Summary Oxford University FHS revision notes: Background to 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.
HANAHAN AND WEINBERG (2011) 10 hallmarks of cancer (defining tumours at the molecular level)
(updated version of HANAHAN’s (2000) 6 hallmarks of cancer)
1) Resisting cell death (e.g. produce IGF survival factors)
a. Apoptosis: programmed cell death - if a cell detects that is has damaged DNA it can activate
apoptosis to remove itself from the population
b. Extremely efficient process: cellular membranes are disrupted, chromosomes are degraded,
DNA breaks up into fragments, the shrinking cell is swallowed up by a neighbouring cell or a
patrolling immune cell
2) Sustaining proliferative signalling (e.g. activate H-Ras oncogene)
3) Evading growth suppressors (e.g. lose retinoblastoma suppressor)
4) Activating invasion and metastasis (e.g. inactivate E-cadherin)
5) Enabling replicative immortality (e.g. turn on telomerase)
6) Inducing angiogenesis (development of new blood vessels) (e.g. produce VEGF inducer)
7) Genome instability and mutation
8) Tumour-promoting inflammation
9) Deregulating cellular energetics
10) Avoiding immune destruction
NOTE importance of specifying “disease state of cancer”: we can use above framework to detect cells with
hallmarks of cancer that are not in a disease state
Cancers can be benign (stop dividing when they get to a certain size)
If a tumour continues to grow and invades healthy surrounding tissue it is known as malignant
(GOLDSBY et al. 2006). The disease state “cancer” refers specifically to malignant tumours which
can be extremely dangerous to an organism’s health
Statistics
Most common cancers
Breast cancer (15% of cancer cases)
Lung cancer (13%)
Colorectal cancer (13%)
Prostate cancer (13%)
o NOTE this rise is probably explained by improved detection
Complexity
The molecular basis of cancer is remarkably complex and varied
Even a single conventional category of tumour represents a heterogeneous collection of disorders
with some common features, but each characterised by its own array of genetic lesions (ALBERTS et
al. 2002)
Different cancers also vary widely in the extent to which susceptibility can be inherited (significance
of genotype as a cancer risk factor)
The molecular/genetic basis of cancer is both complex and highly diverse, requiring a consideration of not
only different cancer types but also the potentially contrasting molecular causes of the same cancer in
different individuals.
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