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Principles of tumour biology for FRCR CO1 > 1.1 Principles of tumour biology > Flashcards

1.1 Principles of tumour biology Flashcards

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1
Q

What are the stages of the cell cycle? (6)

Draw and label the cell cycle from memory

A
  • Interphase
  • Prophase
  • Prometaphase
  • Metaphase
  • Anaphase
  • Telophase
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2
Q

What are the stages within interphase?

A
  • G1
  • S (Synthesis of DNA)
  • G2
  • M (Mitosis)
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3
Q

What occurs during G1?

A
  1. Cell contents duplicate
  2. Receptor ligands (e.g. growth factors or contact with neighbour cells) bind and acitvate Extracellular signal transduction pathways
  3. In the cell if there is serious genomic damage or lack of nutrients (AAs) the cell will arrest in G1
  4. Then either dies or replicates then goes into G0

In cancer:
Restriction point is loosened as cells are able to replicate without the correct extracellular signals

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4
Q

What occurs during ‘S’ (DNA Synthesis)?

A
  1. Thousands of replication origins throughout the genome - ‘fire’ once per cell cycle
  2. at each replication point origin dsDNA is unwound into to ssDNA strands
  3. Large protein complexes that contain DNA polymerase load onto the ssDNA and replicate it
  4. When the two ‘replication forks’ collide replication stops and new strands of DNA are ligated together
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5
Q

What occurs during G2?

A
  • Genetic material organised
  • Proteins synthesised for mitosis and cytokinesis

Signals emenate from the new DNA to advise on the amount of damage that occured during replication.

If lots of damage has occured then entry into mitosis is delayed.

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6
Q

What occurs during ‘M’ (Mitosis)?

A

Centrosomes (organelles) organise microtubules to form the mitotic spindle

Mitotic spindle pulls apart the replicated chromosomes

Drags the two chromatoids to opposite sides of the cell to separate them

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7
Q

What occurs during prophase?

A

Chromosomes condense in the nucleus

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8
Q

What occurs during prometaphase?

A

Envelope of the nucleus breaks down so the microtubule spindle can attach to the chromosome

They start to pull them apart but initially this is only lining them up next to eachother

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9
Q

What occurs during metaphase?

A

All the chromosomes are lined up next to eachother ready for separation

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10
Q

What occurs during anaphase?

A

Anaphase Promoting Complex (APC) drives anaphase

The sister chromosome cohesion is lost, break apart atc entromere and they can be pulled apart to opposite ends of the cell by shortening spindle fibres

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11
Q

What occurs during telophase?

A
  1. Spindle breaks fown
  2. Chromosomes decondense
  3. Nuclear envelope reassembles around them
  4. Cytokinesis - splits the cell in half to form 2 daughter cells
  5. Both daughter cells re-enter G1
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12
Q

What is anaplasia?

A

Lack of differentiation

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13
Q

What is dysplasia?

A

change in phenotype and disordered growth, principally in the epithelium

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14
Q

What is a carcinoma in situ?

A

Full-thickness dysplasia, but basement membrane intact

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15
Q

What is hyperplasia?

A

increase in cell number

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16
Q

What is metaplasia?

A

potentially reversible transformation of one differentiated cell type to another

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17
Q

What is hypertrophy?

A

increase in cell size

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18
Q

What is Neoplasia?

A

abnormal proliferation of cells

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19
Q

What is a carcinoma?

A

Neoplasia of epithelial cells

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20
Q

What is an adenocarcinoma?

A

Neoplasia of glandular/secretory cells

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21
Q

What is sarcoma?

A

Neoplasia of mesodermal (muscle/bone) cells

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22
Q
A
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23
Q

What are the 10 hallmarks of cancer?

A
  1. Proliferative signalling
  2. Evasion of growth suppressors
  3. Avoidance of immune destruction
  4. Replicative immortality
  5. Inflammation that promotes tumour growth
  6. Invasion and metastasis
  7. Angiogenesis
  8. Genome mutation and instability
  9. Apoptosis resistance
  10. Loss of regulation of cell metabolism
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24
Q

What are CDKs and cyclins?

A

Proteins that work together to control the cell cycle.

CDKs are activated by cyclins - CDK engine, cyclin keys

When cyclins bind to CDKs they cause a conformational change of the catalytic subunit of CDK which reveals the CDK active site

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25
Q

What are Cyclin Dependent Kinases?

A

CDKs are enzymes that act like ‘switches’ to activate or deactivate different steps of the cell cycle.

Regulate cell division

Increased activity during G2 due to activation of mitotic CDK cyclins

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26
Q

How do CDKs play a role in cancer?

