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Hallmarks of cancer Flashcards

1
Q

The 10 hallmarks of cancer drugs that target

A

EGFR inhibitors
Cyclin dependent kinase inhibitors
Immune acitvating antiCTLA4 mAb
Telomerase inhibitors
Selective anti inflammatory drugs
Inhibitors of HGF/c-Met
Inhibitors of VEGF signalling
PARP inhibitos
Proapaptotic BH3 mimetics
Aerobic glycolysis inhibitors

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1
Q

How do monoclonal antibodies treat cancer

A

Trastuzumab, cetuximab
Bind to surface expressed receptor and prevents ligand binding (growth factor) preventing signal transducton

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2
Q

What do EGFR inhibitors in cancer cells

A

Sustaining proliferative signalling

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3
Q

10 hallmarks of cancer cells characterisation

A

Sustaining proliferative signalling
Evading growth supressors
Avoiding immune destruction
Enabling replicative immortality
Tumour-promoting inflammation
Acitvating invasion and metastasis
Inducing angiogenesis
Genome instability and mutation
Resisting cell death
Deregulating cellular eneretics

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4
Q

What hallmark does cyclin dependent kindase inhibitors target

A

Evading growth suppressors

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5
Q

What hallmark of cancer does immune activating aanti-CTLA4 mAb target

A

Avoiding immune destruction

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6
Q

What hallmark of cancer do telomerase inhibitors target

A

Enabling replicative immortality

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7
Q

What hallmark of cancer do selective anti-inflammatory drugs target

A

Tumour-promoting inflammation

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8
Q

What hallmark of cancer does inhibitors of HGF/c-Met

A

Activating invasion and metastasis

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9
Q

What hallmark of cancer do inhibitors of VEGF signalling target

A

Inducing angiogenesis

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10
Q

What cancer hallmark do PARP inhibitors target

A

Genome instability and mutation

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11
Q

What cancer hallmark do pro-apoptotic BH3 mimetics target

A

Resisting cell death

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12
Q

What cancer hallmark do aerobic glycolysis inhibitors target

A

Deregulating cellular energetics

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13
Q

Circuits within a cell

A

Motility circuits
Cytostasis and differentiation circuits
Viability circuits

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14
Q

How much of biological mass of tumour are cancer cells

A

40-50%
Enfothelial cells, blood vessels, podocytes, macrophages
Hypoxic and hostile

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15
Q

How do cancer cells sustain proliferation

A

Produce growth factor ligands
Send signals to stimulate normal cells without supporting tumour ass stroma
Elevated levels receptor proteins
Structural alterations in receptor
Somatic mutations activate addiitonal downstream mutations eg EGFR mutation in NSCLC, B-Raf mutation in melanoma

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16
Q

Growth factors.cytokines causing B and T cell prolif

A

Il2, 7, 12
SDF-1
FLT3 ligand
TNF alhpa
TGF beta 1

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17
Q

wHAT IS MOST OMON CYTOKINE CAUSING PROLIFERATION

A

Il3
GCSF/GMSCF

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18
Q

Increase EGFR activaiton in cancer causes

A

Overexpression of EGFR protein
Ligand/autocrine loop
Heterodimerisation and cross talk
Decreased phosphatase
Mutant EGFR

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19
Q

What is heterodimerisation

A

Amplification processs - amplifies process that is triggered by the substance binding to the factor

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20
Q

Anti EGFR therapies

A

Mabs - blocks ligand binding eg citoximab, receptin
Intracellular tyrosine kinase inhibition
Toxin conjugates - modifying ligands into toxins - no viable therapy in humans
Antisense approach - Protein synthesis inhibited downstream

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21
Q

EGFR and affect on cancer

A

Signal transduction - binding of ligand to EGFR receptor activates and cascades affect cell proliferation
EGFR inhibitorn ma inhibit tumour growth

