Cancer Flashcards
(43 cards)
what is cancer and what is it caused by ?
- complex group of more than 100 diseases affecting a wide range of tissues
- caused by mutations in genes controlling cell growth after exposure to carcinogens
how is cancer characterised and how does it differ?
- characterised by loss of growth control leading to an unregulated increase in cell number, metastasis and invasion of other tissues
- cancers differ in tissue or origin, casual factors and molecular mechanisms
How do cancer tumours start?
- when cells that have lost control of growth control proliferate to form a new growth (neoplasia), these cells don’t die via apoptosis which normally keeps number of cells constant
what are the two types of cancer?
- benign
- malignant
Describe Benign tumours?
- well differentiated and look like normal cells
- may perform the normal function of tissue (eg secrete hormones)
- cells grow slowly but this is not suppressed by apoptosis or contact inhibition
- size may be limited to just a few mm due to a lack of blood supply
- surrounded by a fibrous capsule and confined to original location
- they don’t infiltrate, invade or metastasise
- can damage nearby organs by compressing them
Describe Malignant tumours?
- less differentiated and don’t look like normal cells
- don’t perform normal tissue function
- cells grow rapidly since they have lost ability to control proliferation and differentiation
- no fibrous capsule
- cells infiltrate and invade surrounding tissues and metastasise
- can compress and/or destroy surrounding tissues
how are tumours classified?
- classified according to tissue of origin
Benign Tumours: - tissue name + “Oma”
Malignant Tumours: - carcinomas = derived from epithelial cells
- adenocarcinomas = derived from glandular epithelial cells
- sarcoma= derived from mesenchymal cells
- leukaemia = derived from haemopioetic cells
How does the body control cell number?
Most cells in the adult tissues are terminally differentiated and quiescent (non-dividing). within each tissue cell death by apoptosis or necrosis is balanced by cell division often of stem cells leaving the total number of cells constant .
Cell division is tightly regulated by growth factors which allow quiescent cells to enter the cell cycle and divide.
what are the six hallmarks of cancer?
- self sufficiency in growth signals
- in sensitivity to anti- growth signals
- evading apoptosis
- sustained angiogenesis
- tissue invasion and metastasis
- limitless replication potential
how does telomerase help to control cell lifespan?
- telomerase is an enzyme which can elongate telomeres.
- telomerase is essential for allowing cells to keep proliferating
- as cells age, telomerase becomes inactive and hence telomeres shorten and cells lose ability to divide limiting lifespan
- increase telomerase activity allows cells to proliferate indefinitely and leads to cancer
Cell proliferation is regulated by transit through the cell cycle, outline the four stages
- G1 - gap between m and s phase
- s phase- DNA synthesis/ replication
- G2 - gap between S and M phase
- M phase - mitosis, cytokinesis/ Division
cell cycle checkpoints control cell growth what controls these check points?
- cyclin dependent kinases(CDK’s) and CDK inhibitors
what do CDK’s and CDK inhibitors ensure when controlling progression through the cell cycle?
- correct sequence of phases (g1, s, g2,m)
- cellular and environmental conditions are favourable
- DNA is properly replicated and undamaged
what is being checked at the G1/S checkpoint and what is required for cells to progress
- are growth factors present?
- are nutrients available?
- Is Dna changed?
- Is cell big enough?
they need growth factors and intact DNA to progress
what is checked at the G2/M transition checkpoint?
- Has DNA replicated
- Is DNA damaged
cancer is caused by gene mutations controlling cell number what are the two different types?
- mutations that enhance cell proliferation and suppress cell death (apoptosis)
What does does mutation ind DNA repair genes cause and why is this an issue
- it causes genome instability and makes further mutations more likely
What does “multi-hit hypothesis” mean
- a single mutation is not enough , each cancer arises from an accumulation of several mutations over time (2-20 depending on cancer type)
sequencing genes mutated in cancers can give a molecular finger print for each cancer (a list of genes that are mutated) how does this help us?
- diagnosis and targeted treatments
- understanding mechanisms and new development therapies
What are the two main types of mutated genes found in cancer?
- pronto-oncogenes/oncogenes
- tumor supressor genes
what are pronto-oncogenes?
- are mutated forms of normal genes which positively regulate cell division
- they encode components of growth factor signalling pathways allowing the progression of G1 to s Phase when growth factors are not present
what are tumour supressor genes?
- they negatively regulate cell division, preventing abnormal proliferation, suppressing tumorgenesis
- they usually encode proteins at the cell cycle check points that block progression through if there is a problem
what is the Ras-MAPK pathway and what happens when cancer causes a mutation in the ras protein?
the ras-mapk pathway activates cdk 4/6 and allows progression through the g1/s checkpoint and cell division. When cells have an activated ras protein the pathway is always active and cell division is then independent of growth factors
P53 is known as the guardian of the genome what does it do?
it is a transcription factor activated by DNA damage and will cause cell cycle arrest inhibiting the transition from g1 to s phase.
50% of cancers have an inactivating mutation in P53 which consequently allows cells to divide even when dna is damaged
- P53 is a tumor supressor gene
