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a level biology paper 2 > Mutations, Stem Cells and Cancer > Flashcards

Mutations, Stem Cells and Cancer Flashcards

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AP® Biology flashcards
1
Q

Examples of tumour suppressor genes

Off spec, paper 3

A

TP53
BRCA1
BRCA2

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2
Q

What are tumour suppressor genes

A

Genes that slow down cell division by coding for proteins that decrease the rate of cell division

Also code for proteins that repair mistakes in DNA
Also code for proteins that instruct cells to die (apoptosis) (off spec, paper 3)

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3
Q

List 3 mutagenic agents

A

High energy ionising radiation

DNA reactive chemicals

Biological agents

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4
Q

Explain the mutagenic agent of biological agents

A

Viruses and bacteria

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5
Q

Explain the mutagenic agent of high energy ionising radiation

A

Xrays/gamma/alpha/beta
Damage DNA base sequence
Chemicals interfere with DNA replication or structure

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6
Q

Explain the mutagenic agent of DNA reactive chemicals

A

Benzene, bromine, hydrogen peroxide, nitrous acid

Remove amine (NH2) group on cytosine in DNA, converting it to uracil

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7
Q

What are stem cells

A

Undifferentiated cells
Able to express all genes they have
Divide by mitosis OR differentiate into specialised cells

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8
Q

What do stem cells do

A

Differentiate into specialised cells

Mitotic cell division into more stem cells

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9
Q

Types of stem cells

A

Totipotent
Pluripotent
Multipotent
Unipotent

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10
Q

Totipotent

A

Stem cells that can differentiate into all specialised cells available from its genes

Zygote and early embryo (up to 8 cell stage)

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11
Q

Pluripotent

A

Stem cells that can differentiate into most types of cell

Embryonic and fetal stem cells

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12
Q

Multipotent

A

Found in all tissues and can differentiate into a number of cells

Somatic cells/adult stem cells

E.g bone marrow contains multipotent stem cells that can differentiate into various blood cells

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13
Q

Unipotent

A

Can only differentiate into one type of cell

Used in formation of single cell types

E.g cardiomyocytes

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14
Q

What happens to cells as they differentiate

A

Lose their totipotency and become limited in the sections of their DNA that they translate

Because during specialisation only genes required for essential processes in cell and those needed to produce proteins for specialised functions are expressed

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15
Q

iPS

A

Induced pluripotent cells

Lab grown pluripotent cells

Not identical to pluripotent stem cells but can self renew
Providing a limitless supply in medical research

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16
Q

Caution with using stem cells

A

May divide out of control

Leading to formation of a tumour

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17
Q

5 uses of stem cells

A

Producing tissue for skin grafts
Research into producing organs for transplants
Research into how stem cells become specialised
Research into cancer
Research into serious diseases and the use of stem cells to cure them (parkinsons)

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18
Q

Ethical concerns of stem cells (4)

A

Human status from contraception
Potential life/human being so murder
Embryo can’t give consent
Animals must be used in experiments prior to human trials

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19
Q

How can you turn somatic stem cells into desired cell

A

Convert into iPS

Stimulate to differentiate via hormones into desired cell

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20
Q

9 diseases that can be treated with stem cells

A

Heart damage/attack: Heart muscle cells
Muscular dystrophy: Skeletal muscle cells
Type 1 diabetes: Beta cells of pancreas
Parkinsons, MS, stroke, paralysis: Nerve cells
Leukemia, blood diseases: Blood cells
Burns, wounds: Skin cells
Osteoporosis: Bone cells
Osteoarthritis: Cartilage cells
Macular degeneration: Retina cells of eye

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21
Q

Promoter vs transcription factor

A

Promoter is one or more base sequences complementary to transcription factor, found upstream of gene and controls gene expression

Transcription factor is a protein that binds to the promoter when activated and stimulates RNA polymerase to begin transcription

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22
Q

Example of a transcription factor

A

Oestrogen receptor (ER alpha)

23
Q

Explain the activation of transcription

A

1) Oestrogen diffuses through the cell surface membrane (lipid soluble)
2) Diffuses through nuclear envelope
3) Binds to complementary ER alpha receptor
4) Causing a conformational change in shape and releases transcription factor
5) T.f. binds to DNA at complementary promoter region
6) Allowing RNA polymerase to transcribe the gene

24
Q

How is translation controlled

A

RNAi

RNA interference inhibits gene expression via inhibiting translation

Transcribed from cell DNA when needed to stop/slow synthesis of protein

25
Q

Disadvantage of overproduction of a protein

A

Protein synthesis uses lots of ATP
Overproduction is a waste of valuable ATP
That could be used for other processes (e.g active transport)

26
Q

What are the two types of RNAi and what do they do

A

miRNA (micro RNA) and siRNA (small interfering RNA)

Single strands of RNA
Bind to a protein in cytoplasm to form RISC which inhibits gene expression (complementary base sequence to part of specific mRNA molecule)