22
Q

Mabd that inhibit EGFR

A

Trastuzumab, cetuximab

23
Q

Tyrosine kinase inhibitors for EGFR

A

Gefitinib or erlotinib

24
Wyas of growth supression evasion in cancer
pRb and p53 mutations -> loss of contact inhibition Corruption of TGF-beta promotes cacner
25
What is an exmaple of a cancer caused by defective RB1 gene
Retinoblastoma - inherited Ch13 TB1 mutation Rb - cell cycle is continious - no pause Also small cell lung cancer
26
How does p53 work
Increases p21 protein which causes cell arrest
27
What pathway mutations can help predict response to chemotherapy
Abnoramlities in Rb/Cdk4/cyclin D pathway Determine how cell cycle of cancer cell is being altered and whether can be targeted by chemo
28
What protein allows cell to cell adhesions
Integrin - sits across cell membrane layer
29
Why want to give cell adhesion disrupting drug prior to cehmo
For chemo to be effective needs to leave blood vessel -> ECF -> Cel directly Therefore can give adhesion disrupting drug to affect integrin of epithelial vacular cells to allow the next chemo drug through these gpas Therefore sequenzing is important
30
What drugs can cause arrest in G2
Vinca alkaloids Taxanes Target microtubules
31
Combrestatin MOA
Targets microfibrin Interrupts blood supply to tumour as epithelial cells -> shape change due to microtubules
32
How does cancer resist cell death
33
What can change how a ligand signals
Environement that cell is in eg hypoxic etc Heterodimers Receptors on different cells
34
Why is li fraumeni only heterogenous
Homogenous is lethal in utero
35
How is li fraumeni syndrome characterised
Premenopausal breast cancer Childhood sarcoma Brain tumours Leukaemia and lymphoma Adrenocortical carconoma
36
What causes li farumeni syndrme
TP53 germline mutation in chromosome 17 autosomal dominant 50% penetrance by 50 years old
37
What are telomeres
Multiple tandem hexanucleotide repeats Shorten progressively - cells can no longer replicate eventually
38
How do cancer cells become immortal
Telomerase action to restore telomere length
39
What is sorefanib
Tyrosine kinase inhibitor
40
What is bevacizumab
Monoclonal antibody for VEGF - inhibiting
41
What protein is utilised by cancer for metastasis
E-cadherin Downregulating e-cadherin may stop metastasis happening
42
Why are acquired mutations os much more likely in cancer
Cancer cells increased rate of mutation - accelerated by compromising surveillance systems for genomic integrity
43
What genes are required to repair DNA
Tp53 - stops cell cycle to allow time for repairs BRCA1,2, PALB2 - repair double stranded DNA by HRR pathway PARP - single strand breaks repairing
44
MOA of PARPis and why most effective in BRCA/PALB2 + tumours
Means PARP cant repair single strand breaks -> cause multiple double strand breaks Due to mutation in BRCA1,2 or PALB2, double strand breaks cant be repaired and the cell dies
45
What can determine whether a patient will repsond to platinum therapy
Whether they have previously responded to carboplatin
46
How can tumour inflammation aid a cancer
Cytokines -> Proliferation Pro angiogenesis Anti apoptotic
47
Cascade effect
often following bacterial infetion or burns and trauma aswell as cancer Cell derived mediates are joined by acellular biochemidal cascade systems of plasma proteins for an inflammatory response
48
Oxygenation of cancer tumours
Hypoxic - can use both anaerobic and aerobic glycosis in both environments
49
What ligands are found on cytotoxic T lymphocytes and dendritic cells that recognise cancer as foreing
PD1 and PDL1 Cancer can switch them off
50
What is ataxia telagniectasia
Defect in ATM gene 25% lifetime rik of cancer esp haem cancer apraxia and slurring of speech and swallowing problems
51
What cancer stage choose if in doubt
Less advanced category
52
Staging geographical location
Stage I+II - localised to orgna of origin III - locally extensive spread - lymph nodes IV - distant mets

Cancer (22 decks)

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