Week 4 - Cancer Biology Flashcards
What is another name for a tumour
Neoplasm
Describe the growth of a benign tumour
Grows slowly and remains located to the site of origin
Describe the growth of a malignant tumour
They grow fast, invade and spread to different sites
Metastasis
A multistep process by which tumour cells move form a p to a s site
How does cancer cell morphology differ in cancer cells
They have large, variably shaped nuclei
Many dividing cells
Variation in size and shape
Loss of normal features
6 characteristics of cancer
Self-sufficiency in growth signals
Insensitivity to growth-inhibitory signals (inactivation of tumour suppressor genes)
Evasion of programmed cell death
Limited replication potential
Sustained angiogenesis (can draw blood supply)
Tissue invasion and metastasis
What are CDKs
enzymes
Cells receive which signal to enter the cell cycle
Growth factors
What is an oncogene
A gene who’s product in involved in inducing cancer
What is a proto-oncogene
A normal cellular gene that encodes a protein usually involved in regulation of cell growth/differentiation WHEN MUTATED causes ONCOGENE
Which two main factors cause formation of a tumour
Molecules that aree initiate/speed up proliferation are switched on
Molecules that slow down proliferation are switched off
Examples of receptors that when switched on, initiate/speed up proliferation
EGFR
HER2
c-Met
Examples of cytoplasmic signalling intermediates (transducers) when switched on, initiate/speed
Ras
BRAF
Abl, Src (kinases)
Examples of nuclear molecules when initiated/switched speed proliferation
Cyclin D
Myc (transcription factor)
Fos, Jun
Are mutations that cause molecules to initiate/speed up proliferation dominant or recessive
Dominant
What can proto-oncogene RAS cause
RAS -
NORMALLY
produces G protein that transduces signals from cell surface receptors
WHEN POINT MUTATION
‘Ras’ that is always on - repeated stimulation
e.g 30% of tumours
What can proto-oncogene BRAF cause
NORMALLY
produces kinase that transduces signals from cell surface receptors
WHEN POINT MUTATION
Hyperactive kinase activity that is ‘on’ all the time
e.g >50% of all melanomas
What can proto-oncogene EGFR cause
NORMALLY
produces a cell surface receptor that receives an extracellular signal
WHEN DELETION MUTATION
receptor is activated in absence of EGF
e.g non-small cell lung cancer
What can ERB B2 (HER2) proto-oncogene cause
NORMALLY
Produces HER2
WHEN GENE AMPLIFICATION
More receptors equalling more stimulation
What can proto-oncogenes BCR + ABL cause
Philadelphia translation causing bcr-abl hybrid gene - causing persistent activated kinase activity
Found in CML
2 examples of cancers caused by Rb protein mutations
Retinoblastoma
Breast cancer
2 examples of mutated p53 protein cancers
Brain tumours
Leukaemia
Rb tumour supressor- dominant or recessive?
Recessive- two copies of mutated genes required for a cell to become cancerous
(germline + somatic)
p53 tumour supressor - dominant or recessive?
Dominant negative
What is the role of BCL-2
B-cell lymphoma-2 regulates apoptosis
What is different about the BCL-2 gene of cancer cells
They have undergone a translocation mutation, causing increased expression of pro-survival BCL-2 proteins
What do telomerase enzymes do
They add telomeres on which protect chromosome ends
In cancer cells, what is different about telomerase enzymes
They express more telemorases which prevents chromosomes from shortening and results in limitless replicative potential
What is angiogenesis
When tumour grows, cells further away from blood vessels receive insufficient nutrition and become hypoxic. This stimulates tumour cells to produce VEGF (vascular endothelial growth factor) which causes vessels to grow towards the tumour
What happens to the tight junctions of epithelial tumours
They lose epithelial-cadherin which form part of the adherens junction
Metastasis is aided by which group of 23 enzymes and what is their function
Matrix metalloproteinases (MMPs)
They use these specific enzymes to break through structures such as the basement membrane, which gives cancer cells easier access to blood vessels
What does Herceptin target
ERBB2 gene (causes b cancer)
What does Bevacizumab target
VEGF gene (colorectal cancer)
Which gene does imatinib target
ABL (CML)
Venmurafenib targets?
BRAF (melanoma)