A

High CDK activity leads to:

  • Drives cell cycle
  • Errors in G1 DNA replication leading to chromosomal abnormalities
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27
Q

What are cyclins?

A

Subunits that regulate CDK activity

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28
Q

What is the presence of CDK throughout the cell cycle?

A

Constant

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29
Q

What is the presence of cyclins throughout the cell cycle?

A

Varied

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30
Q

How are cyclins destroyed?

A

Proteolysis

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31
Q

What does cyclin D do?

A

Expressed in proliferating cells to prevent the cell becoming inactive

Binds to CDK4/6

D-CDK4/6 phosphorylates and inactivates Rb. If overactive Rb is oversuppressed.

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32
Q

What does CDK activation depend on?

A
  1. Binding to cyclin
  2. Phosphorylation (of Thr161) by CDK- activating kinase (CAK), activates and fine tunes CDK once bound to cyclin
  3. Dephosphorylation of inhibitory phosphate groups by CDC25 (overexpression or dysregulation = bad
  4. No inhibitors
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33
Q

What does INK do to CDKs?

A

Inhibits D/CDK4/6 to control early G1

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34
Q

What do CIP (p21) and KIP (p27 and 57) do to CDKs?

A

Inhibit E/CDK 2 complexes to prevent unscheduled cell progression

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35
Q

How are CDKs inhibited?

A
  1. INK
  2. Cip/Kip
  3. Wee1
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36
Q

What does Wee1 do to CDKs?

A

Phosphorylate at Thr14 and Tyr15 to inactivate CDK

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37
Q

What is Retinoblastoma (Rb)?

A

Tumour suppressor gene that regulates the cell cycle

If Rb is inactivated or suppressed results in unchecked cell division

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38
Q

What does Rb do normally?

A

When active (hypophosphorylated) Keeps the cell in G1

Binds to and inhibits E2F transcription factors which are needed for expressing the genes required for DNA synthesis and entry to S phase

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39
Q

What does suppression/ inactivation of Rb result in?

A

(Rb is inactivated by D-CDK4/6)

E2F is released

This activates transcription of the genes required for DNA replication, pushes the cell into S phase prematurely

This allows the cell to continue to divide, bypassing checkpoints and allowing damaged DNA to replicate

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40
Q

How do cancer cells locally invade tissue?

A
  1. Growth factors secreted from the tumour e.g. HGF, EGF, PDGF, TGF-Beta
  2. The growth factors change the phenotype of the cell changes to Epithelial Mesenchymal Transition (EMT)
  3. Tumour produces proteases which breaks a path through the extracellular matrix
  4. E-cadherin is down regulated allowing cells to detach from other cells
  5. Cells lose polarity and cytoskeleton arrangements
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41
Q

What is E-Cadherin?

A

Protein that sticks cells together (cell-cell adhesion) to maintain the structure and stability of tissue

Play a role in cell-cell signalling

Loss of E-Cadherin allows cells to become mobile and move away

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42
Q

What does the TWIST protein do?

A

Transcription factor (protein that controls gene activity):

  1. Promotes EMT
  2. Reduces expression of E-Cadherin
  3. Activates genes for cell movement and invasion
  4. Promotes metastases
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43
Q

What promotes local tissue invasion?

A
  1. TWIST protein
  2. Hypoxia
  3. Inflammation
  4. Wnt pathway - bind to Frizzled receptors which stabilise beta-catenin which activate genes for cell survival, proliferation, and migration
    4.Notch pathway
  5. Hedgehog pathway
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44
Q

What are the 5 stages of metastasis?

A
  1. Invasion of basement membrane and cell migration
  2. Intravasation into surrounding vessles/lymph nodes
  3. Survive in circulation
  4. Extravasate from vessels to secondary tissue (circulating VEGF and TGF- beta precondition)
  5. Colonisation at secondary site
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45
Q

What is the role of CSF1?

A
  1. Recruits macrophages that remodel extracellular membrane
  2. Induces EMT
  3. Acts directly on cancer cells via CSF1R to support cell movement
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46
Q

What are local effects of tumours?

A
  1. Pain
  2. Pressure/obstruction
  3. Ulceration/bleeding
  4. Invasion - organ dysfunction seizures
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47
Q

What are the distant effects of tumours?

A
  1. Cachexia due to cytokines
  2. Paraneoplastic syndromes
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48
Q

What are some paraneoplastic syndromes?

A
  1. Cushing’s
  2. SIADH
  3. Hypercalcaemia
  4. PTHrp
  5. Hypogylcaemia
  6. Myasthenia
  7. Dermatomyositis
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49
Q

What is sprouting angiogenesis?

