatments and drug resistance
- Targeted therapies & drug development strategies
- Treatment-related late effects
- The Pathology of Cancer
- Molecular studies linking genomic arrays, diagnostics and pathology in cancer detection
- Systems biology, bioinformatic and next-generation approaches to understanding cancer biology
- Cancer stem cells
- Application of experimental models and imaging in cancer
- Leukaemia and its therapy
- Therapy for Prostate Cancer
|Scheduled Learning And Teaching Activities||Lecture||24||1:00||24:00||N/A|
|Scheduled Learning And Teaching Activities||Small group teaching||1||1:00||1:00||Tutorial|
|Guided Independent Study||Independent study||1||175:00||175:00||N/A|
Teaching Rationale And Relationship
Lectures will provide students with key information. Tutorials will encourage increased understanding of the material through discussion. Private study will allow students to extend their knowledge through reading of journal articles and other recommended references.
The format of resits will be determined by the Board of Examiners
|Written Examination||120||2||A||80||Unseen examination ( 2 essays from a choice of 4).|
|Module Code||Module Title||Semester||Comment|
|BGM3024||The Molecular Basis of Cancer||2||N/A|
|BGM3065||Biochemistry of Cancer and Chronic Diseases||2||N/A|
Assessment Rationale And Relationship
The examination provides evidence of knowledge and understanding of the topics.
The open-book essay supports the students’ development of literature-based research, written communication and presentation skills, supplements the main areas of teaching delivered, and helps prepare them for the examination.
FMS Schools offering Semester One modules available as ‘Study Abroad’ will, where required, provide an alternative assessment time for examinations that take place after the Christmas vacation. Coursework with submissions dates after the Christmas vacation will either be submitted at an earlier date or at the same time remotely.
The form of assessment will not vary from the original.