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Cancer > Hallmarks of cancer > Flashcards

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
Q

Wyas of growth supression evasion in cancer

A

pRb and p53 mutations -> loss of contact inhibition
Corruption of TGF-beta promotes cacner

25
Q

What is an exmaple of a cancer caused by defective RB1 gene

A

Retinoblastoma - inherited Ch13 TB1 mutation
Rb - cell cycle is continious - no pause

Also small cell lung cancer

26
Q

How does p53 work

A

Increases p21 protein which causes cell arrest

27
Q

What pathway mutations can help predict response to chemotherapy

A

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
Q

What protein allows cell to cell adhesions

A

Integrin - sits across cell membrane layer

29
Q

Why want to give cell adhesion disrupting drug prior to cehmo

A

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
Q

What drugs can cause arrest in G2

A

Vinca alkaloids
Taxanes
Target microtubules

31
Q

Combrestatin MOA

A

Targets microfibrin
Interrupts blood supply to tumour as epithelial cells -> shape change due to microtubules

32
Q

How does cancer resist cell death

A
33
Q

What can change how a ligand signals

A

Environement that cell is in eg hypoxic etc
Heterodimers
Receptors on different cells

34
Q

Why is li fraumeni only heterogenous

A

Homogenous is lethal in utero

35
Q

How is li fraumeni syndrome characterised

A

Premenopausal breast cancer
Childhood sarcoma
Brain tumours
Leukaemia and lymphoma
Adrenocortical carconoma

36
Q

What causes li farumeni syndrme

A

TP53 germline mutation in chromosome 17
autosomal dominant
50% penetrance by 50 years old

37
Q

What are telomeres

A

Multiple tandem hexanucleotide repeats
Shorten progressively - cells can no longer replicate eventually

38
Q

How do cancer cells become immortal

A

Telomerase action to restore telomere length

39
Q

What is sorefanib

A

Tyrosine kinase inhibitor

40
Q

What is bevacizumab

A

Monoclonal antibody for VEGF - inhibiting

41
Q

What protein is utilised by cancer for metastasis

A

E-cadherin
Downregulating e-cadherin may stop metastasis happening

42
Q

Why are acquired mutations os much more likely in cancer

A

Cancer cells increased rate of mutation - accelerated by compromising surveillance systems for genomic integrity

43
Q

What genes are required to repair DNA

A

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
Q

MOA of PARPis and why most effective in BRCA/PALB2 + tumours

A

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
Q

What can determine whether a patient will repsond to platinum therapy

A

Whether they have previously responded to carboplatin

46
Q

How can tumour inflammation aid a cancer

A

Cytokines ->
Proliferation
Pro angiogenesis
Anti apoptotic

47
Q

Cascade effect

A

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
Q

Oxygenation of cancer tumours

A

Hypoxic - can use both anaerobic and aerobic glycosis in both environments

49
Q

What ligands are found on cytotoxic T lymphocytes and dendritic cells that recognise cancer as foreing

A

PD1 and PDL1

Cancer can switch them off

50
Q

What is ataxia telagniectasia

A

Defect in ATM gene
25% lifetime rik of cancer esp haem cancer
apraxia and slurring of speech and swallowing problems

51
Q

What cancer stage choose if in doubt

A

Less advanced category

52
Q

Staging geographical location

A

Stage I+II - localised to orgna of origin
III - locally extensive spread - lymph nodes
IV - distant mets

Cancer (22 decks)

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