A

Form new blood vessels from existing ones through growth and migration of endothelial cells

50
Q

How does cancer alter angiogenesis?

A

Angiogenesis usually controlled by a balance of pro and anti-angiogenic factors. Tumour creates hypoxic conditions swings in favour of pro angiogenic.

51
Q

What are the pro angiogeneic factors?

A

VEGF
VEGFR
EGF
FGF
HGF
PDGF
Tie receptors

52
Q

What leads to VEGF release?

A

Hypoxia (HIF-1a)
COX-2
NO
H202
Oncogenes

53
Q

What are the anti-angiogenic factors?

A

Angiostatin
Endostatin
Prolactin
p53

Anti-VEGF drugs are cytostatic rather than cytotoxic

54
Q

What are the toxicities associated with anti-VEGF?

A
  • HTN
  • Proteinuria
  • Thrombosis/haemorrhage

Remember a bit like preeclampsia

55
Q

What is the VEGF-A signal transduction pathway?

A

VEGF-A binds to 2 VEGFR-2 receptors causing dimerisation and autophosphorylation

Activates RAS-RAF-MEK-ERK

Activates PI3K-AKT leads to:
- Inhibition of apoptosis
- Endothelial nitric oxide synthase
- Stimulates vascular permeability

56
Q

What is VEGF overexpression associated with?

A
  1. Ovarian cancer
  2. Poor prognosis e.g. colorectal cancer
  3. Peritoneal mets
  4. Ascites
57
Q

What is HIF?

A

Heterodimeric Transciprion factor

1 alpha and 1 beta subunit

58
Q

What does HIF regulate?

A

Angiogenesis (VEGF_
Erythropoesis (epo)
Glycolysis (GLUT-1)
pH (CA9)`

59
Q

What is HIF1-a regulated by?

A

Oxygen concentration
Von-Hippel Lindau tumour suppressor gene

60
Q

What happens if HIF activity is inhibited?

A

Tumour growth is inhibited

61
Q

What happens during normoxia?

A

Prolyl 4-hydroxylase senses oxygen

VHL binds to hydroxylated HIF-a

No angiogenesis occurs

62
Q

What happens during hypoxia?

A

Propyl 4-hydroxylase doesn’t detect oxygen so is inactive

VHL doesn’t bind to HIF-1a

HIF1a then activates hypoxia response enzymes

VEGF gene stimulated

Angiogenesis occurs

63
Q

What are the mechanisms of DNA damage?

A

External e.g. UV, chemicals, viruses

Internal: replication errors, cell metabolism, reactive O2

64
Q

What are the mechanisms of DNA repair?

A
  1. Glycosylase
  2. Endonucleases
  3. Polymerase
  4. Ligase
  5. Exonuclease
65
Q

What does glycosylase do?

A

recognise and remove damaged bases from DNA

66
Q

What do endonucleases do?

A

Cleave phosphodiester bond

67
Q

What do polymerases do?

A

Catalyse DNA/RNA synthesis

68
Q

What do ligases do?

A

facilitate joining two DNA strands together via phosphodiester bond

69
Q

What do exonucelases do?

A

remove nucleotides from the ends of DNA strands

70
Q

What are the single strand break repair types?

A
  1. Base Excision Repair (BER)
  2. Nucleotide Excision Repair (NER)
  3. Mismatch Repair (MMR)
71
Q

What is Base Excision Repair?

A

Corrects small non-helix distorting DNA base lesions caused by oxidation, alkylation, or deamination

72
Q

What happens during Base Excision Repair?

A

DNA glycosylase enzyme identifies and removes the damaged base, creating an abasic (AP) site.

AP endonuclease cleaves the DNA at the AP site.

DNA polymerase inserts the correct nucleotide

DNA lifase seals the gap

Can be short or long patch repair

PARP recognises SSBs during BER - bind to the site and then creates PAR chains which act as a scaffold for BER proteins e.g. XRCC1

73
Q

What is the significance of XRCC1 is mutation?

A

Radiosensitive

74
Q

What is Nucleotide Excision Repair? (NER)

A

Removes bulky helix-distorting lesions

e.g. those created by UV induced pyrimidine dimers

75
Q

What happens during Nucleotide Excision Repair?

A

Damage recognition e.g. Transcription Factor IIH (TFIIH) recruits a protein complex that unwinds the DNA near the lesion

Endonucleases make incisions on both sides of the lesion to remove a short segment of DNA

DNA polymerase makes a new complementary strand

DNA ligase seals it in place

76
Q

What conditions are caused by genetic defects in NER?

