cancer Flashcards

1
Q

what do cancer cells bypass to take over other tissues?

A

normal proliferation controls

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2
Q

what are malignant tumours?

A

theyre tumours which metasase and travel to other parts of the body, they’re harder to get rid of

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3
Q

what type of scan is usually used to detect the spread of cancer and how does it work?

A

its a PET scan reveals the tumour tissue
its detected by the unusually high uptake of radioactive labelled fluro-deoxyglucose (FDG)
this high FGD happens in cells with unusually high glucose uptake and metabolism (like cells which have uncontrolled growth, which are cancerous cells)

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4
Q

what 2 scans are overlayed to see exactly where the cancer is in the body?

A

a PET scan and a CT scan as if it was just a PET scan, you would only see the tumours, not where they are in the bosy

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5
Q

why are the numbers of cancer diagnosis going up?

A

because were getting better at detecting them

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6
Q

what is the difference between benign and malignant tumours?

A

benign- these stay in the basal lamina (this marks the boundary of the normal structure)
malignant- these tumours destroy the integrity of the tissue

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7
Q

what type of graph is a typical human tumour shown on?

A

a logarithmic graph

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8
Q

what mutation is responsible for chronic myelogenous leukaemia?

A

the translocation of chromosome 9 and 22
when transloctaion occurs between than, the result is an abnormal pair of chromosomes (9q+ and 22q-)
22q- is called the Philidelphia chromosome because that’s where it was originally discovered
it generates a fusion gene encoding fusion protein bcr-abl which is an active tyrosine kinase and it drives cell growth

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9
Q

what is the name of the therapy which targets the bcr-abl protein?

A

ematopin

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10
Q

why does the incidence of cancer rise with age?

A

because the evidence suggests that the development of a solid tumour needs 5-8 randomly occurring mutations over time, the older you get the more common mutations are so the more common cancer is

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11
Q

what are the stages of progression in the development of cancer in the epithelium?

A
  1. normal- the dividing cells are confined to the basal layer
  2. low-grade - the dividing cells are found throughout the lower 3rd of the epithelium
  3. high-grade- the cells are proliferating in all layers
  4. true malignancy- the cells move through/destroy the basal layer
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12
Q

what is clonal evolution?

A

its when the tumour develops in repeated rounds of mutation and proliferation, to give rise to fully malignant cells (eventually)

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13
Q

why does proliferaion speed up the occurnce of the next step of the tumours progression?

A

because it’s increasing the rate of the cell population and increasing the risk of undergoing additional mutations

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14
Q

what are the steps of invasion?

A

it happens by the cells invading though the membrane, an essential step in metastasis
there are more than 3 steps in reality and a combination of genetic and epigenetic changes involved

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15
Q

what happens over time in a dangerous cell proliferation?

A

a variety of aubclones arise, this is called heterogeneity and it complicates cancer therapies

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16
Q

what are the usual stains used on cancer cells?

A

a general DNA stain
a combination of fluorescently labelled DNA molecules which show lots of translocations

17
Q

what do cancer cells do when theyre grown in a dish?

A

they do this strange thing called ‘contact inhibition’
most cells just cover the plate then stop growing but cancer cells usually disregard these restraints and just continue to grow on top of one another

18
Q

what does it mean by ‘cancer cells have an altered sugar metabolism’?

A

usually cells oxidise almost all their glucose to make ATP through oxidative phosphorylation in the mitochondria
but tumour cells still produce loads of lactate even of there’s sufficient oxygen to make ATP

19
Q

what is the warburg effect?

A

its the same as the cancer cells haveing an altered sugar metabolism
they usually make too much lactate as they have an increased rate if glycolysis from a very large rate of glucose import, this is usually only seen in rapidly proliferating cells in embryos

20
Q

what can cancer cellshave an abnormal ability to survive?

A

stress and DNA damage
theyre very resiliant cells

21
Q

what is the overractivity mutation?

A

its when tumour cells gain function
its usually a single cell event which creates an oncogen
this activating mutation enables the oncogen to promote cell transfrmation

22
Q

what is the underractivity mutation?

A

this is when a mutation event occurs to inactivate the turnout suppressor gene, this has no effect of the mutation in one gene copy, then there’s a second gene copy which causes 2 inactivating mutations which functionally eliminate the tumour suppressor gene, this promotes cell transformation
this is a cell on its way to become a cancer cells

23
Q

what are the types of chnages in the genome that can convert a proto-oncogene into an oncogene?

A

deletion or point mutaion in coding sequence
regulatory mutation
gene amplification
chromosomal rearrangement

24
Q

what is an oncogene?

A

is a cancer producing gene