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B33 CAN > B33 CAN Biology > Flashcards

B33 CAN Biology Flashcards

1
Q

What is a cancer?

A
  • Uncontrolled growth of abnormal cells in the body

- Balance shifts towards proliferation & survival

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2
Q

What is a gene?

A
  • A gene is a bit of DNA that encodes a protein

- Genes tell cells when to replicate, die or neither

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3
Q

What are mutations?

A
  • Mutations are changes (addition removal or swapping) of nucleotides in a gene that can be ; beneficial, harmful or neutral
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4
Q

How can mutations affect (negatively or positively) cell behaviour?

A

Mutations are changes (additon,removal or swapping) of nucleotides. As proteins are determined by genes a change in the gene sequence confers changes in protein activity or function.

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5
Q

What is a proto-oncogene

A

A proto-oncogene is a gene that is involved in normal cell growth

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6
Q

What is an oncogene

A

An oncogene is a mutated version of a proto-oncogene that may cause cancer

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7
Q

What is a tumour suppresor gene

A

A tumour suppresor gene is a type of gene that makes a tumour suppresor protein that controls cell growth

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8
Q

p53 and RB1 are examples of…?

A

Tumour suppresor genes

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9
Q

MYC and RAB are examples of…?

A

Proto-oncogenes

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10
Q

What does p53 do?

A

Tumour suppresor p53;

  • Blocks cell cycle in response to cellular damage
  • Induces apoptosis if DNA damage is irreprable
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11
Q

What does RB1 do?

A

Tumour suppresor RB1;

  • Binds to & inhbits E2F transcription factors (Blocking cell cycle)
  • Inactivated by phosphorylation
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12
Q

What does MYC do?

A

Proto-oncogene MYC;

  • Transcription factor
  • promotes cell growth
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13
Q

What does RAS do?

A

Proto-oncogene RAS;

  • G-protein
  • Activated by cell growth
  • Activates downstream signalling pathways
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14
Q

What is Senescence? And what is it due to?

A

Cellular old age due to the shortening of telemores

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15
Q

What are Telomeres?

A

Telomeres are repetitive regions at the ends of chromosomes

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16
Q

What happens to telomeres during cell divison?

A

During cell divison telomeres shortern after each ‘divide’

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17
Q

What does telomerase do?

And where are they normally expressed?

A

Telomerase restores telomeres Telomerase is normally expressed in germ cells and stem cells.

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18
Q

What is alternative telomere lengthening? And what can it lead to?

A

In cells that don’t express telomerase
Recombination or fusion between the ends of different chromsomes
It can lead to oncogenic changes

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19
Q

EGFR & Signalling, what does EGFR do?

A

EGFR senses growth signals and transduces a signal that leads to (through changes in DNA) an increase in proteins needed for cell divsion

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20
Q

EGFR Pathway for increased cell divisonal proteins?

A
  • EGF binds to EGFR
  • Phosphorylation cascade occurs
  • RAS -> RAF -> MEK ->ERK
  • ERK activates gene that encodes for more proteins for cell divison
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21
Q

EGFR pathway for decreased cell control etc.

A

-EGF binds to EGFR
- Phosphorylation cascade occurs
- P13K -> AKT
-AKT confers blockage of p53,
Apoptosis and increases protein synthesis

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22
Q

EGFR Mutations, what happens?

A

EGFR is frequently mutated in cancers
-> Change in DNA-> Change in protein sequence -> Change in protein function

EGFR acts as if permantely bound to EGF causing cell to persistenly divide

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23
Q

EGFR as a drug targer?

A
  • Can stop EGF binding to EGFR (Done by MABs)
  • Can stop actiavtion of EGFR
    (done by ErlotNIB)
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24
Q

How can mutations cause sensitivity and resistance to drugs?

