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A Level Biology Paper 2 > Mutations, Stem Cells and Cancer > Flashcards

Mutations, Stem Cells and Cancer 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
Disadvantage of overproduction of a protein
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
What are the two types of RNAi and what do they do
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
What is RISC
RNA Induced Silencing Complex Formed when RNAi binds to a protein (enzyme) in cytoplasm Inhibiting DNA gene expression by binding to complementary mRNA
28
How does RISC inhibit gene expression
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
How can protein still be produced if RNAi used
Not all mRNA hydrolysed so some translation still occurs | RNAi hasn't bound to all mRNA so some translation still occurs
30
Epigenetics
Inheritable changes in gene expression | Without changes to their DNA base sequence
31
How is translation inhibited in epigenetics
Increased methylation of DNA | Decreased acetylation of histones
32
What is methylation
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
Where does methylation occur
CpG Islands Common at the 5' end of many genes Carbon 5 of cytosine base
34
What is acetylation
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
Where does acetylation occur
Amino acid leucine On the tails of histone molecules (side branches) From Acetylecoenzyme A
36
2 types of cancer
Benign | Malignant
37
Compare benign and malignant tumours
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
How are iPS produced
Produced from human somatic cells using certain protein transcription factors
39
What two genes are in control of the rate of cell division
Proto-onco genes | Tumour suppressor genes
40
What are proto-onco genes
Stimulates cell division | by coding for protein that increases the rate of cell division
41
How can cancers cause damage
May damage organ concerned May cause blockages/obstructions (e.g. blood flow) May damage other organs by exerting pressure on them
42
Mutation in a proto-onco gene
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
Mutation in tumour suppressor gene
Gene becomes inactive Stops inhibiting cell division Rate of cell division increases Mass of cells known as tumour form
44
Overmethylated tumour suppressor gene
Gene becomes inactive Stops inhibiting cell division Rate of cell division increases Leading to mass of cells being produced (tumour)
45
Undermethylated onco gene
Gene becomes more activated Cell division switched on Rate of cell division increase
46
Function of stop codons
When read by ribosome during translation, translation stops | So final polypeptide chain detaches from ribosome
47
How do alterations in tumour suppressor genes lead to a tumour
Increased methylation of tumour suppressor gene Mutation in tumour suppressor gene Genes not transcribes/expressed Resulting in uncontrollable cell division via mitosis
48
In microscopy, how do you find the mean ... number per mm2
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
Why doesn't oestrogen affect other cells
Not all cells have the ERalpha receptor/oestrogen receptor
50
Link between sunbathing and cancer
Sun has UV radiation | Causes mutations in the genes responsible for controlling cell division
51
Why are people with a family history of cancer at an increased risk
May inherit onco genes | Giving a predisposition to cancer
52
Consequence of methylation to promoter
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
How can altered DNA cause cancer
``` 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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