27
Q

What is RISC

A

RNA Induced Silencing Complex

Formed when RNAi binds to a protein (enzyme) in cytoplasm

Inhibiting DNA gene expression by binding to complementary mRNA

28
Q

How does RISC inhibit gene expression

A

Binds to complementary mRNA…

-Hydrolyses mRNA by RNA hydrolase, cutting it into fragments
OR
-Inhibits initiation of ribosomal translation (ribosome prevented from attaching to mRNA, mRNA hydrolysed)

Translation does not take place
Polypeptide not produced
EXPRESSION OF GENE IS SILENCED

29
Q

How can protein still be produced if RNAi used

A

Not all mRNA hydrolysed so some translation still occurs

RNAi hasn’t bound to all mRNA so some translation still occurs

30
Q

Epigenetics

A

Inheritable changes in gene expression

Without changes to their DNA base sequence

31
Q

How is translation inhibited in epigenetics

A

Increased methylation of DNA

Decreased acetylation of histones

32
Q

What is methylation

A

The addition of a methyl group to carbon 5 of a cytosine base
Via methyltransferase
Changing the structure of a promoter
So it’s no longer complementary to the transcription factor
Cannot bind and transcription inhibited
No RNA polymerase activation

33
Q

Where does methylation occur

A

CpG Islands
Common at the 5’ end of many genes
Carbon 5 of cytosine base

34
Q

What is acetylation

A

Addition of an acetyl group (COCH3) to leucine
Causing histone winding to losen
Can expose the promoter
Transcription factor can bind so allows RNA polymerase to transcribe target gene
Acetyl group transferred from Acetylcoenzyme-A

35
Q

Where does acetylation occur

A

Amino acid leucine
On the tails of histone molecules (side branches)
From Acetylecoenzyme A

36
Q

2 types of cancer

A

Benign

Malignant

37
Q

Compare benign and malignant tumours

A

Benign cannot metastasise whereas malignant do
Benign surrounded by dense tissue capsule and remains a compact structure whereas malignant are not so grow finger like projections into surrounding tissues
Benign less likely to reoccur after treatment

38
Q

How are iPS produced

A

Produced from human somatic cells using certain protein transcription factors

39
Q

What two genes are in control of the rate of cell division

A

Proto-onco genes

Tumour suppressor genes

40
Q

What are proto-onco genes

A

Stimulates cell division

by coding for protein that increases the rate of cell division

41
Q

How can cancers cause damage

A

May damage organ concerned
May cause blockages/obstructions (e.g. blood flow)
May damage other organs by exerting pressure on them

42
Q

Mutation in a proto-onco gene

A

Alters to become an onco gene
Causing overstimulation of cell division
Cell division permanently switched on
Mass of cells known as a tumour develops

43
Q

Mutation in tumour suppressor gene

A

Gene becomes inactive
Stops inhibiting cell division
Rate of cell division increases
Mass of cells known as tumour form

44
Q

Overmethylated tumour suppressor gene

A

Gene becomes inactive
Stops inhibiting cell division
Rate of cell division increases
Leading to mass of cells being produced (tumour)

45
Q

Undermethylated onco gene

A

Gene becomes more activated
Cell division switched on
Rate of cell division increase

46
Q

Function of stop codons

A

When read by ribosome during translation, translation stops

So final polypeptide chain detaches from ribosome

47
Q

How do alterations in tumour suppressor genes lead to a tumour

A

Increased methylation of tumour suppressor gene
Mutation in tumour suppressor gene
Genes not transcribes/expressed
Resulting in uncontrollable cell division via mitosis

48
Q

In microscopy, how do you find the mean … number per mm2

A

Measure the diameter of the field of view and calculate the area
Using a micrometre slide and eyepiece graticule
Count number of … in field of view in a large number of different fields of view
Selected at random
Calculate mean

49
Q

Why doesn’t oestrogen affect other cells

A

Not all cells have the ERalpha receptor/oestrogen receptor

50
Q

Link between sunbathing and cancer

A

Sun has UV radiation

Causes mutations in the genes responsible for controlling cell division

51
Q

Why are people with a family history of cancer at an increased risk

A

May inherit onco genes

Giving a predisposition to cancer

52
Q

Consequence of methylation to promoter

A

Causes change to the tertiary structure of the promoter
No longer complementary to the RNA polymerase and can’t bind to promoter
RNA polymerase isn’t activated
No transcription
No mRNA produced

53
Q

How can altered DNA cause cancer

A 
DNA altered by mutation
Mutation changes base sequence
Of gene controlling cell growth/division
Of tumour suppressor gene
Change in protein structure/non-functional protein
Tumour suppressor gene codes for protein that inhibits cell division
Mitosis
Uncontrollable cell division
Leading to a malignant tumour

a level biology paper 2 (16 decks)

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