Summary Oxford University FHS revision notes: Cancer Genetics
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Course
Genetics and Evolution
Institution
Oxford University (OX)
My Oxford University notes for the FHS exam in Genetics and Evolution. Useful for Biology, Biomedical Sciences and Human Sciences. I achieved a first and multiple academic prizes. Includes descriptions of concepts and key references/experiments.
How close are we to understanding the genetics behind susceptibility to cancer and tumour progression?
Approaches to identifying genes important in cancer.
Compare and contrast the genome of cells within a tumour both to each other and to cells in the
surrounding tissues.
Cancer-critical genes
Most cancer-critical genes code for components of the pathways that regulate cell proliferation.
All mutations driving cancer fall into two categories: loss of function and gain of function
Loss of function; tumour suppressor gene; recessive as requires both to mutate; the odds of losing
both are low UNLESS you inherit one faulty copy
Gain of function; oncogene; dominant
Cancer-critical genes do not inevitably cause cancer but simply increase the risk
Mutations don’t cause cancer they contribute to cancer
ALBERTS et al. (2002): for example, whilst mice expressing more than one oncogene (e.g. those
bred by mating a pair of transgenic mice, one carrying a Myc oncogene and the other carrying a Ras
oncogene) develop cancers at a much higher rate than either parental strain, cancers originate as
scattered isolated tumours among noncancerous cells (i.e. the vast majority of cells that express the
oncogene do not give rise to cancers and must undergo further, randomly generated changes to
become cancerous
NOTE inherited oncogenes are very rare in humans/nature because the baby normally dies (this
also applies to 2 inherited copies of faulty tumour suppressor genes)
Multi-hit hypothesis: you need lots of mutations in the same cell to cause cancer
Cancer generally arises through multiple mutations in precancerous cells which, when combined,
lead to uncontrolled cell growth
Mutation can increase the rate of mutation in daughter cells -> weird cells (very mutated)
Some will die
^selection (humans are a selective environment for the cells growing within them)
Oncogenes
Mutated proto-oncogene (code for proteins that help to regulate cell growth and differentiation)
Can cause those cells designated for apoptosis to survive and proliferate instead
Dominant
Variety of functions: growth factors, growth factor receptors, signal transducers (involved in
chemical/physical signalling), nuclear oncogenes and transcription factors
Examples of oncogenes in human tumours:
o Brain: ERBB1, SIS
o Breast: ERBB2, HRAS, MYC
Tumour suppressor genes
Involved in control of abnormal cell proliferation (loss of function -> cancer)
Usually recessive (the odds of losing both are low UNLESS you inherit one faulty copy)
Variety of functions: DNA repair (e.g. BRCA1, BRCA2), mismatch repair, cell adhesion, cell cycle,
transcription
Example: p53
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