mechanisms of cell deviance Flashcards

1
Q

how can mutations be prevented

A

cell cycle controle
proof reading
degenerate genetic code

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2
Q

how does cancer occur?

A

if a mutation gives a cell an advantage it will proliferate.
paracrine signalling cause neighbouring cells to proliferate.
mutates again advantage continues to outcompete neighbouring cells
3rd increased advantage leads to too much proliferation and cells become invasive.

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3
Q

what is a gain of function mutation that can lead to cancer

A

Oncogene

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4
Q

what is a proto-oncogene

A

pre oncogone
aka the gene involved in cell growth

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5
Q

what are the functions of RAS proteins?

A

signal cell proliferation

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6
Q

what is neoplasia

A

new growth

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7
Q

what is neoplasm

A

uncontrollable growth

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8
Q

what is oncology

A

swelling

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9
Q

what is anaplasia

A

loss of differentiation

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10
Q

how can a mutation in RAS proteins lead to cancer

A

mutation stops GTP hydrolysing, meaning the RAS will always be active, leading to excess proliferation

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11
Q

what is a tumour supressor gene, and how can a mutation in it lead to cancer?

A

a loss of function
it is recessive so there must be a mutation in both alleles in order for it to no longer inhibit proliferation

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12
Q

what proteins are found in most tumour supressor genes

A

P53

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13
Q

what causes a mutation in both alleles

A

mitotic recombination
gene conversion
frameshift mutations

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14
Q

what is senescence

A

when cells loose their ability to proliferate

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15
Q

give an describe antagonistic pleitropy

A

testosterone producing cells will stop proliferating after pubity

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16
Q

what can cause senescence

A

DNA damage
Chromatin remodelling
chronic age
telomere shortening

17
Q

what is oxidative stress?

A

the imbalance between pro-oxidants species and antioxidants

18
Q

what does too many Reactive Oxidative Species cause

A

in the mitochondria, too many ROS lead to DNA damage

19
Q

what are the enzymatic antioxidants

A

catalase
glutathione
thioredoxin
superoxide dismutase

20
Q

what are the non enzymatic antioxidants

A

reduced glutathione
vitamine C + E

21
Q

what are some pathological responses

A

Cytosine oxidation
lipid peroxidation
mitochondrial disfunction
genetic instability

22
Q

what is AGE

A

advanced glycation end product
sugars attach to proteins, DNA and lipids

23
Q

give an example of AGE

A

pro oxidants
pro inflammitories

24
Q

what causes age

A

nutrition
radiation

25
Q

what are chaperones, how do they work?

A

repair / assist protein folding
sends signal to ER to repair the protein

26
Q

what causes protein misfolding

A

loss/ gain of function mutations

27
Q

what is a prion?

A

protein that triggers a normal protein to fold abnormally

28
Q

give an example of a disease where a prion is found?

A

BSE Mad cow disease
the PrP2 mutated to PrPse prion
Alpha helix mutated to a Beta sheet

29
Q

give an example of a disease where the protein has a loss of function mutation

A

Cystic Fibrosis

30
Q

give an example of a disease where a protein had a gain of function mutation

A

Alzheimer (Beta amyloid)
Parkinsons (alpha synclein)
Hunningtons (HTT mutated)