A

Point mutations in:

  1. Xeroderma Pigmentosum
  2. Cockayne syndrome

UV induced skin cancer

77
Q

What is MisMatch Repair (MMR)?

A

Repairs errors introduced during DNA replication e.g. mismatch or insertion/deletion loops

78
Q

What happens during Mismatch Repair (MMR)?

A
  • hMSH2/3/6 recognise spontaneous replication errors
  • recruit hMLH1/hPSM1/2
  • Mismatch removed by EXO1 (endo+exo nuclease)
  • POLD + LIG1 seal the break
79
Q

What conditions are caused by genetic mutations in MMR?

A
  • HNPCC/Lynch
    (Herditary Nonpolyposis Colorectal Cancer)
  • MMR deficient colorectal cancer - microsatelliye instability and increased mutation frequency - poorer prognosis/outcomes
80
Q

What type of DNA damage does ionising radiation cause?

A

Bases most frequently

Then single strand breaks

Then double strand breaks

81
Q

How are double strand DNA breaks repaired?

A
  1. Homologous Recombination (HR)
  2. Non-homologous end-joining (NHEJ)
82
Q

What is Homologous Recombination?

A

Repairs double stranded DNA breaks using a homologus sequence as a template.

Occurs during S and G2

83
Q

What happens during Homologous Repair?

A
  1. MRN complex detects double stranded break
  2. MRN recuits ataxia telangiectasia mutated kinase (ATM)
  3. ATM phosphorylates key proteins such as BRCA1, p53, CHEK2
  4. End resection creates a 3’ single-stranded DNA
  5. This invades the sister chromatid and DNA polymerase synthesises new DNA using the intact version on the sister chromatid as a template
  6. Strand is ligated back together
84
Q

What do mutations in ATM result in clinically?

A

Chromosomal aberrations or cell-cycle checkpoint mutations

Ataxia Telangiectasia - lymphoma

Li Fraumeni (LiF) - sarcoma and early onset cancers

These patients have the highest sensitivity to ionising radiation

85
Q

What do genetic mutations in Homologous Repair result in?

A

Chromosome Aberrations

  • BRCA 1/2 - breast/ovarian/ prostate
  • Werner
  • Bloom - lymphoma/ leukaemia
86
Q

What is Non-homologous end joining (NHEJ)?

A

Most common pathway for Double Stranded break repair

Takes place in G0/G1

Prone to errors because a homologous template isn’t use so can result in small insertion/deletion mutations at the repair site leading to genetic instability

87
Q

What happens during Non-homologous End-Joining?

A
  1. Ku protein complex (e.g. Ku 70/80) recognises the double stranded break and binds to it
  2. Bound Ku protein acts as a scaffold
  3. Ku protein recruits DNA protein-kinases which stabilises the DNA strands and aligns them for repair
  4. Nucleases such as Artemis remove damage ends. Polymerases such as Pol fill any gaos,
  5. Once two strands are compatible DNA ligase + XRCC4 and XLF 4 joins them back together
88
Q

What do Non-homologous End Joining defects result in clincially?

A

Increased radiosensitivity - even greater than Homologous recombination

89
Q

How does the cell decide between Homologous Recombination and Non-homologous end joining?

A
  1. Stage of the cell cycle HR: S/G2, NHEJ: G0/G1
  2. Type of DNA damage
90
Q

What is Synthetic Lethality?

A

Synthetic lethality is where the disruption of two genes results in cell death, but the disruption of either gene alone is non-lethal.

91
Q

How is Synthetic Lethality relevant clinically?

A

Mutations in tumour suppressor genes such as BRCA1/2 mutations impair homologous recombination (which BRCA1 and 2 are critically involved in). This forces the cell to rely on other DSB repair pathways such as PARP (poly ADP-ribose polymerase).

PARP inhibitors prevent the repair of ssDNA breaks which builds up dsDNA breaks which cannot be repaired due to the defective HR. This can be used to kill cancer cells.

PARP inhibitor e.g. Olaparib in mBRCA positive Triple Negative breast CA

92
Q

What are cancer stem cells?

A

Infrequent cells within tumours - only some cells from a tumour can give rise to a new tumour if transferred to a cancer-free mouse

Capable of self-renewal, differentiation, and tumorigenicity.

Give rise to daughter cells with have limited proliferation potential and differentiate

93
Q

Where do cancer stem cells come from?

A

2 theories:

  1. Normal cells de-differentiate
  2. From tissue step cells
94
Q

How is type of cell death determined?

A
  1. Inflammation and cytoplasmic swelling - necrosis
  2. Chromatin condensation + phagocytosis - apoptosis

Otherwise autophagy

95
Q

What is apoptosis?

