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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
Q

Combination Therapy in combating mutation

A
  • 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

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26
Q

How does the ER: Estrogen receptor work

A

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

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27
Q

Tamoxifen (Prodrug), how does it work?

A

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)

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28
Q

Fulvestrant

A

Pure anti-estrogen)
Prevents Dimersation and activation
Increases degradation (Selective ER down-regulator) SERD)

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29
Q

Gene expression to Protein translation…. is?

A

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
Q

Role of Oncogenes in cancer

A

Oncogenes are mutated forms of proto-oncogenes that promote cell proliferation and survival
Oncogenes are more likely to cause cancer

31
Q

Roles of tumour suppresor genes in cancer

A

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
Q

DNA -> Protein

A

1) Gene encoding protein
2) Trascription of gene to pre-MRNA
3) Splicing out introns to mRNA
4) mRNA translated into proteins

33
Q

Types of gene regulation

A 
Chromatin Remodeling
Transcription
mRNA processing (splicing)
Micro RNAs
Translation (protein synthesis)
Post transitonal modification
34
Q

Chromatin remodelling what does it entail?

A

Each cell has 2m of DNA, supercoiled around histones (to form chromatin) via acetylation(open)and methylation(regulating how tight)

35
Q

Transcription in gene regulation

A 
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
Q

Splicing in gene regulation

A

Single base mutations can cause skipping of exons -> leading to the skipped area not being translated ->
Ultimately dysfunctional protein

37
Q

MicroRNAs in gene regulation

A

MiRNAs/miRs are short RNA molecules
Bind to mRNA target on 3’ side
Bind imperfectly to mRNA targert and repress gene expression

38
Q

Oncomirs are?

A

MicroRNAs that suppress tumour suppressor genes

39
Q

Tumour suppresor miRS are?

A

MicroRNAs that suppres oncogenes

40
Q

Mutation of miRs/MicroRNAs leads to ->

A

Dysregulation of protein synthesis

41
Q

Translation in gene regulation

A

Translational control is complex,

Oncogenic mutations increase the activity of ribosomes and TF (e.g P13k & RAS pathway)

42
Q

Post translational modification in gene regulation

A

Proteins targeted for degradation AFTER translation by adding Ubiquitin onto them -> protesome degrades
When mutated it can degrade many things e.g p53

43
Q

The role of mutations in disrupting gene expression in cancers

A

Cell responses require changes in gene expression patterns

Mutations (changes in DNA sequence) lead to this

44
Q

Types of cancer DNA mutations

A

1) Point Mutation
2) Deletion
3) Amplification
4) Translocation

45
Q

Point mutation (Example + description)

A

E.g p53/RAS

Point mutation is the mutation of a single nucleotide that can have a dramatic effect on protein function

46
Q

Deletion (e.g + Descrip)

A

E.g EGFR
Deletion of a gene (region of DNA) can lead to inactivated genes or truncuated proteins
(Truncated EGFR is persistently active)

47
Q

Amplification (e.g + Description)

A

E.g MDM2
Amplfication of a gene leads to an increase in the No. of copies of that gene.
(more MDM2 = less p53)

48
Q

Translocation (e.g + Description)

A

E.g Philadelphia Chromosome

Translocation of genes entails the rearrangement of chromosomes -> can lead to protein fusion

49
Q

Knowledge of DNA sequences usefull for Diagnosis and Treatment and Prognosis

A

Pharmacgonectics -> effect of genes/genomes on response to treatment
Leads to variation between patients -> Metabolising enzymes
E.g Tamoxifen

50
Q

Role of pharmacist in pharmacogenetics

A

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
Q

Patient DNA influences…

A

Patient DNA influences drug metabolism Rates

52
Q

Tumour DNA can…?

A

Tumour DNA can predict response to treatment

53
Q

Pharmacogenetics can…

A

Pharmacogenetics can inform treatment choices

54
Q

Risk factors for human cancers?

A

Smoking, Obesity, Diet, Exercise, pollution, infection alcohol

55
Q

Risk Factors I: Mutations

A

Permanent changes in the DNA sequence (e.g Point mutation,deletion, amplfication, chromosome rearrangement)

56
Q

Risk factors II: Tumour promoter

A

Once an intiation mutation has occured conditions that increase cell proliferation INCREASE rate of tumour progression

57
Q

Tumour promoters

A

Inflammation, alcohol, chemical promoters

58
Q

Inflammation & Cancer

A

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
Q

ROS/RNS (Reactive oxygen/nitrogen species) Role in cancer

A

ROS and RNS lead to;

  • Oxidies bases and abasic sites
  • Single strand breaks and double strand breaks
60
Q

ROS/RNS endogenous and exogenous sources

A

Endogenous -> Inflammation, immune response

Exogenous -> Radiation (x rays gamma rays chemicals UVA radiation)

61
Q

Chronic Inflammation can lead to mutagenesis through

A

Chronic inflammation produces Cytokines, That then produce ROS/RNS that leads to DNA breaks, DNA adducts, protein damage ——> MUTATION

62
Q

Viruses & Cancer (Example)

A

E.g HPV

  • Produces oncogenic proteins E6 & E7
  • E6 targets p53 for degradation
  • E7 inhibts Rb (RB1)
63
Q

Infections & cancer (example)

A

H.pylori
Causes gastric ulcers (inflammation)
Cytokines released increases ROS/RNS in stomach (Free radicals cause DNA damage)
-> Mutation

64
Q

Describe the potentials of gene therapy against cancers

A

Potentials

  • Gene repair: correction of mutation
  • Pro-drug metabolising enzymes therapy to sensitize cancer cells
  • Modification tumour microevironment
65
Q

Describe the limitations of gene therapy against cancers

A

Commercial barriers

  • Expensive materials
  • Individualised therapies

Biological barriers

  • Many genes may be mutated
  • Variation in tumours
  • Variation in patients
66
Q

Describe the roles of Monoclonal Antibodies (Mabs) in cancer

A

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
Q

Mabs as drugs

A

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
Q

Advantages of Mabs

A

Good Specficity

Large quantities can be made

69
Q

Advantages and disadvantages of recombinant Mabs

A

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
Q

How do cancer vaccines work?

A

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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