Biological Flashcards

1
Q

Currrnt approaches for angiogenesis

A

Antisense RNA - single oligo nucleotide that’s complementary to coding mRNA which hybridise so that it can’t be translated
Mab Avastin
VEGFR inhibitors - sunitinib, sorafenib
Activation of p53 TSG- p53 up reg anti angiogenic factor eg angiostatin, endostatin

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2
Q

Avastin is cytocidal or cytostatic agent, why

A

Cytostatic it limits tumour growth instead of killing it directly. It starve the tumour so takes long time to work

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3
Q

Novel therapies that target neo vasculature

A

1 vitaxin - mab against interin (like bind that links cell tgt)
2 thalidomide
3 ANET
4 direct cytotoxic drug eg adriamycin to EC
5 aflibercept VEGFR ligand binding domain fused w Ig (prevent VEGF binding)

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4
Q

Drugs that Destroy existing Tumour Vasculature

A

Combretastatin (colchicine) - destroy tubulin cytoskeleton

Nanoparticle technology- within it inhibitory drug

Particles contain proteasome inhibitor - bortezomib for trt of neuronlastoma

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5
Q

How is leukaemia diagnosed

A
  • milky blood
  • immature looking WBC
  • blood test (see all stages granulocyte differentiation)
  • increased Myeloid to erythroid ratio
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6
Q

What are the symptoms of CML

A

Fatigue
Anaemia
Splenimegally
Hepatomegly due to ex. WBC produced and broken up and accumulated there

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7
Q

What are the three clinical faces of CML

A

1 initial chronic phase -mild
2 accelerated phase
3 acute leukaemia phase - emergency

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8
Q

Advantages and disadvantages of tyrosine kinase inhibitor eg gefotinib

A

Block triggering of growth pathways
Orally active

Not specific
Want to dampen down not wipe off all act,

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9
Q

Advantages and disadvantages of monoclonal antibody eg avastin herceptin

A
Highly specific 
Cancer specific 
But prone to mutation Induced r 
Target extracellular only
Require IV
Expensive
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