A

Programmed cell death

96
Q

What occurs during apoptosis?

A
  1. Nuclear volume reduces
  2. Cell shrinks
  3. Chromatin condenses
  4. DNA fragments - non-random cleavage
  5. Membrane blebs
  6. Caspases control destruction
  7. Phagocytosis of dead cell prevents inflammation
97
Q

Why is apoptosis important?

A
  1. Suppress tumours (successful tumour cells inhibit apoptosis)
  2. Regulate the number of cells
  3. Remove redundant cells
  4. Control and limit proliferation (c-MYC)
  5. Remove damage cells
98
Q

What is autophagy?

A

Lysosomes degrade unnecessary or dysfunctional organelles and proteins

99
Q

What is the extrinsic cell death pathway?

A

Cells die due to external stimuli

100
Q

What is extrinsic cell death mediated by?

A
  1. Membrane death receptors (Fas (CD95, TNF)
  2. Form the Death-Inducing Signalling Complex (DISC) made up of: Death ligands, receptors, adaptors and initiator caspases
101
Q

What are the initiator caspases in the extrinsic cell death pathway?

A

8 and 10

102
Q

What are the effector caspases in the extrinsic cell death pathway?

A

3, 6, 7

Executioner caspases

103
Q

What is the caspase cascade int he extrinsic cell death pathway?

A
  1. DISC initiates Pro-caspase 8 by cleavage
  2. Caspase 8 directly cleave executioner caspases (3 and 7) Effector caspases
  3. Cell death
104
Q

What are the inhibitors of the extrinsic cell death pathway?

A

Inhibitors of Apoptosis Proteins (IAP)
c-Flip

105
Q

What causes the intrinsic cell death pathway?

A

Internal cellular stress factors
1. Drugs
2. DNA damage e.g. UV radiation
3. Oxidative stress
4. Growth factir deoruvation

106
Q

What is the intrinsic cell death pathway mediated by?

A
  1. Mitochondria releases SMAC, diablo and cytochrome C
  2. Bcl-2 family which are pro and anti-apoptotic proteins
107
Q

What happens during the intrinsic cell death pathway?

A
  1. Cell responds to stress by activating pro-apoptotic BCL-2 proteins such as Bax and Bak
  2. Bax and bap cause permeability of the mitochondrial outer membrane (MOMP) which releases apoptogenic factors e.g. cytochrome c
  3. Cytochrome c binds to APAF-1 (apoptotic protease activating factor) and ATP forming the apoptosome
  4. Apoptosone acitvates caspase 9 (initator caspase)
  5. Caspase 9 activates executionare caspases 3 and 7
108
Q

What inhibits the intrinsic cell death pathway?

A

Inhibitors of Apoptosis proteins - block caspases

These can be used therapeutically to sensitise cells to chemo

109
Q

What is an oncogene addiction?

A

The cancer cell depends on a specific oncogene for its maintainance

110
Q

What do humanised MABs end in?

A

-umab

111
Q

What do non-humanised MABs end in?

A

-imab

112
Q

What drug targets the c-kit oncogene?

A

Imatinib

Inhibits Bcr-Abl

e.g. in CML

113
Q

What drug targets BRAF mutation?

A

DeBRAFenib
VemuRAFenib

Inhibit BRAF

BRAF V600EM e.g. colorectal, NSCLC, thyroid

V600KM melanoma

114
Q

What drugs target EGFR mutations?

  • EXON 19
  • on chromosome 7
A

Cetuximab - K-Ras wild type CRC and head and Neck

Trastuzumab, Pertuzumab, Kadcyla HER2 positive breast CA

115
Q

What drugs target NTRK fusion oncogene?

A

Entrectanib
Larotrectinib

116
Q

What drugs target mTOR oncogene?

A

Everolimus

117
Q

What drugs target CDK 4/6 oncogene?

A

Palbociclib, Ribociclib, Abemaciclib

118
Q

What cancers are RAS mutations found in?

A
  • NSCLC (30%)
  • Colorectal
  • Pancreatic
119
Q

What is the most common RAS mutation and what drug is used to target this?

A

Majority of mutations are wild-type
KRAS G12C

Sotorasib in lung and CRC

120
Q

What cancer is ALK mutation found in?

A

Adenocarcinomas (2-4%)

Usually younger, often CNS spread

121
Q

What is the ALK mutation?

A

EML4-ALK gene fusion caused by inversion on chromosome 2

122
Q

What drug is used to target ROS1 mutation?

A

Crizotinib

Alectanib
Brigatinib

Principles of tumour biology for FRCR CO1 (4 decks)

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