A

Can cause changes in downstream signalling and/or receptor affinity

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25
Combination Therapy in combating mutation
- Combinations of treatments makes it more difficult for them to become resistant Multiple mutations must occur in the same cell for resistance to treatment to all drugs occur
26
How does the ER: Estrogen receptor work
1) Estorgen diffuses into cell 2) Estrogen binds to receptor, displacing chaperone proteins 3) ER dimerises and migrates to nucleus 4) ER dimer binds with Co-activators or Co-repressors to modifty transcription of target genes
27
Tamoxifen (Prodrug), how does it work?
1) Metabolised to active metabolites by CYP 2) Binds to ER with high affinity than E Mostly Anti-estrogenic (Except Uterus and bone) -> SERM (Selective ER modifier)
28
Fulvestrant
Pure anti-estrogen) Prevents Dimersation and activation Increases degradation (Selective ER down-regulator) SERD)
29
Gene expression to Protein translation.... is?
1) 2 Copies of each gene for parents 2) Changes in DNA 3) Changes in gene sequence 4) changes in protein sequence 5) Change in protein activity/function
30
Role of Oncogenes in cancer
Oncogenes are mutated forms of proto-oncogenes that promote cell proliferation and survival Oncogenes are more likely to cause cancer
31
Roles of tumour suppresor genes in cancer
Tumour suppresor genes (such as p53) protect against cancer initiation and progression (pro-apoptotic0 If tumour suppresor genes are mutated cancer is more likely
32
DNA -> Protein
1) Gene encoding protein 2) Trascription of gene to pre-MRNA 3) Splicing out introns to mRNA 4) mRNA translated into proteins
33
Types of gene regulation
``` Chromatin Remodeling Transcription mRNA processing (splicing) Micro RNAs Translation (protein synthesis) Post transitonal modification ```
34
Chromatin remodelling what does it entail?
Each cell has 2m of DNA, supercoiled around histones (to form chromatin) via acetylation(open)and methylation(regulating how tight)
35
Transcription in gene regulation
``` The level of transcription of a gene determines amount proteins expressed Affected by; Changes in protein levels e.g p53 Changes in DNA structure Changes in DNA sequence ```
36
Splicing in gene regulation
Single base mutations can cause skipping of exons -> leading to the skipped area not being translated -> Ultimately dysfunctional protein
37
MicroRNAs in gene regulation
MiRNAs/miRs are short RNA molecules Bind to mRNA target on 3' side Bind imperfectly to mRNA targert and repress gene expression
38
Oncomirs are?
MicroRNAs that suppress tumour suppressor genes
39
Tumour suppresor miRS are?
MicroRNAs that suppres oncogenes
40
Mutation of miRs/MicroRNAs leads to ->
Dysregulation of protein synthesis
41
Translation in gene regulation
Translational control is complex, | Oncogenic mutations increase the activity of ribosomes and TF (e.g P13k & RAS pathway)
42
Post translational modification in gene regulation
Proteins targeted for degradation AFTER translation by adding Ubiquitin onto them -> protesome degrades When mutated it can degrade many things e.g p53
43
The role of mutations in disrupting gene expression in cancers
Cell responses require changes in gene expression patterns | Mutations (changes in DNA sequence) lead to this
44
Types of cancer DNA mutations
1) Point Mutation 2) Deletion 3) Amplification 4) Translocation
45
Point mutation (Example + description)
E.g p53/RAS | Point mutation is the mutation of a single nucleotide that can have a dramatic effect on protein function
46
Deletion (e.g + Descrip)
E.g EGFR Deletion of a gene (region of DNA) can lead to inactivated genes or truncuated proteins (Truncated EGFR is persistently active)
47
Amplification (e.g + Description)
E.g MDM2 Amplfication of a gene leads to an increase in the No. of copies of that gene. (more MDM2 = less p53)
48
Translocation (e.g + Description)
E.g Philadelphia Chromosome | Translocation of genes entails the rearrangement of chromosomes -> can lead to protein fusion
49
Knowledge of DNA sequences usefull for Diagnosis and Treatment and Prognosis
Pharmacgonectics -> effect of genes/genomes on response to treatment Leads to variation between patients -> Metabolising enzymes E.g Tamoxifen
50
Role of pharmacist in pharmacogenetics
Explain the genetic testing and why DTC genetic testing may report false postitive Genetic dispostion for a disease doesnt mean that they will develope disease
51
Patient DNA influences...
Patient DNA influences drug metabolism Rates
52
Tumour DNA can...?
Tumour DNA can predict response to treatment
53
Pharmacogenetics can...
Pharmacogenetics can inform treatment choices
54
Risk factors for human cancers?
Smoking, Obesity, Diet, Exercise, pollution, infection alcohol
55
Risk Factors I: Mutations
Permanent changes in the DNA sequence (e.g Point mutation,deletion, amplfication, chromosome rearrangement)
56
Risk factors II: Tumour promoter
Once an intiation mutation has occured conditions that increase cell proliferation INCREASE rate of tumour progression
57
Tumour promoters
Inflammation, alcohol, chemical promoters
58
Inflammation & Cancer
Chronic inflammation is a MAJOR cancer risk as; - Promotes mutagenisis (ROS & RNS produced in inflammation) -Promotes tumour progression (induces cytokines, prevents apoptosis) -Promotes metastasis (Angiogensis & migration)
59
ROS/RNS (Reactive oxygen/nitrogen species) Role in cancer
ROS and RNS lead to; - Oxidies bases and abasic sites - Single strand breaks and double strand breaks
60
ROS/RNS endogenous and exogenous sources
Endogenous -> Inflammation, immune response Exogenous -> Radiation (x rays gamma rays chemicals UVA radiation)
61
Chronic Inflammation can lead to mutagenesis through
Chronic inflammation produces Cytokines, That then produce ROS/RNS that leads to DNA breaks, DNA adducts, protein damage ------> MUTATION
62
Viruses & Cancer (Example)
E.g HPV - Produces oncogenic proteins E6 & E7 - E6 targets p53 for degradation - E7 inhibts Rb (RB1)
63
Infections & cancer (example)
H.pylori Causes gastric ulcers (inflammation) Cytokines released increases ROS/RNS in stomach (Free radicals cause DNA damage) -> Mutation
64
Describe the potentials of gene therapy against cancers
Potentials - Gene repair: correction of mutation - Pro-drug metabolising enzymes therapy to sensitize cancer cells - Modification tumour microevironment
65
Describe the limitations of gene therapy against cancers
Commercial barriers - Expensive materials - Individualised therapies Biological barriers - Many genes may be mutated - Variation in tumours - Variation in patients
66
Describe the roles of Monoclonal Antibodies (Mabs) in cancer
Mabs are proteins produed by the B-lymphocytes to bind to foreign antigens Mabs come from single-cloned B-lymphocytes and target a single Epitope Mabs makes cells visible to the immune system Stop cells dividing
67
Mabs as drugs
E.g Rituximab -> Targets CD20 on B cells Kills B cells in lymphomas and leukaemias (and healthy cells) (Antibody Drug Conjugate) ADC Drug delivery system like in emtansine
68
Advantages of Mabs
Good Specficity | Large quantities can be made
69
Advantages and disadvantages of recombinant Mabs
Reduced immune response as not recognised as foreign, Smaller molecules extravasate and distribute more Disadvanntages -Reduced circulation (1/2t controlled by Fc region & glycosylation)
70
How do cancer vaccines work?
Cancer vaccines contain A tumour-associated antigen (TAA) which induces a immune response against tumour cells Induces cytotoxic T-lympocyes

B33 CAN (5 decks)

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